PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
30157179-8	2018	There was a strong, positive correlation between the change in the absolute concentration of NAA and the change in the absolute concentration of tCr (p<0.001) suggesting an effect of tDCS.	N-acetylaspartate	93-96	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	145-148
29980225-4	2018	CONCLUSION: These findings suggested that EA is a potential therapeutic for ameliorate cognitive dysfunction, and it might be due to EA could improve NAA and Glu metabolism by upregulation of BDNF in APP/PS1 mice.	N-acetylaspartate	150-153	brain derived neurotrophic factor	Mus musculus	192-196
29859874-2	2018	Based on its unique tertiary structure, we explored the potential of NAA to modulate aggregation of amyloid-beta (Abeta) peptide 1-42 via multiple corroborating aggregation assays along with electron microscopy.	N-acetylaspartate	69-72	amyloid beta precursor protein	Homo sapiens	114-119
29859874-3	2018	Thioflavin-T fluorescence assay demonstrated that at physiological concentrations, NAA substantially inhibited the initiation of Abeta fibril formation.	N-acetylaspartate	83-86	amyloid beta precursor protein	Homo sapiens	129-134
29859874-6	2018	Furthermore, fluorescence correlation spectroscopy and dynamic light scattering measurements confirmed significant reductions in Abeta fibril hydrodynamic radius following treatment with NAA.	N-acetylaspartate	187-190	amyloid beta precursor protein	Homo sapiens	129-134
29745082-13	2018	Cho/NAA and Cho/Cr in the tumor were positively correlated with p53 in the tumor, but negatively correlated with PTEN in the tumor.	N-acetylaspartate	4-7	tumor protein p53	Homo sapiens	64-67
29438199-9	2018	A greater increase in frontal grey matter N-acetyl aspartate/creatine ratio was observed in Arm1 [ratio change of 0.071 (SD 0.16)] versus Arm2 [change -0.097 (SD 0.18), P = 0.009], although this was not associated with changes in cognitive function (P = 0.17).	N-acetylaspartate	42-60	ADRM1 26S proteasome ubiquitin receptor	Homo sapiens	92-96
29438199-9	2018	A greater increase in frontal grey matter N-acetyl aspartate/creatine ratio was observed in Arm1 [ratio change of 0.071 (SD 0.16)] versus Arm2 [change -0.097 (SD 0.18), P = 0.009], although this was not associated with changes in cognitive function (P = 0.17).	N-acetylaspartate	42-60	Jupiter microtubule associated homolog 1	Homo sapiens	138-142
29438199-11	2018	Greater improvement in neuronal metabolites (N-acetyl aspartate/creatine) was observed with standard ART.	N-acetylaspartate	45-63	artemin	Homo sapiens	101-104
29456021-2	2018	ASPA encodes aspartoacylase, an oligodendroglial enzyme that cleaves the abundant brain amino acid N-acetyl-L-aspartate (NAA) to L-aspartate and acetate.	N-acetylaspartate	99-119	aspartoacylase	Mus musculus	0-4
29456021-2	2018	ASPA encodes aspartoacylase, an oligodendroglial enzyme that cleaves the abundant brain amino acid N-acetyl-L-aspartate (NAA) to L-aspartate and acetate.	N-acetylaspartate	121-124	aspartoacylase	Mus musculus	0-4
29456021-4	2018	Prior studies showed that homozygous constitutive knockout of Nat8l, the gene encoding the neuronal NAA synthesizing enzyme N-acetyltransferase 8-like, prevents aspartoacylase-deficient mice from developing spongiform leukodystrophy.	N-acetylaspartate	100-103	N-acetyltransferase 8-like	Mus musculus	62-67
29456021-4	2018	Prior studies showed that homozygous constitutive knockout of Nat8l, the gene encoding the neuronal NAA synthesizing enzyme N-acetyltransferase 8-like, prevents aspartoacylase-deficient mice from developing spongiform leukodystrophy.	N-acetylaspartate	100-103	N-acetyltransferase 8-like	Mus musculus	124-150
29341105-10	2018	Distinct concentration variations for glutamine, glutamate, and N-acetylaspartate (NAA) were observed between HS1 and HS2.	N-acetylaspartate	64-81	eukaryotic translation elongation factor 1 alpha 2	Homo sapiens	110-113
29341105-10	2018	Distinct concentration variations for glutamine, glutamate, and N-acetylaspartate (NAA) were observed between HS1 and HS2.	N-acetylaspartate	64-81	spectrin beta, erythrocytic	Homo sapiens	118-121
29341105-10	2018	Distinct concentration variations for glutamine, glutamate, and N-acetylaspartate (NAA) were observed between HS1 and HS2.	N-acetylaspartate	83-86	eukaryotic translation elongation factor 1 alpha 2	Homo sapiens	110-113
29341105-10	2018	Distinct concentration variations for glutamine, glutamate, and N-acetylaspartate (NAA) were observed between HS1 and HS2.	N-acetylaspartate	83-86	spectrin beta, erythrocytic	Homo sapiens	118-121
28334553-1	2017	A multi-matrix hydrophilic interaction liquid chromatography tandem mass spectrometric method (HILIC-MS/MS) was developed for the quantitation of N-Acetyl Aspartic acid (NAA) using stable isotope labeled internal standard, D3-NAA in various biological matrices such as human plasma, human CSF, mouse plasma, brain and spinal cord.	N-acetylaspartate	146-168	colony stimulating factor 2	Homo sapiens	289-292
29116375-8	2018	In fact, in transgenic mice overexpressing the NAA synthesising enzyme Nat8l in neurons, supra-physiological NAA levels were uncoupled from neurological deficits.	N-acetylaspartate	47-50	N-acetyltransferase 8-like	Mus musculus	71-76
29116375-8	2018	In fact, in transgenic mice overexpressing the NAA synthesising enzyme Nat8l in neurons, supra-physiological NAA levels were uncoupled from neurological deficits.	N-acetylaspartate	109-112	N-acetyltransferase 8-like	Mus musculus	71-76
29336203-6	2018	There were positive correlations between Lip09a/tCr and myo-inositol/tCr, between Lip13a/tCr and N-acetylaspartate (NAA)/tCr, and between Lip09/tCr and NAA/tCr in healthy controls.	N-acetylaspartate	97-114	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	82-92
29336203-6	2018	There were positive correlations between Lip09a/tCr and myo-inositol/tCr, between Lip13a/tCr and N-acetylaspartate (NAA)/tCr, and between Lip09/tCr and NAA/tCr in healthy controls.	N-acetylaspartate	116-119	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	82-92
29310864-5	2018	Abeta (beta = 0.45, p = 0.018) and white matter hyperintensities (beta = 0.40, p = 0.046) were independently and interactively (beta = -0.49, p = 0.026) associated with a higher ratio of mI over NAA (mI/NAA) in the posterior cingulate and precuneus gray matter but not in the white matter.	N-acetylaspartate	195-198	amyloid beta precursor protein	Homo sapiens	0-5
29310864-5	2018	Abeta (beta = 0.45, p = 0.018) and white matter hyperintensities (beta = 0.40, p = 0.046) were independently and interactively (beta = -0.49, p = 0.026) associated with a higher ratio of mI over NAA (mI/NAA) in the posterior cingulate and precuneus gray matter but not in the white matter.	N-acetylaspartate	203-206	amyloid beta precursor protein	Homo sapiens	0-5
29020418-3	2017	Shati/Nat8l synthesizes N-acetylaspartate from L-aspartate and acetyl-coenzyme A.	N-acetylaspartate	24-41	N-acetyltransferase 8-like	Mus musculus	0-5
29020418-3	2017	Shati/Nat8l synthesizes N-acetylaspartate from L-aspartate and acetyl-coenzyme A.	N-acetylaspartate	24-41	N-acetyltransferase 8-like	Mus musculus	6-11
29020418-4	2017	Further, N-acetylaspartate is converted into N-acetylaspartylglutamate, a neurotransmitter for metabotropic glutamate receptor 3.	N-acetylaspartate	9-26	glutamate receptor, metabotropic 3	Mus musculus	95-128
29020418-9	2017	Furthermore, the metabolism of N-acetylaspartate to N-acetylaspartylglutamate was decreased in the dorsal striatum of the dS-Shati/Nat8l mice.	N-acetylaspartate	31-48	N-acetyltransferase 8-like	Mus musculus	125-130
29020418-9	2017	Furthermore, the metabolism of N-acetylaspartate to N-acetylaspartylglutamate was decreased in the dorsal striatum of the dS-Shati/Nat8l mice.	N-acetylaspartate	31-48	N-acetyltransferase 8-like	Mus musculus	131-136
28879565-1	2017	Aspartoacylase (ASPA) is a zinc-dependent abundant enzyme in the brain, which catalyzes the conversion of N-acetyl aspartate (NAA) into acetate and aspartate.	N-acetylaspartate	106-124	aspartoacylase	Homo sapiens	0-14
28879565-1	2017	Aspartoacylase (ASPA) is a zinc-dependent abundant enzyme in the brain, which catalyzes the conversion of N-acetyl aspartate (NAA) into acetate and aspartate.	N-acetylaspartate	106-124	aspartoacylase	Homo sapiens	16-20
28879565-1	2017	Aspartoacylase (ASPA) is a zinc-dependent abundant enzyme in the brain, which catalyzes the conversion of N-acetyl aspartate (NAA) into acetate and aspartate.	N-acetylaspartate	126-129	aspartoacylase	Homo sapiens	0-14
28879565-1	2017	Aspartoacylase (ASPA) is a zinc-dependent abundant enzyme in the brain, which catalyzes the conversion of N-acetyl aspartate (NAA) into acetate and aspartate.	N-acetylaspartate	126-129	aspartoacylase	Homo sapiens	16-20
28334553-1	2017	A multi-matrix hydrophilic interaction liquid chromatography tandem mass spectrometric method (HILIC-MS/MS) was developed for the quantitation of N-Acetyl Aspartic acid (NAA) using stable isotope labeled internal standard, D3-NAA in various biological matrices such as human plasma, human CSF, mouse plasma, brain and spinal cord.	N-acetylaspartate	170-173	colony stimulating factor 2	Homo sapiens	289-292
28334553-10	2017	NAA CSF levels in control human subjects (73.3+-31.0ng/mL,N=10) were found to be slightly higher than ALS patients (46.1+-22.6ng/mL, N=10) (P=0.04).	N-acetylaspartate	0-3	colony stimulating factor 2	Homo sapiens	4-7
28626388-1	2017	Canavan disease is caused by mutations in the gene encoding aspartoacylase (ASPA), a deacetylase that catabolizes N-acetylaspartate (NAA).	N-acetylaspartate	114-131	aspartoacylase	Mus musculus	60-74
28626388-1	2017	Canavan disease is caused by mutations in the gene encoding aspartoacylase (ASPA), a deacetylase that catabolizes N-acetylaspartate (NAA).	N-acetylaspartate	114-131	aspartoacylase	Mus musculus	76-80
28626388-1	2017	Canavan disease is caused by mutations in the gene encoding aspartoacylase (ASPA), a deacetylase that catabolizes N-acetylaspartate (NAA).	N-acetylaspartate	133-136	aspartoacylase	Mus musculus	60-74
28626388-1	2017	Canavan disease is caused by mutations in the gene encoding aspartoacylase (ASPA), a deacetylase that catabolizes N-acetylaspartate (NAA).	N-acetylaspartate	133-136	aspartoacylase	Mus musculus	76-80
28626388-5	2017	This treatment increased NAA levels in the brain to those observed in the brains of Nur7 mice, an established model of Canavan disease.	N-acetylaspartate	25-28	aspartoacylase	Mus musculus	84-88
28626388-10	2017	These results show that ASPA expression prevents the pathologies associated with excessive NAA concentrations in the brain during postnatal myelination.	N-acetylaspartate	91-94	aspartoacylase	Mus musculus	24-28
28235644-0	2017	Down-regulation of the mitochondrial aspartate-glutamate carrier isoform 1 AGC1 inhibits proliferation and N-acetylaspartate synthesis in Neuro2A cells.	N-acetylaspartate	107-124	solute carrier family 25 member 12	Homo sapiens	75-79
28235644-3	2017	Defects in the AGC1 gene cause AGC1 deficiency, an infantile encephalopathy with delayed myelination and reduced brain N-acetylaspartate (NAA) levels, the precursor of myelin synthesis in the CNS.	N-acetylaspartate	119-136	solute carrier family 25 member 12	Homo sapiens	15-19
28235644-3	2017	Defects in the AGC1 gene cause AGC1 deficiency, an infantile encephalopathy with delayed myelination and reduced brain N-acetylaspartate (NAA) levels, the precursor of myelin synthesis in the CNS.	N-acetylaspartate	138-141	solute carrier family 25 member 12	Homo sapiens	15-19
28194442-1	2017	Canavan disease (CD) is a debilitating and lethal leukodystrophy caused by mutations in the aspartoacylase (ASPA) gene and the resulting defect in N-acetylaspartate (NAA) metabolism in the CNS and peripheral tissues.	N-acetylaspartate	147-164	cathepsin D	Mus musculus	17-19
28253907-8	2017	Time-matched (acquired within 5 h of each other) serum cytokine and MRS showed correlations between Lac/NAA and serum IL-1beta and IL-10 (all p < 0.01).	N-acetylaspartate	104-107	interleukin 1 beta	Homo sapiens	118-126
28319198-3	2017	We recently found that Shati/Nat8L overexpression in NAc regulates the dopaminergic neuronal system via the activation of group II mGluRs by elevated N-acetylaspartylglutamate following N-acetylaspartate increase due to the overexpression.	N-acetylaspartate	186-203	N-acetyltransferase 8-like	Mus musculus	23-28
28319198-3	2017	We recently found that Shati/Nat8L overexpression in NAc regulates the dopaminergic neuronal system via the activation of group II mGluRs by elevated N-acetylaspartylglutamate following N-acetylaspartate increase due to the overexpression.	N-acetylaspartate	186-203	N-acetyltransferase 8-like	Mus musculus	29-34
28194442-1	2017	Canavan disease (CD) is a debilitating and lethal leukodystrophy caused by mutations in the aspartoacylase (ASPA) gene and the resulting defect in N-acetylaspartate (NAA) metabolism in the CNS and peripheral tissues.	N-acetylaspartate	147-164	aspartoacylase	Mus musculus	108-112
28194442-1	2017	Canavan disease (CD) is a debilitating and lethal leukodystrophy caused by mutations in the aspartoacylase (ASPA) gene and the resulting defect in N-acetylaspartate (NAA) metabolism in the CNS and peripheral tissues.	N-acetylaspartate	166-169	cathepsin D	Mus musculus	17-19
28194442-1	2017	Canavan disease (CD) is a debilitating and lethal leukodystrophy caused by mutations in the aspartoacylase (ASPA) gene and the resulting defect in N-acetylaspartate (NAA) metabolism in the CNS and peripheral tissues.	N-acetylaspartate	166-169	aspartoacylase	Mus musculus	108-112
27531131-1	2017	Canavan disease (CD) is a rare fatal childhood neurological autosomal recessive genetic disease caused by mutations in the ASPA gene, which lead to catalytic deficiency of the ASPA enzyme, which catalyzes the hydrolysis of N-acetyl-L-aspartate (NAA) into aspartate and acetate.	N-acetylaspartate	223-243	aspartoacylase	Homo sapiens	123-127
27531131-1	2017	Canavan disease (CD) is a rare fatal childhood neurological autosomal recessive genetic disease caused by mutations in the ASPA gene, which lead to catalytic deficiency of the ASPA enzyme, which catalyzes the hydrolysis of N-acetyl-L-aspartate (NAA) into aspartate and acetate.	N-acetylaspartate	223-243	aspartoacylase	Homo sapiens	176-180
27531131-1	2017	Canavan disease (CD) is a rare fatal childhood neurological autosomal recessive genetic disease caused by mutations in the ASPA gene, which lead to catalytic deficiency of the ASPA enzyme, which catalyzes the hydrolysis of N-acetyl-L-aspartate (NAA) into aspartate and acetate.	N-acetylaspartate	245-248	aspartoacylase	Homo sapiens	123-127
27531131-1	2017	Canavan disease (CD) is a rare fatal childhood neurological autosomal recessive genetic disease caused by mutations in the ASPA gene, which lead to catalytic deficiency of the ASPA enzyme, which catalyzes the hydrolysis of N-acetyl-L-aspartate (NAA) into aspartate and acetate.	N-acetylaspartate	245-248	aspartoacylase	Homo sapiens	176-180
27129239-0	2016	RhoC GTPase Is a Potent Regulator of Glutamine Metabolism and N-Acetylaspartate Production in Inflammatory Breast Cancer Cells.	N-acetylaspartate	62-79	ras homolog family member C	Homo sapiens	0-11
28077719-2	2017	The lack of functional ASPA, an enzyme enriched in oligodendroglia that cleaves N-acetyl-l-aspartate (NAA) to acetate and l-aspartic acid, elevates brain NAA and causes "spongiform" vacuolation of superficial brain white matter and neighboring gray matter.	N-acetylaspartate	80-100	aspartoacylase	Mus musculus	23-27
28077719-2	2017	The lack of functional ASPA, an enzyme enriched in oligodendroglia that cleaves N-acetyl-l-aspartate (NAA) to acetate and l-aspartic acid, elevates brain NAA and causes "spongiform" vacuolation of superficial brain white matter and neighboring gray matter.	N-acetylaspartate	102-105	aspartoacylase	Mus musculus	23-27
28077719-2	2017	The lack of functional ASPA, an enzyme enriched in oligodendroglia that cleaves N-acetyl-l-aspartate (NAA) to acetate and l-aspartic acid, elevates brain NAA and causes "spongiform" vacuolation of superficial brain white matter and neighboring gray matter.	N-acetylaspartate	154-157	aspartoacylase	Mus musculus	23-27
28077719-7	2017	This neuronal pathology is prevented by constitutive disruption of Nat8l, which encodes the neuronal NAA-synthetic enzyme N-acetyltransferase-8-like.	N-acetylaspartate	101-104	N-acetyltransferase 8-like	Mus musculus	67-72
28077719-7	2017	This neuronal pathology is prevented by constitutive disruption of Nat8l, which encodes the neuronal NAA-synthetic enzyme N-acetyltransferase-8-like.	N-acetylaspartate	101-104	N-acetyltransferase 8-like	Mus musculus	122-148
27709268-2	2017	NAA is synthesized in neurons by the enzyme N-acetyltransferase-8-like (NAT8L) and broken down in oligodendrocytes by aspartoacylase (ASPA) into acetate and aspartate.	N-acetylaspartate	0-3	N-acetyltransferase 8-like	Mus musculus	44-70
27709268-2	2017	NAA is synthesized in neurons by the enzyme N-acetyltransferase-8-like (NAT8L) and broken down in oligodendrocytes by aspartoacylase (ASPA) into acetate and aspartate.	N-acetylaspartate	0-3	N-acetyltransferase 8-like	Mus musculus	72-77
27709268-2	2017	NAA is synthesized in neurons by the enzyme N-acetyltransferase-8-like (NAT8L) and broken down in oligodendrocytes by aspartoacylase (ASPA) into acetate and aspartate.	N-acetylaspartate	0-3	aspartoacylase	Mus musculus	134-138
26650045-5	2016	However, reliable PLS-DA models can be developed between control and PD groups as well as between PD and bFGF groups, which is attributed to changes in a series of metabolites including GABA, glutamate (Glu), glutamine (Gln), lactate, N-acetylaspartate, creatine, taurine, and myo-inositol.	N-acetylaspartate	235-252	fibroblast growth factor 2	Rattus norvegicus	105-109
27288788-3	2016	The physiological role of ASPA is to hydrolyse N-acetyl-l-aspartic acid (NAA), producing l-aspartic acid and acetate; as a result, its deficiency leads to abnormally high central nervous system NAA levels.	N-acetylaspartate	47-71	aspartoacylase	Homo sapiens	26-30
27288788-3	2016	The physiological role of ASPA is to hydrolyse N-acetyl-l-aspartic acid (NAA), producing l-aspartic acid and acetate; as a result, its deficiency leads to abnormally high central nervous system NAA levels.	N-acetylaspartate	73-76	aspartoacylase	Homo sapiens	26-30
27288788-3	2016	The physiological role of ASPA is to hydrolyse N-acetyl-l-aspartic acid (NAA), producing l-aspartic acid and acetate; as a result, its deficiency leads to abnormally high central nervous system NAA levels.	N-acetylaspartate	194-197	aspartoacylase	Homo sapiens	26-30
27089868-3	2016	The method, called HERMES (Hadamard Encoding and Reconstruction of MEGA-Edited Spectroscopy), was optimized to detect NAA and NAAG simultaneously using density-matrix simulations and validated in phantoms at 3T.	N-acetylaspartate	118-121	RNA binding protein, mRNA processing factor	Homo sapiens	19-25
27129239-5	2016	We also report that the oncogene RhoC, a driver of metastatic potential, modulates glutamine and N-acetylaspartate metabolism in IBC cells in vitro, revealing a novel role for RhoC as a regulator of tumor cell metabolism that extends beyond its well known role in cytoskeletal rearrangement.	N-acetylaspartate	97-114	ras homolog family member C	Homo sapiens	33-37
27129239-5	2016	We also report that the oncogene RhoC, a driver of metastatic potential, modulates glutamine and N-acetylaspartate metabolism in IBC cells in vitro, revealing a novel role for RhoC as a regulator of tumor cell metabolism that extends beyond its well known role in cytoskeletal rearrangement.	N-acetylaspartate	97-114	ras homolog family member C	Homo sapiens	176-180
26959509-7	2016	The CD4/CD8 ratio at baseline correlated with N-acetyl-aspartate (r = 0.56, P = 0.003) and choline (r = 0.36, P = 0.03) at 5 years, irrespective of treatment regimen and ART interruption.	N-acetylaspartate	46-64	CD4 molecule	Homo sapiens	4-7
26959509-7	2016	The CD4/CD8 ratio at baseline correlated with N-acetyl-aspartate (r = 0.56, P = 0.003) and choline (r = 0.36, P = 0.03) at 5 years, irrespective of treatment regimen and ART interruption.	N-acetylaspartate	46-64	CD8a molecule	Homo sapiens	8-11
26526126-5	2016	LCModel was used in analyzing the spectra to measure the levels of N-Acetyl aspartate (NAA), choline (Cho), creatine (Cr), and glutamate/glutamine (Glx) in dACC and PCC.	N-acetylaspartate	67-85	Acetyl-CoA carboxylase	Drosophila melanogaster	156-160
26526126-8	2016	A reduction in NAA/Cr in dACC was found in ASD participants, compared to their TD peers.	N-acetylaspartate	15-18	Acetyl-CoA carboxylase	Drosophila melanogaster	25-29
27338073-8	2016	RESULTS: The levels of NAA, Cr, and Cho in the PFC and ACC of patients with the SNAP-25 Ddel and Mnll polymorphism genotypes did not significantly differ before and after the administration of MPH.	N-acetylaspartate	23-26	synaptosome associated protein 25	Homo sapiens	80-87
27338073-9	2016	However, in patients with the SNAP-25 Ddel polymorphism T/T genotype and the Mnll polymorphism G/G genotype, there was a significant increase in NAA levels in the ACC after MPH treatment compared with before MPH treatment.	N-acetylaspartate	145-148	synaptosome associated protein 25	Homo sapiens	30-37
27338073-9	2016	However, in patients with the SNAP-25 Ddel polymorphism T/T genotype and the Mnll polymorphism G/G genotype, there was a significant increase in NAA levels in the ACC after MPH treatment compared with before MPH treatment.	N-acetylaspartate	145-148	NADH:ubiquinone oxidoreductase subunit B1	Homo sapiens	77-81
27338073-10	2016	CONCLUSION: The present results suggest that the SNAP-25 Ddel and Mnll polymorphisms might be associated with MPH-related changes in NAA levels in the ACC.	N-acetylaspartate	133-136	synaptosome associated protein 25	Homo sapiens	49-56
27338073-10	2016	CONCLUSION: The present results suggest that the SNAP-25 Ddel and Mnll polymorphisms might be associated with MPH-related changes in NAA levels in the ACC.	N-acetylaspartate	133-136	NADH:ubiquinone oxidoreductase subunit B1	Homo sapiens	66-70
26853538-9	2016	CONCLUSIONS: This study extends the literature by demonstrating inverse associations between recent heavy drinking and dACC glutamate and NAA concentrations in a sample of nonsevere, non-treatment-seeking individuals with AD.	N-acetylaspartate	138-141	Acetyl-CoA carboxylase	Drosophila melanogaster	119-123
26656908-3	2016	Separate measurement of NAA and NAAG using MRS is difficult due to large superposition of their spectra.	N-acetylaspartate	24-27	MROS	Homo sapiens	43-46
26586007-8	2016	Classical elevation of NAA in brain and urine was present and genetic analysis identified mutations in the ASPA gene.	N-acetylaspartate	23-26	aspartoacylase	Homo sapiens	107-111
26797702-1	2016	Aspartoacylase (ASPA) is an abundant enzyme in the brain, which catalyzes the conversion of N-acetylaspartate into acetate and aspartate, deficiency in its activity leads to degeneration of the white matter of the brain and is a recognized cause of Canavan disease (CD), which affect children.	N-acetylaspartate	92-109	aspartoacylase	Homo sapiens	0-14
26797702-1	2016	Aspartoacylase (ASPA) is an abundant enzyme in the brain, which catalyzes the conversion of N-acetylaspartate into acetate and aspartate, deficiency in its activity leads to degeneration of the white matter of the brain and is a recognized cause of Canavan disease (CD), which affect children.	N-acetylaspartate	92-109	aspartoacylase	Homo sapiens	16-20
27089954-1	2016	The complete catalytic cycle of aspartoacylase (ASPA), a zinc-dependent enzyme responsible for cleavage of N-acetyl-l-aspartate, is characterized by the methods of molecular modeling.	N-acetylaspartate	107-127	aspartoacylase	Homo sapiens	32-46
27089954-1	2016	The complete catalytic cycle of aspartoacylase (ASPA), a zinc-dependent enzyme responsible for cleavage of N-acetyl-l-aspartate, is characterized by the methods of molecular modeling.	N-acetylaspartate	107-127	aspartoacylase	Homo sapiens	48-52
27036033-6	2016	Moreover, NAA-treated SH-SY5Y cells exhibited morphological changes accompanied with increase of the neurogenic markers TH and MAP2 and down-regulation of the pluripotency markers OCT4 and CXCR4/CD184.	N-acetylaspartate	10-13	microtubule associated protein 2	Homo sapiens	127-131
27036033-6	2016	Moreover, NAA-treated SH-SY5Y cells exhibited morphological changes accompanied with increase of the neurogenic markers TH and MAP2 and down-regulation of the pluripotency markers OCT4 and CXCR4/CD184.	N-acetylaspartate	10-13	POU class 5 homeobox 1	Homo sapiens	180-184
27036033-6	2016	Moreover, NAA-treated SH-SY5Y cells exhibited morphological changes accompanied with increase of the neurogenic markers TH and MAP2 and down-regulation of the pluripotency markers OCT4 and CXCR4/CD184.	N-acetylaspartate	10-13	C-X-C motif chemokine receptor 4	Homo sapiens	189-194
27036033-6	2016	Moreover, NAA-treated SH-SY5Y cells exhibited morphological changes accompanied with increase of the neurogenic markers TH and MAP2 and down-regulation of the pluripotency markers OCT4 and CXCR4/CD184.	N-acetylaspartate	10-13	C-X-C motif chemokine receptor 4	Homo sapiens	195-200
27110360-7	2016	Starting without a priori knowledge, we detect metabolic flux changes, leading to an increased glutamine contribution to acetyl-CoA production, reveal biosynthesis of N-acetylaspartate by N-acetyltransferase 8-like (NAT8L) in lung cancer cells and show that NAT8L silencing inhibits proliferation of A549, JHH-4, PH5CH8, and BEAS-2B cells.	N-acetylaspartate	167-184	N-acetyltransferase 8 like	Homo sapiens	188-214
27110360-7	2016	Starting without a priori knowledge, we detect metabolic flux changes, leading to an increased glutamine contribution to acetyl-CoA production, reveal biosynthesis of N-acetylaspartate by N-acetyltransferase 8-like (NAT8L) in lung cancer cells and show that NAT8L silencing inhibits proliferation of A549, JHH-4, PH5CH8, and BEAS-2B cells.	N-acetylaspartate	167-184	N-acetyltransferase 8 like	Homo sapiens	216-221
27110360-7	2016	Starting without a priori knowledge, we detect metabolic flux changes, leading to an increased glutamine contribution to acetyl-CoA production, reveal biosynthesis of N-acetylaspartate by N-acetyltransferase 8-like (NAT8L) in lung cancer cells and show that NAT8L silencing inhibits proliferation of A549, JHH-4, PH5CH8, and BEAS-2B cells.	N-acetylaspartate	167-184	N-acetyltransferase 8 like	Homo sapiens	258-263
27045997-8	2016	Combinations of approaches to increase intracellular NAA levels showed additive effects on lipolysis and gene repression, nearly abolishing the expression of Ucp1, Cidea, Prdm16, and Ppara.	N-acetylaspartate	53-56	uncoupling protein 1	Homo sapiens	158-162
27045997-8	2016	Combinations of approaches to increase intracellular NAA levels showed additive effects on lipolysis and gene repression, nearly abolishing the expression of Ucp1, Cidea, Prdm16, and Ppara.	N-acetylaspartate	53-56	cell death inducing DFFA like effector a	Homo sapiens	164-169
27045997-8	2016	Combinations of approaches to increase intracellular NAA levels showed additive effects on lipolysis and gene repression, nearly abolishing the expression of Ucp1, Cidea, Prdm16, and Ppara.	N-acetylaspartate	53-56	PR/SET domain 16	Homo sapiens	171-177
27045997-8	2016	Combinations of approaches to increase intracellular NAA levels showed additive effects on lipolysis and gene repression, nearly abolishing the expression of Ucp1, Cidea, Prdm16, and Ppara.	N-acetylaspartate	53-56	peroxisome proliferator activated receptor alpha	Homo sapiens	183-188
25925982-7	2015	RESULTS: Among all 13 FMR1 premutation carriers, significant correlations were found between N-acetyl aspartate/creatine and choline/creatine in the MCP and COWAT scores, and between FA in the genu and performance on the Behavioral Dyscontrol Scale, COWAT, and Symbol Digit Modalities Test; a correlation was also found between FA in the splenium and COWAT performance.	N-acetylaspartate	93-111	fragile X messenger ribonucleoprotein 1	Homo sapiens	22-26
26361739-0	2015	Deletion of SHATI/NAT8L decreases the N-acetylaspartate content in the brain and induces behavioral deficits, which can be ameliorated by administering N-acetylaspartate.	N-acetylaspartate	38-55	N-acetyltransferase 8-like	Mus musculus	12-17
26361739-0	2015	Deletion of SHATI/NAT8L decreases the N-acetylaspartate content in the brain and induces behavioral deficits, which can be ameliorated by administering N-acetylaspartate.	N-acetylaspartate	38-55	N-acetyltransferase 8-like	Mus musculus	18-23
26361739-0	2015	Deletion of SHATI/NAT8L decreases the N-acetylaspartate content in the brain and induces behavioral deficits, which can be ameliorated by administering N-acetylaspartate.	N-acetylaspartate	152-169	N-acetyltransferase 8-like	Mus musculus	12-17
26361739-0	2015	Deletion of SHATI/NAT8L decreases the N-acetylaspartate content in the brain and induces behavioral deficits, which can be ameliorated by administering N-acetylaspartate.	N-acetylaspartate	152-169	N-acetyltransferase 8-like	Mus musculus	18-23
26361739-2	2015	Recently, it has been reported that SHATI might function as an aspartate N-acetyltransferase, which synthesizes N-acetylaspartate (NAA) in vitro.	N-acetylaspartate	112-129	N-acetyltransferase 8-like	Mus musculus	36-41
26361739-2	2015	Recently, it has been reported that SHATI might function as an aspartate N-acetyltransferase, which synthesizes N-acetylaspartate (NAA) in vitro.	N-acetylaspartate	112-129	N-acetyltransferase 8-like	Mus musculus	63-92
26361739-2	2015	Recently, it has been reported that SHATI might function as an aspartate N-acetyltransferase, which synthesizes N-acetylaspartate (NAA) in vitro.	N-acetylaspartate	131-134	N-acetyltransferase 8-like	Mus musculus	36-41
26361739-2	2015	Recently, it has been reported that SHATI might function as an aspartate N-acetyltransferase, which synthesizes N-acetylaspartate (NAA) in vitro.	N-acetylaspartate	131-134	N-acetyltransferase 8-like	Mus musculus	63-92
26361739-3	2015	However, whether SHATI actually synthesizes NAA in vivo in the brain is still unclear.	N-acetylaspartate	44-47	N-acetyltransferase 8-like	Mus musculus	17-22
26361739-4	2015	In this study, we found that both Shati-deleted mice showed significantly lower NAA levels in all brain areas than wild-type (Shati(+/+)) mice using HPLC and fluorescence detection, suggesting that SHATI regulates NAA content in the brain.	N-acetylaspartate	80-83	N-acetyltransferase 8-like	Mus musculus	34-39
26361739-4	2015	In this study, we found that both Shati-deleted mice showed significantly lower NAA levels in all brain areas than wild-type (Shati(+/+)) mice using HPLC and fluorescence detection, suggesting that SHATI regulates NAA content in the brain.	N-acetylaspartate	80-83	N-acetyltransferase 8-like	Mus musculus	198-203
26361739-4	2015	In this study, we found that both Shati-deleted mice showed significantly lower NAA levels in all brain areas than wild-type (Shati(+/+)) mice using HPLC and fluorescence detection, suggesting that SHATI regulates NAA content in the brain.	N-acetylaspartate	214-217	N-acetyltransferase 8-like	Mus musculus	34-39
26361739-4	2015	In this study, we found that both Shati-deleted mice showed significantly lower NAA levels in all brain areas than wild-type (Shati(+/+)) mice using HPLC and fluorescence detection, suggesting that SHATI regulates NAA content in the brain.	N-acetylaspartate	214-217	N-acetyltransferase 8-like	Mus musculus	198-203
26511242-9	2015	In contrast, Aspa(nur7/nur7) mice with only one intact Nat8L allele accumulated less NAA, developed a less severe pathology, phenotypic improvements, and, importantly, an almost normal survival time.	N-acetylaspartate	85-88	aspartoacylase	Mus musculus	13-17
26511242-9	2015	In contrast, Aspa(nur7/nur7) mice with only one intact Nat8L allele accumulated less NAA, developed a less severe pathology, phenotypic improvements, and, importantly, an almost normal survival time.	N-acetylaspartate	85-88	aspartoacylase	Mus musculus	18-22
26511242-9	2015	In contrast, Aspa(nur7/nur7) mice with only one intact Nat8L allele accumulated less NAA, developed a less severe pathology, phenotypic improvements, and, importantly, an almost normal survival time.	N-acetylaspartate	85-88	N-acetyltransferase 8-like	Mus musculus	55-60
26132508-0	2015	In vivo topical application of acetyl aspartic acid increases fibrillin-1 and collagen IV deposition leading to a significant improvement of skin firmness.	N-acetylaspartate	31-51	fibrillin 1	Homo sapiens	62-73
25872793-2	2015	In the nervous system, glia-bound GCPII mediates the hydrolysis of the neurotransmitter N-acetylaspartylglutamate (NAAG) into glutamate and N-acetylaspartate.	N-acetylaspartate	140-157	folate hydrolase 1	Mus musculus	34-39
26341904-4	2016	Both sexes showed negative correlations between alexithymia and N-acetylaspartate (NAA) in pregenual ACC (pgACC).	N-acetylaspartate	64-81	Acetyl-CoA carboxylase	Drosophila melanogaster	101-104
26341904-4	2016	Both sexes showed negative correlations between alexithymia and N-acetylaspartate (NAA) in pregenual ACC (pgACC).	N-acetylaspartate	83-86	Acetyl-CoA carboxylase	Drosophila melanogaster	101-104
26341904-5	2016	Women showed a robust negative correlation of the joint measure of glutamate and glutamine (Glx) to NAA in posterior cingulate cortex (PCC), whereas men showed a weak positive association of Glx to NAA in dorsal ACC (dACC).	N-acetylaspartate	198-201	Acetyl-CoA carboxylase	Drosophila melanogaster	212-215
26819345-7	2016	RESULTS: Patients with high levels of tumoral NAA and its biosynthetic enzyme, aspartate N-acetyltransferase (NAT8L), had worse overall survival than patients with low levels of NAA and NAT8L.	N-acetylaspartate	46-49	N-acetyltransferase 8 like	Homo sapiens	110-115
26819345-7	2016	RESULTS: Patients with high levels of tumoral NAA and its biosynthetic enzyme, aspartate N-acetyltransferase (NAT8L), had worse overall survival than patients with low levels of NAA and NAT8L.	N-acetylaspartate	46-49	N-acetyltransferase 8 like	Homo sapiens	186-191
26511490-0	2016	Cancer-Specific Production of N-Acetylaspartate via NAT8L Overexpression in Non-Small Cell Lung Cancer and Its Potential as a Circulating Biomarker.	N-acetylaspartate	30-47	N-acetyltransferase 8 like	Homo sapiens	52-57
26511490-4	2016	NAA"s cancer specificity was further supported in our analysis of NAA synthetase (gene symbol: NAT8L) gene expression levels in The Cancer Genome Atlas: elevated NAT8L expression in approximately 40% of adenocarcinoma and squamous cell carcinoma cases (N = 577), with minimal expression in all nonmalignant lung tissues (N = 74).	N-acetylaspartate	0-3	N-acetyltransferase 8 like	Homo sapiens	66-80
26511490-4	2016	NAA"s cancer specificity was further supported in our analysis of NAA synthetase (gene symbol: NAT8L) gene expression levels in The Cancer Genome Atlas: elevated NAT8L expression in approximately 40% of adenocarcinoma and squamous cell carcinoma cases (N = 577), with minimal expression in all nonmalignant lung tissues (N = 74).	N-acetylaspartate	0-3	N-acetyltransferase 8 like	Homo sapiens	95-100
26511490-4	2016	NAA"s cancer specificity was further supported in our analysis of NAA synthetase (gene symbol: NAT8L) gene expression levels in The Cancer Genome Atlas: elevated NAT8L expression in approximately 40% of adenocarcinoma and squamous cell carcinoma cases (N = 577), with minimal expression in all nonmalignant lung tissues (N = 74).	N-acetylaspartate	0-3	N-acetyltransferase 8 like	Homo sapiens	162-167
26511490-5	2016	We then showed that NAT8L is functionally involved in NAA production of NSCLC cells through siRNA-mediated suppression of NAT8L, which caused selective reduction of intracellular and secreted NAA.	N-acetylaspartate	54-57	N-acetyltransferase 8 like	Homo sapiens	20-25
26511490-5	2016	We then showed that NAT8L is functionally involved in NAA production of NSCLC cells through siRNA-mediated suppression of NAT8L, which caused selective reduction of intracellular and secreted NAA.	N-acetylaspartate	54-57	N-acetyltransferase 8 like	Homo sapiens	122-127
26511490-5	2016	We then showed that NAT8L is functionally involved in NAA production of NSCLC cells through siRNA-mediated suppression of NAT8L, which caused selective reduction of intracellular and secreted NAA.	N-acetylaspartate	192-195	N-acetyltransferase 8 like	Homo sapiens	20-25
26511490-5	2016	We then showed that NAT8L is functionally involved in NAA production of NSCLC cells through siRNA-mediated suppression of NAT8L, which caused selective reduction of intracellular and secreted NAA.	N-acetylaspartate	192-195	N-acetyltransferase 8 like	Homo sapiens	122-127
26511490-8	2016	Taken together, these results indicate that NAA is produced specifically in NSCLC tumors through NAT8L overexpression, and its extracellular secretion can be detected in blood.	N-acetylaspartate	44-47	N-acetyltransferase 8 like	Homo sapiens	97-102
26575297-5	2016	Bipolar disorders complicated by insulin resistance/T2DM are associated with smaller hippocampal and cortical gray matter volumes and lower prefrontal N-acetyl aspartate (neuronal marker).	N-acetylaspartate	151-169	insulin	Homo sapiens	33-40
26459214-1	2015	Glutamate carboxypeptidase II (GCPII) is a zinc metalloprotease on the surface of astrocytes which cleaves N-acetylaspartylglutamate to release N-acetylaspartate and glutamate.	N-acetylaspartate	144-161	folate hydrolase 1	Homo sapiens	0-29
26459214-1	2015	Glutamate carboxypeptidase II (GCPII) is a zinc metalloprotease on the surface of astrocytes which cleaves N-acetylaspartylglutamate to release N-acetylaspartate and glutamate.	N-acetylaspartate	144-161	folate hydrolase 1	Homo sapiens	31-36
26361739-9	2015	administration of NAA prior to the test in Shati(+/-) but not in Shati(-/-) mice.	N-acetylaspartate	18-21	N-acetyltransferase 8-like	Mus musculus	43-48
26361739-11	2015	preinjection of NAA inhibited dopamine release after high K(+) stimulation in the NAc of Shati(+/+) and Shati(+/-) mice, but not Shati(-/-) mice.	N-acetylaspartate	16-19	N-acetyltransferase 8-like	Mus musculus	89-94
26361739-11	2015	preinjection of NAA inhibited dopamine release after high K(+) stimulation in the NAc of Shati(+/+) and Shati(+/-) mice, but not Shati(-/-) mice.	N-acetylaspartate	16-19	N-acetyltransferase 8-like	Mus musculus	104-109
26361739-11	2015	preinjection of NAA inhibited dopamine release after high K(+) stimulation in the NAc of Shati(+/+) and Shati(+/-) mice, but not Shati(-/-) mice.	N-acetylaspartate	16-19	N-acetyltransferase 8-like	Mus musculus	104-109
26361739-12	2015	These results suggested that the behavioral deficits in Shati-deleted mice were caused by dopaminergic abnormality via deprivation of NAA.	N-acetylaspartate	134-137	N-acetyltransferase 8-like	Mus musculus	56-61
26511242-1	2015	Canavan disease (CD) is a severe, lethal leukodystrophy caused by deficiency in aspartoacylase (ASPA), which hydrolyzes N-acetylaspartate (NAA).	N-acetylaspartate	120-137	aspartoacylase	Mus musculus	96-100
26511242-1	2015	Canavan disease (CD) is a severe, lethal leukodystrophy caused by deficiency in aspartoacylase (ASPA), which hydrolyzes N-acetylaspartate (NAA).	N-acetylaspartate	139-142	aspartoacylase	Mus musculus	96-100
26164607-3	2015	Shati/Nat8l produces N-acetylaspartate from aspartate and acetyl-CoA.	N-acetylaspartate	21-38	N-acetyltransferase 8-like	Mus musculus	0-5
26164607-3	2015	Shati/Nat8l produces N-acetylaspartate from aspartate and acetyl-CoA.	N-acetylaspartate	21-38	N-acetyltransferase 8-like	Mus musculus	6-11
26164607-4	2015	Previously, we reported that overexpression of Shati/Nat8l in nucleus accumbens attenuates the response to METH by N-acetylaspartylglutamate (which is derived from N-acetylaspartate)-mGluR3 signaling in the mice brain.	N-acetylaspartate	164-181	N-acetyltransferase 8-like	Mus musculus	47-52
26164607-4	2015	Previously, we reported that overexpression of Shati/Nat8l in nucleus accumbens attenuates the response to METH by N-acetylaspartylglutamate (which is derived from N-acetylaspartate)-mGluR3 signaling in the mice brain.	N-acetylaspartate	164-181	N-acetyltransferase 8-like	Mus musculus	53-58
26164607-4	2015	Previously, we reported that overexpression of Shati/Nat8l in nucleus accumbens attenuates the response to METH by N-acetylaspartylglutamate (which is derived from N-acetylaspartate)-mGluR3 signaling in the mice brain.	N-acetylaspartate	164-181	glutamate receptor, ionotropic, AMPA3 (alpha 3)	Mus musculus	183-189
26339674-8	2015	RESULTS: In INCL patients, N-acetylaspartate (NAA) was abnormally low at all locations upon initial measurement, and further declined throughout the follow-up period.	N-acetylaspartate	27-44	palmitoyl-protein thioesterase 1	Homo sapiens	12-16
26339674-8	2015	RESULTS: In INCL patients, N-acetylaspartate (NAA) was abnormally low at all locations upon initial measurement, and further declined throughout the follow-up period.	N-acetylaspartate	46-49	palmitoyl-protein thioesterase 1	Homo sapiens	12-16
25573156-4	2015	N-acetyl-l-aspartate (NAA), the primary storage form of brain acetate, and aspartoacylase (ASPA), the enzyme responsible for NAA catalysis, are significantly reduced in GBM tumors.	N-acetylaspartate	125-128	aspartoacylase	Homo sapiens	91-95
25833344-3	2015	Unexpectedly, we found that CNTF expression through lentiviral gene transfer in the rat striatum significantly decreased the levels of neuronal metabolites (N-acetyl-aspartate, N-acetyl-aspartyl-glutamate, and glutamate).	N-acetylaspartate	157-175	ciliary neurotrophic factor	Rattus norvegicus	28-32
24559655-8	2014	In the AAV vector-injected NAc, the tissue contents of both N-acetylaspartate and N-acetylaspartylglutamate (NAAG), endogenous mGluR3 agonist, were elevated.	N-acetylaspartate	60-77	glutamate receptor, ionotropic, AMPA3 (alpha 3)	Mus musculus	127-133
26701952-5	2015	Long echo-time (TE: 270 ms) MRS showed decreased N-acetyl-aspartate/creatine and elevated choline/creatine and lactate; short echo-time MRS (TE: 30 ms) revealed increased myoinositol at 3.56 ppm and lipid peaks at 0.9 and 1.3 ppm.	N-acetylaspartate	49-67	MROS	Homo sapiens	28-31
25189319-3	2015	NAA is catabolized by the enzyme aspartoacylase (ASPA) which is predominantly expressed in oligodendrocytes.	N-acetylaspartate	0-3	aspartoacylase	Homo sapiens	49-53
25766789-3	2015	We have undertaken an analysis of abnormalities in NAA during early stage pathology in the 5xFAD mouse model of familial Alzheimer"s disease and show here that dysregulated expression of the gene encoding for the rate-limiting NAA synthetic enzyme (Nat8L) is associated with deficits in mitochondrial oxidative phosphorylation in this model system.	N-acetylaspartate	51-54	N-acetyltransferase 8-like	Mus musculus	249-254
25766789-3	2015	We have undertaken an analysis of abnormalities in NAA during early stage pathology in the 5xFAD mouse model of familial Alzheimer"s disease and show here that dysregulated expression of the gene encoding for the rate-limiting NAA synthetic enzyme (Nat8L) is associated with deficits in mitochondrial oxidative phosphorylation in this model system.	N-acetylaspartate	227-230	N-acetyltransferase 8-like	Mus musculus	249-254
25766789-4	2015	Downreguation of Nat8L is particularly pronounced in the 5xFAD hippocampus, and is preceded by a significant upregulation of oligodendrocytic aspartoacylase (aspa), which encodes for the sole known NAA-catabolizing enzyme in the brain.	N-acetylaspartate	198-201	N-acetyltransferase 8-like	Mus musculus	17-22
25766789-4	2015	Downreguation of Nat8L is particularly pronounced in the 5xFAD hippocampus, and is preceded by a significant upregulation of oligodendrocytic aspartoacylase (aspa), which encodes for the sole known NAA-catabolizing enzyme in the brain.	N-acetylaspartate	198-201	aspartoacylase	Mus musculus	142-146
26269888-37	2015	The excessive NAA/Na(+) cotransport into astrocytes after TBI initiates a pathological cascade in astrocytes related to elevated [Na(+)]i. Glutamate/Na(+) cotransporters (GLT-1 and GLAST) located on astrocytes also initiates a Na(+)-dependent pathological cascade in astrocytes that eventually impacts upon survival of nearby neurons (Floyd et al., 2005).	N-acetylaspartate	14-17	solute carrier family 1 member 2	Homo sapiens	171-176
26269888-37	2015	The excessive NAA/Na(+) cotransport into astrocytes after TBI initiates a pathological cascade in astrocytes related to elevated [Na(+)]i. Glutamate/Na(+) cotransporters (GLT-1 and GLAST) located on astrocytes also initiates a Na(+)-dependent pathological cascade in astrocytes that eventually impacts upon survival of nearby neurons (Floyd et al., 2005).	N-acetylaspartate	14-17	solute carrier family 1 member 3	Homo sapiens	181-186
25712859-1	2015	Canavan disease is caused by inactivating ASPA (aspartoacylase) mutations that prevent cleavage of N-acetyl-L-aspartate (NAA), resulting in marked elevations in central nervous system (CNS) NAA and progressively worsening leukodystrophy.	N-acetylaspartate	99-119	aspartoacylase	Mus musculus	42-46
25712859-1	2015	Canavan disease is caused by inactivating ASPA (aspartoacylase) mutations that prevent cleavage of N-acetyl-L-aspartate (NAA), resulting in marked elevations in central nervous system (CNS) NAA and progressively worsening leukodystrophy.	N-acetylaspartate	121-124	aspartoacylase	Mus musculus	42-46
25712859-1	2015	Canavan disease is caused by inactivating ASPA (aspartoacylase) mutations that prevent cleavage of N-acetyl-L-aspartate (NAA), resulting in marked elevations in central nervous system (CNS) NAA and progressively worsening leukodystrophy.	N-acetylaspartate	190-193	aspartoacylase	Mus musculus	42-46
25712859-2	2015	We now report that ablating NAA synthesis by constitutive genetic disruption of Nat8l (N-acetyltransferase-8 like) permits normal CNS myelination and prevents leukodystrophy in a murine Canavan disease model.	N-acetylaspartate	28-31	N-acetyltransferase 8-like	Mus musculus	80-85
25712859-2	2015	We now report that ablating NAA synthesis by constitutive genetic disruption of Nat8l (N-acetyltransferase-8 like) permits normal CNS myelination and prevents leukodystrophy in a murine Canavan disease model.	N-acetylaspartate	28-31	N-acetyltransferase 8-like	Mus musculus	87-113
25622053-6	2015	RESULTS: Increases in plasma or CSF MCP-1 were associated with lower NAA/Cr in the MFC and BG, whereas metabolite changes in the frontal white matter for NAA/Cr, GlxCr, and Cho/Cr were explained almost exclusively by a single factor, sCD14.	N-acetylaspartate	69-72	C-C motif chemokine ligand 2	Homo sapiens	36-41
25750529-6	2015	RESULTS: The BAFME patients exhibited a decreased N-acetylaspartate (NAA)/choline (Cho) ratio in the cerebellar cortex, whereas there were no significant differences in the NAA/creatine (Cr), Cho/Cr, and NAA/(Cr+Cho) ratios compared with healthy controls.	N-acetylaspartate	50-67	benign adult familial myoclonic epilepsy 1	Homo sapiens	13-18
25750529-6	2015	RESULTS: The BAFME patients exhibited a decreased N-acetylaspartate (NAA)/choline (Cho) ratio in the cerebellar cortex, whereas there were no significant differences in the NAA/creatine (Cr), Cho/Cr, and NAA/(Cr+Cho) ratios compared with healthy controls.	N-acetylaspartate	69-72	benign adult familial myoclonic epilepsy 1	Homo sapiens	13-18
24585452-2	2015	METHODS: Using density matrix simulations, a PRESS sequence with (TE1 , TE2 ) = (69, 37) ms and an inserted 90  J-suppression pulse were found to minimize the NAA multiplet at 2.49 ppm.	N-acetylaspartate	159-162	N-alpha-acetyltransferase 10, NatA catalytic subunit	Homo sapiens	72-75
25169676-5	2015	NAA was lower in Pittsburgh Compound B-positive subjects and APOE epsilon4 allele carriers.	N-acetylaspartate	0-3	apolipoprotein E	Homo sapiens	61-65
25523827-12	2014	NAA and glutamate decreased with decreased SYN and MAG.	N-acetylaspartate	0-3	synaptophysin	Homo sapiens	43-46
25471565-9	2014	Higher amyloid-beta burden was associated with elevated mI/Cr and lower NAA/mI ratios, but not with NAA/Cr.	N-acetylaspartate	72-75	amyloid beta precursor protein	Homo sapiens	7-19
24222427-6	2014	Further, serum IL-6 was increased in fatigued women compared to non-fatigued women (P = 0.03), Using receiver operator curves (ROC) we determined that the posterior insula Glx/NAA ratio was the best predictor of fatigue with an overall area under the receiver operating characteristic curve (AUROC) of 79%, with a sensitivity of 81% and a specificity of 69%.	N-acetylaspartate	176-179	interleukin 6	Homo sapiens	15-19
25173431-8	2014	Glx in dACC significantly correlated with CTh in healthy controls but not MDD patients, while NAA and CTh in dACC significantly correlated in both groups.	N-acetylaspartate	94-97	Acetyl-CoA carboxylase	Drosophila melanogaster	109-113
25003821-1	2014	Canavan disease (CD) is a fatal, childhood neurological disorder caused by mutations in the ASPA gene, leading to catalytic deficiencies in the aspartoacylase (ASPA) enzyme and impaired N-acetyl-l-aspartic acid metabolism in the brain.	N-acetylaspartate	186-210	aspartoacylase	Homo sapiens	92-96
24977939-2	2014	CD is characterized by mutations in the gene encoding aspartoacylase (ASPA), the substrate enzyme that hydrolyzes N-acetylaspartic acid (NAA) to acetate and aspartate.	N-acetylaspartate	114-135	aspartoacylase	Homo sapiens	70-74
24977939-2	2014	CD is characterized by mutations in the gene encoding aspartoacylase (ASPA), the substrate enzyme that hydrolyzes N-acetylaspartic acid (NAA) to acetate and aspartate.	N-acetylaspartate	137-140	aspartoacylase	Homo sapiens	70-74
24031048-8	2014	The NAA/tCr ratio in the pACC of patients with MDD showed a significant decrease in the follow-up scan (P=0.032), and the NAA/tCr ratio of the baseline scan showed logarithmic negative association with illness duration (P=0.024).	N-acetylaspartate	122-125	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	126-129
24902613-8	2014	RESULTS: In patients with JME, GABA and NAA were reduced in the thalamus (p = 0.03 and p = 0.02), whereas frontal GABA and glutamine were elevated (p = 0.046 and p = 0.03).	N-acetylaspartate	40-43	myoclonic epilepsy, juvenile, 2	Homo sapiens	26-29
24808185-5	2014	In addition to citric acid cycle intermediates such as alpha-ketoglutarate and succinate, NaDC3 transports other compounds into cells, including N-acetyl aspartate, mercaptosuccinate, and glutathione, in keeping with its dual roles in cell nutrition and detoxification.	N-acetylaspartate	145-163	solute carrier family 13 member 3	Homo sapiens	90-95
24031048-9	2014	CONCLUSION: A progressive decrease in the NAA/tCr ratio in the pACC of patients with MDD was demonstrated and the decrease in this ratio was at the highest rate in the early period after illness onset.	N-acetylaspartate	42-45	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	46-49
24515258-2	2014	The reversible changes in NAA induced by mild TBI were due to a combination of transient mitochondrial malfunctioning with energy crisis (decrease in ATP and in the ATP/ADP ratio) and modulation in the gene and protein levels of N-acetyltransferase 8-like and increase of aspartoacylase levels.	N-acetylaspartate	26-29	N-acetyltransferase 8-like	Rattus norvegicus	229-255
24792733-8	2014	The results revealed a significant reduction in metabolite to total creatine ratios of N-acetylaspartate (NAA/tCr) in the left prefrontal cortex and the pons for children with PMNE compared to healthy children.	N-acetylaspartate	87-104	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	110-113
24826990-2	2014	ASPA-deficiency is characterized by severe psychomotor retardation, and excessive levels of the ASPA substrate N-acetylaspartate (NAA).	N-acetylaspartate	111-128	aspartoacylase	Mus musculus	0-4
24826990-2	2014	ASPA-deficiency is characterized by severe psychomotor retardation, and excessive levels of the ASPA substrate N-acetylaspartate (NAA).	N-acetylaspartate	111-128	aspartoacylase	Mus musculus	96-100
24826990-2	2014	ASPA-deficiency is characterized by severe psychomotor retardation, and excessive levels of the ASPA substrate N-acetylaspartate (NAA).	N-acetylaspartate	130-133	aspartoacylase	Mus musculus	0-4
24826990-2	2014	ASPA-deficiency is characterized by severe psychomotor retardation, and excessive levels of the ASPA substrate N-acetylaspartate (NAA).	N-acetylaspartate	130-133	aspartoacylase	Mus musculus	96-100
24493094-4	2014	An increase in the amounts of GABA, NAA and choline compounds in the brain occurred in mice treated with LPS.	N-acetylaspartate	36-39	toll-like receptor 4	Mus musculus	105-108
24515258-2	2014	The reversible changes in NAA induced by mild TBI were due to a combination of transient mitochondrial malfunctioning with energy crisis (decrease in ATP and in the ATP/ADP ratio) and modulation in the gene and protein levels of N-acetyltransferase 8-like and increase of aspartoacylase levels.	N-acetylaspartate	26-29	aspartoacylase	Rattus norvegicus	272-286
24515258-3	2014	The irreversible decrease in NAA following severe TBI, was instead characterized by profound mitochondrial malfunctioning (constant 65% decrease of the ATP/ADP indicating permanent impairment of the mitochondrial phosphorylating capacity), dramatic repression of the N-acetyltransferase 8-like gene and concomitant remarkable increase in the aspartoacylase gene and protein levels.	N-acetylaspartate	29-32	N-acetyltransferase 8-like	Rattus norvegicus	267-293
24515258-3	2014	The irreversible decrease in NAA following severe TBI, was instead characterized by profound mitochondrial malfunctioning (constant 65% decrease of the ATP/ADP indicating permanent impairment of the mitochondrial phosphorylating capacity), dramatic repression of the N-acetyltransferase 8-like gene and concomitant remarkable increase in the aspartoacylase gene and protein levels.	N-acetylaspartate	29-32	aspartoacylase	Rattus norvegicus	342-356
24393355-0	2014	Possible association between the oxytocin receptor gene and N-acetylaspartate of the right medial temporal lobe in autism spectrum disorders.	N-acetylaspartate	60-77	oxytocin receptor	Homo sapiens	33-50
23996800-2	2014	Levels of N-acetyl-L-aspartate (NAA), the primary storage form of acetate in the brain, and aspartoacylase (ASPA), the enzyme responsible for NAA catalysis to generate acetate, are reduced in glioma; yet, few studies have investigated acetate as a potential therapeutic agent.	N-acetylaspartate	142-145	aspartoacylase	Homo sapiens	108-112
23892392-5	2014	RESULTS: NF1 patients, compared to healthy controls, showed (a) decreased NAA in all the four ROI, (b) increased Cho and decreased Cr in three of the four ROI, (c) decreased NAA/Cho ratio in three ROI, and (d) increased ADC in all the four ROI.	N-acetylaspartate	74-77	neurofibromin 1	Homo sapiens	9-12
23892392-5	2014	RESULTS: NF1 patients, compared to healthy controls, showed (a) decreased NAA in all the four ROI, (b) increased Cho and decreased Cr in three of the four ROI, (c) decreased NAA/Cho ratio in three ROI, and (d) increased ADC in all the four ROI.	N-acetylaspartate	174-177	neurofibromin 1	Homo sapiens	9-12
24338370-4	2014	Compared with McGill-R-Thy1-APP females, McGill-R-Thy1-APP males had lower levels of myo-inositol and N-acetylaspartate (NAA).	N-acetylaspartate	102-119	Thy-1 cell surface antigen	Rattus norvegicus	50-54
24338370-4	2014	Compared with McGill-R-Thy1-APP females, McGill-R-Thy1-APP males had lower levels of myo-inositol and N-acetylaspartate (NAA).	N-acetylaspartate	121-124	Thy-1 cell surface antigen	Rattus norvegicus	50-54
24338370-5	2014	No differences in metabolite levels were evident when female control and McGill-R-Thy1-APP rats were compared, whereas McGill-R-Thy1-APP males had lower levels of glutamate, NAA and total choline compared with male controls.	N-acetylaspartate	174-177	Thy-1 cell surface antigen	Rattus norvegicus	128-132
24055700-1	2014	2-Phosphonomethyl pentanedioic acid (2-PMPA) is a potent and selective inhibitor of glutamate carboxypeptidase-II, an enzyme which catabolizes the abundant neuropeptide N-acetyl-aspartyl-glutamate (NAAG) to N-acetylaspartate (NAA) and glutamate.	N-acetylaspartate	207-224	folate hydrolase 1	Rattus norvegicus	84-113
24055700-1	2014	2-Phosphonomethyl pentanedioic acid (2-PMPA) is a potent and selective inhibitor of glutamate carboxypeptidase-II, an enzyme which catabolizes the abundant neuropeptide N-acetyl-aspartyl-glutamate (NAAG) to N-acetylaspartate (NAA) and glutamate.	N-acetylaspartate	198-201	folate hydrolase 1	Rattus norvegicus	84-113
24515575-10	2014	One prior reported SLC25A12 mutation caused complete loss of AGC1 activity in a child with epilepsy, hypotonia, hypomyelination, and reduced brain NAA.	N-acetylaspartate	147-150	solute carrier family 25 member 12	Homo sapiens	19-27
24515575-10	2014	One prior reported SLC25A12 mutation caused complete loss of AGC1 activity in a child with epilepsy, hypotonia, hypomyelination, and reduced brain NAA.	N-acetylaspartate	147-150	solute carrier family 25 member 12	Homo sapiens	61-65
24515575-12	2014	SLC25A12 sequencing should be considered in children with infantile epilepsy, congenital hypotonia, global delay, abnormal myelination, and reduced brain NAA.	N-acetylaspartate	154-157	solute carrier family 25 member 12	Homo sapiens	0-8
24155240-1	2013	NAT8L (N-acetyltransferase 8-like) catalyzes the formation of N-acetylaspartate (NAA) from acetyl-CoA and aspartate.	N-acetylaspartate	62-79	N-acetyltransferase 8-like	Mus musculus	0-5
24155240-1	2013	NAT8L (N-acetyltransferase 8-like) catalyzes the formation of N-acetylaspartate (NAA) from acetyl-CoA and aspartate.	N-acetylaspartate	62-79	N-acetyltransferase 8-like	Mus musculus	7-33
24155240-1	2013	NAT8L (N-acetyltransferase 8-like) catalyzes the formation of N-acetylaspartate (NAA) from acetyl-CoA and aspartate.	N-acetylaspartate	81-84	N-acetyltransferase 8-like	Mus musculus	0-5
24155240-1	2013	NAT8L (N-acetyltransferase 8-like) catalyzes the formation of N-acetylaspartate (NAA) from acetyl-CoA and aspartate.	N-acetylaspartate	81-84	N-acetyltransferase 8-like	Mus musculus	7-33
24155240-11	2013	Taken together, our data show that Nat8l impacts on the brown adipogenic phenotype and suggests the existence of the NAT8L-driven NAA metabolism as a novel pathway to provide cytosolic acetyl-CoA for lipid synthesis in adipocytes.	N-acetylaspartate	130-133	N-acetyltransferase 8-like	Mus musculus	35-40
24155240-11	2013	Taken together, our data show that Nat8l impacts on the brown adipogenic phenotype and suggests the existence of the NAT8L-driven NAA metabolism as a novel pathway to provide cytosolic acetyl-CoA for lipid synthesis in adipocytes.	N-acetylaspartate	130-133	N-acetyltransferase 8-like	Mus musculus	117-122
24278309-2	2013	N-acetyl-L-aspartate (NAA), the primary storage form of acetate in the brain, and aspartoacylase (ASPA), the enzyme responsible for NAA catalysis to generate acetate and ultimately acetyl-Coenzyme A for histone acetylation, are reduced in oligodendroglioma.	N-acetylaspartate	132-135	aspartoacylase	Homo sapiens	98-102
25206655-6	2013	Hydrogen proton magnetic resonance spectroscopy analysis showed that the N-acetylaspartate/creatine ratio in the hippocampal CA3 region was significantly increased at 1 week, and the N-acetylaspartate/choline ratio was significantly increased at 2 weeks after hyperbaric oxygen therapy.	N-acetylaspartate	73-90	carbonic anhydrase 3	Rattus norvegicus	125-128
25206655-6	2013	Hydrogen proton magnetic resonance spectroscopy analysis showed that the N-acetylaspartate/creatine ratio in the hippocampal CA3 region was significantly increased at 1 week, and the N-acetylaspartate/choline ratio was significantly increased at 2 weeks after hyperbaric oxygen therapy.	N-acetylaspartate	183-200	carbonic anhydrase 3	Rattus norvegicus	125-128
25069253-4	2013	Recently, it has been demonstrated that the substrate for shati/nat81 is aspaltate and shati/nat8l biosynthesizes N-acetylaspartate, which exists abundantly in the mammalian brain.	N-acetylaspartate	114-131	N-acetyltransferase 8 like	Homo sapiens	93-98
23884408-5	2013	Although the NAA dicarboxylate transporter NaDC3 is primarily thought to be expressed by astrocytes, all cell lines expressed NaDC3 and, thus, are capable of NAA up-take.	N-acetylaspartate	13-16	solute carrier family 13 member 3	Homo sapiens	43-48
23884408-6	2013	Treatment with NAA or NAAG significantly increased GSC growth and suppressed differentiation of Oli-Neu cells and proneural GSCs.	N-acetylaspartate	15-18	neuralized E3 ubiquitin protein ligase 1	Homo sapiens	100-103
23884408-8	2013	Both NAA and NAAG elicited the expression of a novel immunoreactive ASPA species in select GSC nuclei, suggesting differential ASPA regulation in response to these metabolites.	N-acetylaspartate	5-8	aspartoacylase	Homo sapiens	68-72
23884408-8	2013	Both NAA and NAAG elicited the expression of a novel immunoreactive ASPA species in select GSC nuclei, suggesting differential ASPA regulation in response to these metabolites.	N-acetylaspartate	5-8	aspartoacylase	Homo sapiens	127-131
23596182-10	2013	Insulin infusion resulted in an increase in frontal NAA/Cr and NAA/H2O and frontal and temporal Glx/Cr and Glx/H2O and a decrease in frontal Cho/Cr and temporal Cho/H2O and myo-inositol/H2O (all P < 0.05, except temporal Glx/H2O, P = 0.054, NS) in the high-IS, but not in the low-IS, group.	N-acetylaspartate	52-55	insulin	Homo sapiens	0-7
23596182-10	2013	Insulin infusion resulted in an increase in frontal NAA/Cr and NAA/H2O and frontal and temporal Glx/Cr and Glx/H2O and a decrease in frontal Cho/Cr and temporal Cho/H2O and myo-inositol/H2O (all P < 0.05, except temporal Glx/H2O, P = 0.054, NS) in the high-IS, but not in the low-IS, group.	N-acetylaspartate	63-66	insulin	Homo sapiens	0-7
23596182-11	2013	Insulin sensitivity correlated positively with frontal NAA/Cr and NAA/H2O and temporal Glx/H2O and negatively with temporal myo-inositol/Cr and myo-inositol/H2O assessed during the second (1)H-MRS (all P < 0.05).	N-acetylaspartate	55-58	insulin	Homo sapiens	0-7
23596182-11	2013	Insulin sensitivity correlated positively with frontal NAA/Cr and NAA/H2O and temporal Glx/H2O and negatively with temporal myo-inositol/Cr and myo-inositol/H2O assessed during the second (1)H-MRS (all P < 0.05).	N-acetylaspartate	66-69	insulin	Homo sapiens	0-7
23608100-8	2013	Our results showed that N-acetylaspartate (NAA) levels increased and myo-inositol levels decreased in Tg-BDNF mice compared with Tg-PBS mice.	N-acetylaspartate	24-41	brain derived neurotrophic factor	Mus musculus	105-109
23608100-9	2013	But NAA level in Tg-BDNF mice was still lower than that in wild-type mice at 6weeks after infusion.	N-acetylaspartate	4-7	brain derived neurotrophic factor	Mus musculus	20-24
23936155-12	2013	Plasma CD14(+) HIV DNA was associated with plasma and CSF neopterin (p = 0.023) and with MRS markers of neuronal injury (lower N-acetyl aspartate) and glial dysfunction (higher myoinositol) in multiple brain regions.	N-acetylaspartate	127-145	CD14 molecule	Homo sapiens	7-11
23253771-0	2013	Age-modulated association between prefrontal NAA and the BDNF gene.	N-acetylaspartate	45-48	brain derived neurotrophic factor	Homo sapiens	57-61
23525278-1	2013	Glutamate carboxypeptidase II (GCPII) is an exopeptidase that catalyzes the hydrolysis of N-acetylated aspartate-glutamate (NAAG) to N-acetyl aspartate (NAA) and glutamate.	N-acetylaspartate	133-151	folate hydrolase 1	Homo sapiens	0-29
23525278-1	2013	Glutamate carboxypeptidase II (GCPII) is an exopeptidase that catalyzes the hydrolysis of N-acetylated aspartate-glutamate (NAAG) to N-acetyl aspartate (NAA) and glutamate.	N-acetylaspartate	133-151	folate hydrolase 1	Homo sapiens	31-36
23525278-1	2013	Glutamate carboxypeptidase II (GCPII) is an exopeptidase that catalyzes the hydrolysis of N-acetylated aspartate-glutamate (NAAG) to N-acetyl aspartate (NAA) and glutamate.	N-acetylaspartate	124-127	folate hydrolase 1	Homo sapiens	0-29
23525278-1	2013	Glutamate carboxypeptidase II (GCPII) is an exopeptidase that catalyzes the hydrolysis of N-acetylated aspartate-glutamate (NAAG) to N-acetyl aspartate (NAA) and glutamate.	N-acetylaspartate	124-127	folate hydrolase 1	Homo sapiens	31-36
23253771-3	2013	However, few studies have explored the relationship between BDNF polymorphisms and NAA levels directly.	N-acetylaspartate	83-86	brain derived neurotrophic factor	Homo sapiens	60-64
23253771-4	2013	Here, we present data from a single-voxel proton magnetic resonance spectroscopy study of 64 individuals and explore the relationship between BDNF polymorphisms and prefrontal NAA level.	N-acetylaspartate	176-179	brain derived neurotrophic factor	Homo sapiens	142-146
23253771-5	2013	Our results indicate an association between a single nucleotide polymorphism (SNP) within BDNF, known as rs1519480, and reduced NAA level (p = 0.023).	N-acetylaspartate	128-131	brain derived neurotrophic factor	Homo sapiens	90-94
23253771-10	2013	The rs1519480 SNP influences BDNF mRNA expression and has an impact on prefrontal NAA level over time.	N-acetylaspartate	82-85	brain derived neurotrophic factor	Homo sapiens	29-33
23315172-7	2013	Our results showed that N-acetylaspartate (NAA) levels increased and myoinositol levels decreased in the BDNF group compared with the PBS group.	N-acetylaspartate	24-41	brain derived neurotrophic factor	Mus musculus	105-109
23633398-4	2013	We have generated an Nat8l transgenic knockout mouse line to study the functions of NAA in the nervous system.	N-acetylaspartate	84-87	N-acetyltransferase 8-like	Mus musculus	21-26
23633398-6	2013	MRS analysis of the Nat8l(+/-) mice indicated significant reductions in NAA in cortex (-38%) and hypothalamus (-29%) compared with wild-type controls, which was confirmed using HPLC (-29% in forebrain).	N-acetylaspartate	72-75	N-acetyltransferase 8-like	Mus musculus	20-25
23633398-9	2013	Nat8l(+/-) mice also showed atypical locomotor responses to methamphetamine administration, suggesting that NAA is involved in modulating the hyperactivity effect of methamphetamine.	N-acetylaspartate	108-111	N-acetyltransferase 8-like	Mus musculus	0-5
23315172-7	2013	Our results showed that N-acetylaspartate (NAA) levels increased and myoinositol levels decreased in the BDNF group compared with the PBS group.	N-acetylaspartate	43-46	brain derived neurotrophic factor	Mus musculus	105-109
23315172-8	2013	However, the BDNF group NAA level was still lower than the control group at 6 weeks after infusion.	N-acetylaspartate	24-27	brain derived neurotrophic factor	Mus musculus	13-17
23211962-9	2013	Using (1)H-MRS (proton magnetic resonance spectroscopy), increases in N-acetylaspartate levels were found in the lesioned cortex after CART treatment in stroke brain.	N-acetylaspartate	70-87	CART prepropeptide	Rattus norvegicus	135-139
23151389-4	2013	Canavan disease (CD) is a globally occurring but rare early-onset human spongiform leukodystrophy associated with inborn genetic errors affecting the activity of aspartoacylase (ASPA), the enzyme highly expressed in oligodendrocytes that hydrolyzes NAA.	N-acetylaspartate	249-252	aspartoacylase	Homo sapiens	162-176
23151389-4	2013	Canavan disease (CD) is a globally occurring but rare early-onset human spongiform leukodystrophy associated with inborn genetic errors affecting the activity of aspartoacylase (ASPA), the enzyme highly expressed in oligodendrocytes that hydrolyzes NAA.	N-acetylaspartate	249-252	aspartoacylase	Homo sapiens	178-182
23255614-9	2013	N-acetyl aspartate weakly interacted with OAT1, but aspartate did not.	N-acetylaspartate	0-18	solute carrier family 22 member 6	Homo sapiens	42-46
23046047-5	2012	MRS revealed significant developmental changes in the ratios of hippocampal metabolites N-acetylaspartate (NAA), myo-inositol (Ins), and taurine to total creatine (tCr) in Fmr1 KO mice compared with WT controls.	N-acetylaspartate	88-105	fragile X messenger ribonucleoprotein 1	Mus musculus	172-176
22850825-2	2013	The enzyme aspartoacylase catalyzes the deacetylation of N-acetylaspartate to produce acetate required for fatty acid biosynthesis in the brain.	N-acetylaspartate	57-74	aspartoacylase	Homo sapiens	11-25
23253610-1	2012	Canavan disease is a hereditary leukodystrophy caused by mutations in the aspartoacylase gene (ASPA), leading to loss of enzyme activity and increased concentrations of the substrate N-acetyl-aspartate (NAA) in the brain.	N-acetylaspartate	183-201	aspartoacylase	Homo sapiens	95-99
23253610-1	2012	Canavan disease is a hereditary leukodystrophy caused by mutations in the aspartoacylase gene (ASPA), leading to loss of enzyme activity and increased concentrations of the substrate N-acetyl-aspartate (NAA) in the brain.	N-acetylaspartate	203-206	aspartoacylase	Homo sapiens	95-99
23253610-8	2012	AAV2-ASPA gene therapy resulted in a decrease in elevated NAA in the brain and slowed progression of brain atrophy, with some improvement in seizure frequency and with stabilization of overall clinical status.	N-acetylaspartate	58-61	aspartoacylase	Homo sapiens	5-9
23579327-10	2013	Higher hippocampal NAA/Cr was related to higher CSF Abeta42, while lower parietal NAA/Cr was associated with a higher CSF total tau (t-tau) and p-tau181P.	N-acetylaspartate	82-85	microtubule associated protein tau	Homo sapiens	128-131
23579327-10	2013	Higher hippocampal NAA/Cr was related to higher CSF Abeta42, while lower parietal NAA/Cr was associated with a higher CSF total tau (t-tau) and p-tau181P.	N-acetylaspartate	82-85	microtubule associated protein tau	Homo sapiens	135-138
23099815-8	2013	Phenomena we observed could potentially explain why cholinesterase inhibitor therapy increases AD brain glucose utilization and N-acetyl aspartate levels.	N-acetylaspartate	128-146	butyrylcholinesterase	Homo sapiens	52-66
23046047-5	2012	MRS revealed significant developmental changes in the ratios of hippocampal metabolites N-acetylaspartate (NAA), myo-inositol (Ins), and taurine to total creatine (tCr) in Fmr1 KO mice compared with WT controls.	N-acetylaspartate	107-110	fragile X messenger ribonucleoprotein 1	Mus musculus	172-176
22070551-7	2012	Patients with SCA6 had more severe overall atrophy of the vermis and hemispheres, but relatively preserved N-acetyl-aspartate/creatine (NAA/Cr).	N-acetylaspartate	107-125	calcium voltage-gated channel subunit alpha1 A	Homo sapiens	14-18
22503310-8	2012	RESULTS: ALC at baseline had lower concentrations of Glu, N-acetylaspartate (NAA), choline- (Cho) and creatine-containing metabolites (Cr) than LD in the ACC, but had normal GABA and myo-inositol (mI) levels.	N-acetylaspartate	58-75	allantoicase	Homo sapiens	9-12
22503310-8	2012	RESULTS: ALC at baseline had lower concentrations of Glu, N-acetylaspartate (NAA), choline- (Cho) and creatine-containing metabolites (Cr) than LD in the ACC, but had normal GABA and myo-inositol (mI) levels.	N-acetylaspartate	77-80	allantoicase	Homo sapiens	9-12
22335434-0	2012	Deletion of beta-2-microglobulin ameliorates spinal cord lesion load and promotes recovery of brainstem NAA levels in a murine model of multiple sclerosis.	N-acetylaspartate	104-107	beta-2 microglobulin	Mus musculus	12-32
22335434-5	2012	Early in the disease, brainstem NAA levels drop in both strains, but accordingly with remyelination and axonal preservation, NAA recover in beta2m(-/-) mice despite equivalent brainstem pathology.	N-acetylaspartate	125-128	beta-2 microglobulin	Mus musculus	140-146
22909248-0	2012	Effect of metabotropic glutamate receptor 3 genotype on N-acetylaspartate levels and neurocognition in non-smoking, active alcoholics.	N-acetylaspartate	56-73	glutamate metabotropic receptor 3	Homo sapiens	10-43
22909248-1	2012	BACKGROUND: We studied the effects of single nucleotide polymorphisms (SNPs) in the metabotropic glutamate receptor 3 (GRM3) gene on brain N-acetylaspartate (NAA) concentrations and executive function (EF) skills in non-smoking, active alcoholics, and evaluated associations between these variables.	N-acetylaspartate	139-156	glutamate metabotropic receptor 3	Homo sapiens	84-117
22729482-7	2012	Logistic regression analysis was used to determine the relationship between Cho/NAA and MIB-1, p53, CD34, and the degree of tumour infiltration.	N-acetylaspartate	80-83	MIB E3 ubiquitin protein ligase 1	Homo sapiens	88-93
22070551-7	2012	Patients with SCA6 had more severe overall atrophy of the vermis and hemispheres, but relatively preserved N-acetyl-aspartate/creatine (NAA/Cr).	N-acetylaspartate	136-139	calcium voltage-gated channel subunit alpha1 A	Homo sapiens	14-18
22729482-9	2012	RESULTS: In HGG, higher Cho/NAA ratios were associated with a greater probability of higher MIB-1 counts, stronger CD34 expression, and tumour infiltration.	N-acetylaspartate	28-31	MIB E3 ubiquitin protein ligase 1	Homo sapiens	92-97
22468686-2	2012	The human aspartoacylase (ASPA) gene, which catalyzes the deacetylation of N-acetyl-L-aspartate, is mutated in Canavan disease.	N-acetylaspartate	75-95	aspartoacylase	Homo sapiens	10-24
22729482-9	2012	RESULTS: In HGG, higher Cho/NAA ratios were associated with a greater probability of higher MIB-1 counts, stronger CD34 expression, and tumour infiltration.	N-acetylaspartate	28-31	CD34 molecule	Homo sapiens	115-119
22468686-2	2012	The human aspartoacylase (ASPA) gene, which catalyzes the deacetylation of N-acetyl-L-aspartate, is mutated in Canavan disease.	N-acetylaspartate	75-95	aspartoacylase	Homo sapiens	26-30
21940617-6	2011	RESULTS: NAA/Cr and NAA/Myo ratios are reduced in both SOD1+ subjects (39.7%, p = 0.001 and 18.0%, p = 0.02) and patients with ALS (41.2%, p < 0.001 and 24.0%, p = 0.01) compared to controls.	N-acetylaspartate	9-12	superoxide dismutase 1	Homo sapiens	55-59
22522288-2	2012	We studied in the rat the effect of prolonged exposure to a low-dose of the NMDA glutamate receptor antagonist phencyclidine (PCP) on levels of NAA, glutamate and glutamine in several brain regions where metabolite reductions have been reported in chronically medicated patients with schizophrenia.	N-acetylaspartate	144-147	glutamate ionotropic receptor NMDA type subunit 2C	Rattus norvegicus	76-99
22283763-11	2012	In addition, the weak association between DTNBP1 genotype and NAA is in line with a regulatory influence of dysbindin on synaptogenesis and neuronal survival.	N-acetylaspartate	62-65	dystrobrevin binding protein 1	Homo sapiens	42-48
22283763-11	2012	In addition, the weak association between DTNBP1 genotype and NAA is in line with a regulatory influence of dysbindin on synaptogenesis and neuronal survival.	N-acetylaspartate	62-65	dystrobrevin binding protein 1	Homo sapiens	108-117
22124883-1	2012	Glutamate carboxypeptidase II (GCPII) catalyzes the hydrolysis of N-acetylaspartylglutamate into N-acetylaspartate and glutamate in the brain.	N-acetylaspartate	97-114	folate hydrolase 1	Homo sapiens	0-29
22124883-1	2012	Glutamate carboxypeptidase II (GCPII) catalyzes the hydrolysis of N-acetylaspartylglutamate into N-acetylaspartate and glutamate in the brain.	N-acetylaspartate	97-114	folate hydrolase 1	Homo sapiens	31-36
21509595-2	2012	The aim of the present study was to replicate and to extend prior findings of BDNF val66met genotype effects on hippocampal volume and N-acetyl aspartate (NAA) levels.	N-acetylaspartate	135-153	brain derived neurotrophic factor	Homo sapiens	78-82
21509595-2	2012	The aim of the present study was to replicate and to extend prior findings of BDNF val66met genotype effects on hippocampal volume and N-acetyl aspartate (NAA) levels.	N-acetylaspartate	155-158	brain derived neurotrophic factor	Homo sapiens	78-82
22611636-2	2012	The deficiency of aspartoacylase (ASPA), resulting in the accumulation of N-acetyl aspartic acid (NAA) in the brain, plays an important role in the pathogenesis of the disease.	N-acetylaspartate	74-96	aspartoacylase	Homo sapiens	34-38
22611636-2	2012	The deficiency of aspartoacylase (ASPA), resulting in the accumulation of N-acetyl aspartic acid (NAA) in the brain, plays an important role in the pathogenesis of the disease.	N-acetylaspartate	98-101	aspartoacylase	Homo sapiens	34-38
22567176-8	2012	Finally, multivariate statistical modeling revealed that the concentration of N-acetyl-aspartate [NAA] in the occipital cortex was negatively associated with [TNF-alpha].	N-acetylaspartate	78-96	tumor necrosis factor	Homo sapiens	159-168
22567176-8	2012	Finally, multivariate statistical modeling revealed that the concentration of N-acetyl-aspartate [NAA] in the occipital cortex was negatively associated with [TNF-alpha].	N-acetylaspartate	98-101	tumor necrosis factor	Homo sapiens	159-168
23094053-4	2012	V-NAA and patient age were used to calculate the predicted age at which a patient with SCA2 or SCA3 would reach an onset V-NAA value.	N-acetylaspartate	2-5	ataxin 2	Homo sapiens	87-91
23094053-4	2012	V-NAA and patient age were used to calculate the predicted age at which a patient with SCA2 or SCA3 would reach an onset V-NAA value.	N-acetylaspartate	123-126	ataxin 2	Homo sapiens	87-91
21598311-1	2011	Aspartoacylase (ASPA) catalyzes deacetylation of N-acetylaspartate (NAA) to generate acetate and aspartate.	N-acetylaspartate	49-66	aspartoacylase	Rattus norvegicus	0-14
21598311-1	2011	Aspartoacylase (ASPA) catalyzes deacetylation of N-acetylaspartate (NAA) to generate acetate and aspartate.	N-acetylaspartate	49-66	aspartoacylase	Rattus norvegicus	16-20
21598311-1	2011	Aspartoacylase (ASPA) catalyzes deacetylation of N-acetylaspartate (NAA) to generate acetate and aspartate.	N-acetylaspartate	68-71	aspartoacylase	Rattus norvegicus	0-14
21598311-1	2011	Aspartoacylase (ASPA) catalyzes deacetylation of N-acetylaspartate (NAA) to generate acetate and aspartate.	N-acetylaspartate	68-71	aspartoacylase	Rattus norvegicus	16-20
21598311-12	2011	Strong ASPA expression in cell nuclei is consistent with a role for NAA-derived acetate in nuclear acetylation reactions, including histone acetylation.	N-acetylaspartate	68-71	aspartoacylase	Rattus norvegicus	7-11
21608034-1	2011	Aspartoacylase (ASPA) is an enzyme that functions to catabolize the neuronal amino acid derivative N-acetyl-L-aspartic acid (NAA).	N-acetylaspartate	99-123	aspartoacylase	Rattus norvegicus	16-20
21608034-1	2011	Aspartoacylase (ASPA) is an enzyme that functions to catabolize the neuronal amino acid derivative N-acetyl-L-aspartic acid (NAA).	N-acetylaspartate	125-128	aspartoacylase	Rattus norvegicus	16-20
21608034-3	2011	NAA synthesis and catabolism are tightly compartmentalized within neurons and oligodendrocytes, respectively, and there is evidence to suggest the developmental regulation of ASPA activity is transcriptional.	N-acetylaspartate	0-3	aspartoacylase	Rattus norvegicus	175-179
22909248-1	2012	BACKGROUND: We studied the effects of single nucleotide polymorphisms (SNPs) in the metabotropic glutamate receptor 3 (GRM3) gene on brain N-acetylaspartate (NAA) concentrations and executive function (EF) skills in non-smoking, active alcoholics, and evaluated associations between these variables.	N-acetylaspartate	139-156	glutamate metabotropic receptor 3	Homo sapiens	119-123
22909248-1	2012	BACKGROUND: We studied the effects of single nucleotide polymorphisms (SNPs) in the metabotropic glutamate receptor 3 (GRM3) gene on brain N-acetylaspartate (NAA) concentrations and executive function (EF) skills in non-smoking, active alcoholics, and evaluated associations between these variables.	N-acetylaspartate	158-161	glutamate metabotropic receptor 3	Homo sapiens	84-117
22909248-1	2012	BACKGROUND: We studied the effects of single nucleotide polymorphisms (SNPs) in the metabotropic glutamate receptor 3 (GRM3) gene on brain N-acetylaspartate (NAA) concentrations and executive function (EF) skills in non-smoking, active alcoholics, and evaluated associations between these variables.	N-acetylaspartate	158-161	glutamate metabotropic receptor 3	Homo sapiens	119-123
22909248-13	2012	It is possible that certain GRM3 SNP genotypes (the A/A genotype of rs6465084 and the T allele of rs1468412) may further lower NAA/Cr levels and EF skills in addition to the effect of alcohol.	N-acetylaspartate	127-130	glutamate metabotropic receptor 3	Homo sapiens	28-32
21936773-1	2012	Aspartate N-acetyltransferase (NAT8L, N-acetyltransferase 8-like), the enzyme that synthesizes N-acetylaspartate, is membrane-bound and is at least partially associated with the ER (endoplasmic reticulum).	N-acetylaspartate	95-112	N-acetyltransferase 8 like	Homo sapiens	31-36
21936773-1	2012	Aspartate N-acetyltransferase (NAT8L, N-acetyltransferase 8-like), the enzyme that synthesizes N-acetylaspartate, is membrane-bound and is at least partially associated with the ER (endoplasmic reticulum).	N-acetylaspartate	95-112	N-acetyltransferase 8 like	Homo sapiens	38-65
22304714-6	2012	It is cleaved by a specific peptidase located on astrocytes, glutamate carboxypeptidase type II (GCP-II), to N-acetylaspartate (NAA) and glutamate.	N-acetylaspartate	109-126	folate hydrolase 1	Homo sapiens	61-95
22304714-6	2012	It is cleaved by a specific peptidase located on astrocytes, glutamate carboxypeptidase type II (GCP-II), to N-acetylaspartate (NAA) and glutamate.	N-acetylaspartate	109-126	folate hydrolase 1	Homo sapiens	97-103
22304714-6	2012	It is cleaved by a specific peptidase located on astrocytes, glutamate carboxypeptidase type II (GCP-II), to N-acetylaspartate (NAA) and glutamate.	N-acetylaspartate	128-131	folate hydrolase 1	Homo sapiens	61-95
22304714-6	2012	It is cleaved by a specific peptidase located on astrocytes, glutamate carboxypeptidase type II (GCP-II), to N-acetylaspartate (NAA) and glutamate.	N-acetylaspartate	128-131	folate hydrolase 1	Homo sapiens	97-103
22304717-1	2012	Glutamate carboxypeptidase II (GCPII, EC 3.4.17.21) is a zinc metallopeptidase that hydrolyzes N-acetylaspartylglutamate (NAAG) into N-acetylaspartate (NAA) and glutamate in the nervous system.	N-acetylaspartate	133-150	folate hydrolase 1	Homo sapiens	0-29
22304717-1	2012	Glutamate carboxypeptidase II (GCPII, EC 3.4.17.21) is a zinc metallopeptidase that hydrolyzes N-acetylaspartylglutamate (NAAG) into N-acetylaspartate (NAA) and glutamate in the nervous system.	N-acetylaspartate	133-150	folate hydrolase 1	Homo sapiens	31-36
22304717-1	2012	Glutamate carboxypeptidase II (GCPII, EC 3.4.17.21) is a zinc metallopeptidase that hydrolyzes N-acetylaspartylglutamate (NAAG) into N-acetylaspartate (NAA) and glutamate in the nervous system.	N-acetylaspartate	122-125	folate hydrolase 1	Homo sapiens	0-29
22304717-1	2012	Glutamate carboxypeptidase II (GCPII, EC 3.4.17.21) is a zinc metallopeptidase that hydrolyzes N-acetylaspartylglutamate (NAAG) into N-acetylaspartate (NAA) and glutamate in the nervous system.	N-acetylaspartate	122-125	folate hydrolase 1	Homo sapiens	31-36
21963649-6	2011	The NAA-to-myo-inositol ratio was significantly different between the treated vs. untreated SCA1 mice and demonstrated partial reversal to WT values both at early and mid-stage, consistent with the histological measures.	N-acetylaspartate	4-7	ataxin 1	Mus musculus	92-96
21608011-1	2011	The aralar/AGC1 knockout (KO) mouse shows a drastic decrease in brain aspartate and N-acetylaspartate levels and global hypomyelination, which are attributed to the lack of neuron-produced NAA used by oligodendrocytes as precursor of myelin lipid synthesis.	N-acetylaspartate	84-101	aggrecan	Mus musculus	11-15
21608011-1	2011	The aralar/AGC1 knockout (KO) mouse shows a drastic decrease in brain aspartate and N-acetylaspartate levels and global hypomyelination, which are attributed to the lack of neuron-produced NAA used by oligodendrocytes as precursor of myelin lipid synthesis.	N-acetylaspartate	189-192	aggrecan	Mus musculus	11-15
21625935-10	2011	On (1)H-MRSI, NAA/Cr values were lower in SPG11 patients than in HC (p = 0.002).	N-acetylaspartate	14-17	SPG11 vesicle trafficking associated, spatacsin	Homo sapiens	42-47
21872444-4	2011	CSF-corrected "total NAA" (tNAA; N-acetyl-aspartate + N-acetyl-aspartyl-glutamate), glutamate + glutamine (Glx), creatine + phosphocreatine (Cr + PCr), choline compounds (Cho), and myo-inositol (mI) were assayed in manually drawn regions-of-interest partitioned into gray matter, white matter, and CSF and then coregistered with MRSI.	N-acetylaspartate	21-24	colony stimulating factor 2	Homo sapiens	0-3
21940617-6	2011	RESULTS: NAA/Cr and NAA/Myo ratios are reduced in both SOD1+ subjects (39.7%, p = 0.001 and 18.0%, p = 0.02) and patients with ALS (41.2%, p < 0.001 and 24.0%, p = 0.01) compared to controls.	N-acetylaspartate	20-23	superoxide dismutase 1	Homo sapiens	55-59
21750421-11	2011	Plasma IP-10 correlated significantly and inversely with ACC NAA, which was lower in HIV-positive patients with mild compared to no cognitive impairment.	N-acetylaspartate	61-64	C-X-C motif chemokine ligand 10	Homo sapiens	7-12
21071619-0	2011	Performance-related increases in hippocampal N-acetylaspartate (NAA) induced by spatial navigation training are restricted to BDNF Val homozygotes.	N-acetylaspartate	45-62	brain derived neurotrophic factor	Homo sapiens	126-130
21627621-2	2011	METHOD: We assessed right anterior cingulate cortex (ACC) and amygdala-hippocampal region (Am + Hpp) N-acetyl-aspartate (NAA), choline (Cho) and creatine (Cr) concentrations and NAA/Cr and Cho/Cr ratios using single-voxel proton magnetic resonance spectroscopy in 15 patients with autogenous obsessions (OCD-A), 15 patients with reactive obsessions (OCD-R) and 15 healthy controls (HC).	N-acetylaspartate	101-119	familial progressive hyperpigmentation 1	Homo sapiens	96-99
21627621-5	2011	OCD-A group had significantly lower baseline NAA/Cr ratios in the Am + Hpp than other groups.	N-acetylaspartate	45-48	familial progressive hyperpigmentation 1	Homo sapiens	71-74
21627621-8	2011	Significant increase in NAA/Cr ratios of OCD-A group found in the Am + Hpp was more likely to be explained by increased NAA levels.	N-acetylaspartate	24-27	familial progressive hyperpigmentation 1	Homo sapiens	71-74
21627621-8	2011	Significant increase in NAA/Cr ratios of OCD-A group found in the Am + Hpp was more likely to be explained by increased NAA levels.	N-acetylaspartate	120-123	familial progressive hyperpigmentation 1	Homo sapiens	71-74
21474353-3	2011	CD is caused by mutations in the ASPA gene, which codes for the enzyme aspartoacylase (ASPA), which breaks down N-acetylaspartate (NAA) to acetate and aspartic acid.	N-acetylaspartate	112-129	aspartoacylase	Homo sapiens	33-37
21474353-3	2011	CD is caused by mutations in the ASPA gene, which codes for the enzyme aspartoacylase (ASPA), which breaks down N-acetylaspartate (NAA) to acetate and aspartic acid.	N-acetylaspartate	112-129	aspartoacylase	Homo sapiens	87-91
21474353-3	2011	CD is caused by mutations in the ASPA gene, which codes for the enzyme aspartoacylase (ASPA), which breaks down N-acetylaspartate (NAA) to acetate and aspartic acid.	N-acetylaspartate	131-134	aspartoacylase	Homo sapiens	33-37
21474353-3	2011	CD is caused by mutations in the ASPA gene, which codes for the enzyme aspartoacylase (ASPA), which breaks down N-acetylaspartate (NAA) to acetate and aspartic acid.	N-acetylaspartate	131-134	aspartoacylase	Homo sapiens	87-91
21071619-0	2011	Performance-related increases in hippocampal N-acetylaspartate (NAA) induced by spatial navigation training are restricted to BDNF Val homozygotes.	N-acetylaspartate	64-67	brain derived neurotrophic factor	Homo sapiens	126-130
21071619-4	2011	Training-induced changes in NAA were, however, absent in carriers of the Met substitution in the brain-derived neurotrophic factor (BDNF) gene, which is known to reduce activity-dependent secretion of BDNF.	N-acetylaspartate	28-31	brain derived neurotrophic factor	Homo sapiens	97-130
21071619-4	2011	Training-induced changes in NAA were, however, absent in carriers of the Met substitution in the brain-derived neurotrophic factor (BDNF) gene, which is known to reduce activity-dependent secretion of BDNF.	N-acetylaspartate	28-31	brain derived neurotrophic factor	Homo sapiens	132-136
21071619-4	2011	Training-induced changes in NAA were, however, absent in carriers of the Met substitution in the brain-derived neurotrophic factor (BDNF) gene, which is known to reduce activity-dependent secretion of BDNF.	N-acetylaspartate	28-31	brain derived neurotrophic factor	Homo sapiens	201-205
21071619-5	2011	Among BDNF Val homozygotes, increases in NAA were strongly related to the degree of practice-related improvement in navigation performance and normalized to pretraining levels 4 months after the last training session.	N-acetylaspartate	41-44	brain derived neurotrophic factor	Homo sapiens	6-10
21494901-8	2011	Greater numbers of CD16+ monocytes were associated with lower N-acetylaspartate levels and higher choline levels in the brain.	N-acetylaspartate	62-79	Fc gamma receptor IIIa	Homo sapiens	19-23
21144647-9	2011	Univariate statistical analysis revealed greater 1H-MRS-detected Cho content (P=0.0444) and lower normalized NAA/Cho ratio (P=0.0203) in tumors with MIB-1 index 5% and more.	N-acetylaspartate	109-112	MIB E3 ubiquitin protein ligase 1	Homo sapiens	149-154
21743142-5	2011	RESULTS: The ratio of NAA/Cr in SCA3/MJD patients showed a significant reduction in the cerebellar cortex, dentatum, cerebellar vermis and medipeduncle (P<0.01) compared with the controls.	N-acetylaspartate	22-25	ataxin 3	Homo sapiens	32-36
21743142-5	2011	RESULTS: The ratio of NAA/Cr in SCA3/MJD patients showed a significant reduction in the cerebellar cortex, dentatum, cerebellar vermis and medipeduncle (P<0.01) compared with the controls.	N-acetylaspartate	22-25	ataxin 3	Homo sapiens	37-40
21246320-6	2011	Specifically, (1) higher IP-10 levels correlated with lower N-acetyl aspartate (NAA)/creatine (Cr) ratios in the frontal white matter and higher MI/Cr ratios in all three brain regions considered and (2) higher MCP-1 levels correlated with lower NAA/Cr ratios in frontal white matter and the parietal cortex.	N-acetylaspartate	60-78	C-X-C motif chemokine ligand 10	Homo sapiens	25-30
21172405-6	2011	Our data show that basal glutamate+glutamine (Glx), glutamate, glutamine and N-acetylaspartatic acid (NAA) levels are increased in the nucleus accumbens (NAc) of ENT1(-/-) compared to wild-type mice.	N-acetylaspartate	77-100	solute carrier family 29 (nucleoside transporters), member 1	Mus musculus	162-166
21093418-1	2011	Glutamate carboxypeptidase II (GCP II) is a glial enzyme responsible for the hydrolysis of N-acetylaspartylglutamate (NAAG) into glutamate and N-acetylaspartate (NAA).	N-acetylaspartate	143-160	folate hydrolase 1	Mus musculus	0-29
21093418-1	2011	Glutamate carboxypeptidase II (GCP II) is a glial enzyme responsible for the hydrolysis of N-acetylaspartylglutamate (NAAG) into glutamate and N-acetylaspartate (NAA).	N-acetylaspartate	143-160	folate hydrolase 1	Mus musculus	31-37
21093418-1	2011	Glutamate carboxypeptidase II (GCP II) is a glial enzyme responsible for the hydrolysis of N-acetylaspartylglutamate (NAAG) into glutamate and N-acetylaspartate (NAA).	N-acetylaspartate	118-121	folate hydrolase 1	Mus musculus	0-29
21093418-1	2011	Glutamate carboxypeptidase II (GCP II) is a glial enzyme responsible for the hydrolysis of N-acetylaspartylglutamate (NAAG) into glutamate and N-acetylaspartate (NAA).	N-acetylaspartate	118-121	folate hydrolase 1	Mus musculus	31-37
21246320-6	2011	Specifically, (1) higher IP-10 levels correlated with lower N-acetyl aspartate (NAA)/creatine (Cr) ratios in the frontal white matter and higher MI/Cr ratios in all three brain regions considered and (2) higher MCP-1 levels correlated with lower NAA/Cr ratios in frontal white matter and the parietal cortex.	N-acetylaspartate	80-83	C-X-C motif chemokine ligand 10	Homo sapiens	25-30
21246320-6	2011	Specifically, (1) higher IP-10 levels correlated with lower N-acetyl aspartate (NAA)/creatine (Cr) ratios in the frontal white matter and higher MI/Cr ratios in all three brain regions considered and (2) higher MCP-1 levels correlated with lower NAA/Cr ratios in frontal white matter and the parietal cortex.	N-acetylaspartate	246-249	C-X-C motif chemokine ligand 10	Homo sapiens	25-30
21841259-2	2011	We tested the association of the putative marker of mitochondrial function N-acetylaspartate (NAA) as measured by proton magnetic resonance spectroscopy within the medial temporal lobe and cerebrospinal fluid amyoid-beta42 (Abeta42), total Tau and pTau181.	N-acetylaspartate	94-97	microtubule associated protein tau	Homo sapiens	240-243
20643647-3	2010	NAAG is synthesized by a NAAG synthetase catalyzing the ATP-dependent condensation of N-acetylaspartate and glutamate.	N-acetylaspartate	86-103	ribosomal modification protein rimK like family member A	Homo sapiens	25-40
21625469-1	2011	Canavan Disease (CD) is a recessive leukodystrophy caused by loss of function mutations in the gene encoding aspartoacylase (ASPA), an oligodendrocyte-enriched enzyme that hydrolyses N-acetylaspartate (NAA) to acetate and aspartate.	N-acetylaspartate	183-200	aspartoacylase	Mus musculus	125-129
21625469-1	2011	Canavan Disease (CD) is a recessive leukodystrophy caused by loss of function mutations in the gene encoding aspartoacylase (ASPA), an oligodendrocyte-enriched enzyme that hydrolyses N-acetylaspartate (NAA) to acetate and aspartate.	N-acetylaspartate	202-205	aspartoacylase	Mus musculus	125-129
21625469-7	2011	Non-invasive ultrahigh field proton magnetic resonance spectroscopy revealed increased levels of NAA, myo-inositol and taurine in the aspa(lacZ/lacZ) brain.	N-acetylaspartate	97-100	aspartoacylase	Mus musculus	134-138
20739347-11	2010	In patients there was significant decline in N-acetyl-aspartate:creatine/phosphocreatine (mean: 2.2%/year; 95% confidence interval: 0.9-3.5) and N-acetyl-aspartate:myo-inositol (mean: 3.7%/year; 95% confidence interval: 1.7-5.7), with no evidence for influence by age, disease severity or acetylcholinesterase inhibitor use.	N-acetylaspartate	45-63	acetylcholinesterase (Cartwright blood group)	Homo sapiens	289-309
20806406-0	2010	Reduction of hippocampal N-acetyl aspartate level in aged APP(Swe)/PS1(dE9) transgenic mice is associated with degeneration of CA3 pyramidal neurons.	N-acetylaspartate	25-43	presenilin 1	Mus musculus	67-70
20806406-0	2010	Reduction of hippocampal N-acetyl aspartate level in aged APP(Swe)/PS1(dE9) transgenic mice is associated with degeneration of CA3 pyramidal neurons.	N-acetylaspartate	25-43	anon-E9	Drosophila melanogaster	71-74
20806406-0	2010	Reduction of hippocampal N-acetyl aspartate level in aged APP(Swe)/PS1(dE9) transgenic mice is associated with degeneration of CA3 pyramidal neurons.	N-acetylaspartate	25-43	carbonic anhydrase 3	Mus musculus	127-130
20806406-3	2010	The results showed that the APP(Swe)/PS1(dE9) mice had significantly decreased hippocampal N-acetyl aspartate (NAA)/total creatine (tCr) level at 16 months of age, which was associated with degeneration of and intracellular deposition of thioflavine S-positive materials in hippocampal CA3 pyramidal neurons.	N-acetylaspartate	91-109	presenilin 1	Mus musculus	37-40
20806406-3	2010	The results showed that the APP(Swe)/PS1(dE9) mice had significantly decreased hippocampal N-acetyl aspartate (NAA)/total creatine (tCr) level at 16 months of age, which was associated with degeneration of and intracellular deposition of thioflavine S-positive materials in hippocampal CA3 pyramidal neurons.	N-acetylaspartate	91-109	anon-E9	Drosophila melanogaster	41-44
20806406-3	2010	The results showed that the APP(Swe)/PS1(dE9) mice had significantly decreased hippocampal N-acetyl aspartate (NAA)/total creatine (tCr) level at 16 months of age, which was associated with degeneration of and intracellular deposition of thioflavine S-positive materials in hippocampal CA3 pyramidal neurons.	N-acetylaspartate	111-114	presenilin 1	Mus musculus	37-40
20806406-3	2010	The results showed that the APP(Swe)/PS1(dE9) mice had significantly decreased hippocampal N-acetyl aspartate (NAA)/total creatine (tCr) level at 16 months of age, which was associated with degeneration of and intracellular deposition of thioflavine S-positive materials in hippocampal CA3 pyramidal neurons.	N-acetylaspartate	111-114	anon-E9	Drosophila melanogaster	41-44
20686917-8	2010	CAT, GPx activities, and total antioxidant potential were significantly reduced, while hydrogen peroxide content, TBA-RS, spontaneous chemiluminescence, and protein carbonyl content were significantly enhanced by acute administration of NAA.	N-acetylaspartate	237-240	catalase	Rattus norvegicus	0-3
20673702-0	2010	Upregulation of N-acetylaspartic acid resulting nitric oxide toxicity induces aspartoacylase mutations and protein interaction to cause pathophysiology seen in Canavan disease.	N-acetylaspartate	16-37	aspartoacylase	Homo sapiens	78-92
20673702-1	2010	Aspartoacylase (ASPA) converts N-acetylaspartic acid into aspartate and acetate.	N-acetylaspartate	31-52	aspartoacylase	Homo sapiens	0-14
20673702-1	2010	Aspartoacylase (ASPA) converts N-acetylaspartic acid into aspartate and acetate.	N-acetylaspartate	31-52	aspartoacylase	Homo sapiens	16-20
20673702-2	2010	In Canavan disease (CD), N-acetylaspartic acid (NAA) is found to be increased and over 65 mutations including IVS4+1 G   T, deletion of introns and exons have been reported in the ASPA gene.	N-acetylaspartate	25-46	aspartoacylase	Homo sapiens	180-184
20673702-2	2010	In Canavan disease (CD), N-acetylaspartic acid (NAA) is found to be increased and over 65 mutations including IVS4+1 G   T, deletion of introns and exons have been reported in the ASPA gene.	N-acetylaspartate	48-51	aspartoacylase	Homo sapiens	180-184
20673702-5	2010	We have reported that elevated levels of NAA induce inducible nitric oxide (iNOS) to produce nitric oxide toxicity in CD.	N-acetylaspartate	41-44	nitric oxide synthase 2	Homo sapiens	76-80
20673702-7	2010	Therefore we hypothesize that upregulation of NAA stimulates NOS and the resulting nitric oxide toxicity induces ASPA mutations and protein interaction to result pathophysiological abnormalities seen in patients with CD.	N-acetylaspartate	46-49	aspartoacylase	Homo sapiens	113-117
20657015-7	2010	RIMKLA catalyzed the ATP-dependent synthesis of N-acetylaspartylglutamate from N-acetylaspartate and l-glutamate.	N-acetylaspartate	79-96	ribosomal modification protein rimK like family member A	Homo sapiens	0-6
20805522-4	2010	RESULTS: Symptomatic MAPT mutation carriers were characterized by decreased N-acetylaspartate/creatine (NAA/Cr) ratio, an index of neuronal integrity, increased myoinositol (mI)/Cr ratio, a possible marker for glial activity, decreased NAA/mI, and hippocampal atrophy (p < 0.001).	N-acetylaspartate	76-93	regulator of microtubule dynamics 1	Homo sapiens	21-25
20805522-4	2010	RESULTS: Symptomatic MAPT mutation carriers were characterized by decreased N-acetylaspartate/creatine (NAA/Cr) ratio, an index of neuronal integrity, increased myoinositol (mI)/Cr ratio, a possible marker for glial activity, decreased NAA/mI, and hippocampal atrophy (p < 0.001).	N-acetylaspartate	104-107	regulator of microtubule dynamics 1	Homo sapiens	21-25
20805522-4	2010	RESULTS: Symptomatic MAPT mutation carriers were characterized by decreased N-acetylaspartate/creatine (NAA/Cr) ratio, an index of neuronal integrity, increased myoinositol (mI)/Cr ratio, a possible marker for glial activity, decreased NAA/mI, and hippocampal atrophy (p < 0.001).	N-acetylaspartate	236-239	regulator of microtubule dynamics 1	Homo sapiens	21-25
20805522-5	2010	Whereas presymptomatic MAPT mutation carriers had elevated mI/Cr and decreased NAA/mI (p < 0.001), NAA/Cr levels and hippocampal volumes were not different from controls.	N-acetylaspartate	79-82	regulator of microtubule dynamics 1	Homo sapiens	23-27
20805522-8	2010	CONCLUSION: (1)H MRS metabolite abnormalities characterized by an elevated mI/Cr and decreased NAA/mI are present several years before the onset of symptoms in MAPT mutation carriers.	N-acetylaspartate	95-98	regulator of microtubule dynamics 1	Homo sapiens	160-164
20619617-2	2010	Individuals with the S/S genotype of the 5-HTTLPR polymorphism showed significantly lower levels of N-acetylaspartate/creatine in the right medial prefrontal cortex compared with those with the S/L genotype.	N-acetylaspartate	100-117	solute carrier family 6 member 4	Homo sapiens	41-49
20488677-5	2010	NAA concentration tended to increase in CBTp+SC patients at follow-up (n=7 with usable data) concomitant with improvement in positive symptoms.	N-acetylaspartate	0-3	opsin 1, short wave sensitive	Homo sapiens	40-44
19457086-5	2009	Interestingly, over-expression of Folh1 would be expected to result in accumulation of its enzymatic product N-acetyl-aspartate, an event known to be linked to Canavan disease, a human cerebral degenerative syndrome often involving blindness and hearing loss.	N-acetylaspartate	109-127	folate hydrolase 1	Homo sapiens	34-39
20392701-1	2010	Our goal was to identify the reaction catalyzed by NAT8 (N-acetyltransferase 8), a putative N-acetyltransferase homologous to the enzyme (NAT8L) that produces N-acetylaspartate in brain.	N-acetylaspartate	159-176	N-acetyltransferase 8 (putative)	Homo sapiens	51-55
20392701-1	2010	Our goal was to identify the reaction catalyzed by NAT8 (N-acetyltransferase 8), a putative N-acetyltransferase homologous to the enzyme (NAT8L) that produces N-acetylaspartate in brain.	N-acetylaspartate	159-176	N-acetyltransferase 8 (putative)	Homo sapiens	57-78
20392701-1	2010	Our goal was to identify the reaction catalyzed by NAT8 (N-acetyltransferase 8), a putative N-acetyltransferase homologous to the enzyme (NAT8L) that produces N-acetylaspartate in brain.	N-acetylaspartate	159-176	N-alpha-acetyltransferase 30, NatC catalytic subunit	Homo sapiens	83-111
20392701-1	2010	Our goal was to identify the reaction catalyzed by NAT8 (N-acetyltransferase 8), a putative N-acetyltransferase homologous to the enzyme (NAT8L) that produces N-acetylaspartate in brain.	N-acetylaspartate	159-176	N-acetyltransferase 8 like	Homo sapiens	138-143
20385109-0	2010	Methamphetamine-induced neuronal protein NAT8L is the NAA biosynthetic enzyme: implications for specialized acetyl coenzyme A metabolism in the CNS.	N-acetylaspartate	54-57	N-acetyltransferase 8 like	Homo sapiens	41-46
20385109-5	2010	A very recent report has identified Nat8l as the gene encoding Asp-NAT and confirmed that the only child diagnosed with a lack of NAA on brain magnetic resonance spectrograms has a 19-bp deletion in this gene.	N-acetylaspartate	130-133	N-acetyltransferase 8 like	Homo sapiens	36-41
20385109-7	2010	In studies done concurrently in our laboratory we have demonstrated via cloning, expression, specificity for acetylation of aspartate, responsiveness to methamphetamine treatment, molecular modeling and comparative immunolocalization that NAT8L is the NAA biosynthetic enzyme Asp-NAT.	N-acetylaspartate	252-255	N-acetyltransferase 8 like	Homo sapiens	239-244
20394738-2	2010	N-acetylaspartylglutamate (NAAG) is an acetylated dipeptide formed from NAA, and may be an agonist of the mGluR3 receptor.	N-acetylaspartate	27-30	glutamate receptor, ionotropic, AMPA3 (alpha 3)	Mus musculus	106-112
20043005-3	2010	We hypothesized that the prefrontal levels of N-acetyl-aspartate (NAA), a neuronal marker, and choline-containing compound (Cho), which are related to membrane turnover, would increase with CDP-choline treatment in MA-dependent patients.	N-acetylaspartate	46-64	cut like homeobox 1	Homo sapiens	190-193
20043005-3	2010	We hypothesized that the prefrontal levels of N-acetyl-aspartate (NAA), a neuronal marker, and choline-containing compound (Cho), which are related to membrane turnover, would increase with CDP-choline treatment in MA-dependent patients.	N-acetylaspartate	66-69	cut like homeobox 1	Homo sapiens	190-193
20043005-7	2010	Generalized estimating equation regression analyses showed that the rate of change in prefrontal NAA (p=0.005) and Cho (p=0.03) levels were greater with CDP-choline treatment than with placebo.	N-acetylaspartate	97-100	cut like homeobox 1	Homo sapiens	153-156
20043005-8	2010	In the CDP-choline-treated patients, changes in prefrontal NAA levels were positively associated with the total number of negative urine results (p=0.03).	N-acetylaspartate	59-62	cut like homeobox 1	Homo sapiens	7-10
19347959-3	2009	Glutamate Carboxypeptidase II (GCP II) hydrolyzes N-acetyl-alpha L-aspartyl-L-glutamate (NAAG) into glutamate and N-acetyl-aspartate.	N-acetylaspartate	114-132	folate hydrolase 1	Mus musculus	0-29
19347959-3	2009	Glutamate Carboxypeptidase II (GCP II) hydrolyzes N-acetyl-alpha L-aspartyl-L-glutamate (NAAG) into glutamate and N-acetyl-aspartate.	N-acetylaspartate	114-132	folate hydrolase 1	Mus musculus	31-37
20464498-3	2010	ASPA produces free acetate from the concentrated brain metabolite, N-acetylaspartate (NAA).	N-acetylaspartate	67-84	aspartoacylase	Rattus norvegicus	0-4
20464498-3	2010	ASPA produces free acetate from the concentrated brain metabolite, N-acetylaspartate (NAA).	N-acetylaspartate	86-89	aspartoacylase	Rattus norvegicus	0-4
20437087-2	2010	Considering that the mechanisms of brain damage in this disease remain poorly understood, in the present study we investigated the in vitro and in vivo effects of N-acetylaspartic acid on the activities of catalase, superoxide dismutase and glutathione peroxidase, as well as on hydrogen peroxide concentration in cerebral cortex of 14-day-old rats.	N-acetylaspartate	163-184	catalase	Rattus norvegicus	206-214
20220018-3	2010	Cerebellar concentrations of N-acetylaspartate (NAA), myo-inositol, and glutamate as measured by magnetic resonance spectroscopy (MRS) correlate with ataxia scores of patients with SCA1, indicating their potential as reliable biomarkers of neurodegeneration.	N-acetylaspartate	29-46	ataxin 1	Homo sapiens	181-185
20220018-3	2010	Cerebellar concentrations of N-acetylaspartate (NAA), myo-inositol, and glutamate as measured by magnetic resonance spectroscopy (MRS) correlate with ataxia scores of patients with SCA1, indicating their potential as reliable biomarkers of neurodegeneration.	N-acetylaspartate	48-51	ataxin 1	Homo sapiens	181-185
19874395-9	2010	The changes in the NAA/creatine ratio in the PCG correlated significantly with the changes in the ADAS-cog (P = 0.004).	N-acetylaspartate	19-22	alkylglycerone phosphate synthase	Homo sapiens	98-102
19683059-0	2010	Met carriers of BDNF Val66Met genotype show increased N-acetylaspartate concentration in the anterior cingulate cortex.	N-acetylaspartate	54-71	brain derived neurotrophic factor	Homo sapiens	16-20
19683059-2	2010	We previously found that BDNF serum concentration was predicted by the concentration of NAA in the ACC, indicating that neuronal integrity and vitality of a cortical region like the ACC, as reflected by a high concentration of NAA, might be related to high concentrations of BDNF in serum.	N-acetylaspartate	88-91	brain derived neurotrophic factor	Homo sapiens	25-29
19683059-2	2010	We previously found that BDNF serum concentration was predicted by the concentration of NAA in the ACC, indicating that neuronal integrity and vitality of a cortical region like the ACC, as reflected by a high concentration of NAA, might be related to high concentrations of BDNF in serum.	N-acetylaspartate	227-230	brain derived neurotrophic factor	Homo sapiens	25-29
19807691-4	2009	The molecular identity of the NAT (N-acetyltransferase) that catalyses NAA synthesis has remained unknown, because the enzyme is membrane-bound and difficult to purify.	N-acetylaspartate	71-74	bromodomain containing 2	Homo sapiens	30-33
19807691-4	2009	The molecular identity of the NAT (N-acetyltransferase) that catalyses NAA synthesis has remained unknown, because the enzyme is membrane-bound and difficult to purify.	N-acetylaspartate	71-74	bromodomain containing 2	Homo sapiens	35-54
19807691-6	2009	Transfection studies in HEK-293T [human embryonic kidney-293 cells expressing the large T-antigen of SV40 (simian virus 40)] indicated that NAT8L, but not NAT14, catalysed the synthesis of NAA from L-aspartate and acetyl-CoA.	N-acetylaspartate	189-192	N-acetyltransferase 8 like	Homo sapiens	140-145
19807691-9	2009	A mutation search in the NAT8L gene of the only patient known to be deficient in NAA disclosed the presence of a homozygous 19 bp deletion, resulting in a change in reading frame and the absence of production of a functional protein.	N-acetylaspartate	81-84	N-acetyltransferase 8 like	Homo sapiens	25-30
19807691-10	2009	We conclude that NAT8L, a neuron-specific protein, is responsible for NAA synthesis and is mutated in primary NAA deficiency (hypoacetylaspartia).	N-acetylaspartate	70-73	N-acetyltransferase 8 like	Homo sapiens	17-22
19319678-5	2009	However, finding the links between the lacks of ASPA activity in oligodendrocytes, the buildup of NAA in white matter (WM) and the mechanisms underlying the edematous spongiform leukodystrophy have remained elusive.	N-acetylaspartate	98-101	aspartoacylase	Homo sapiens	48-52
19457086-6	2009	Consistently, in vivo brain nuclear magnetic resonance spectroscopy identified higher levels of N-acetyl-aspartate in our RasGRF1-/- mice and immunohistochemical analysis detected reduced levels of aspartoacylase, the enzyme which degrades N-acetyl-aspartate.	N-acetylaspartate	96-114	RAS protein-specific guanine nucleotide-releasing factor 1	Mus musculus	122-129
19294497-5	2009	NAA significantly reduced total radical-trapping antioxidant potential, catalase and glucose 6-phosphate dehydrogenase activities, whereas protein carbonyl content and superoxide dismutase activity were significantly enhanced.	N-acetylaspartate	0-3	catalase	Rattus norvegicus	72-80
19294497-5	2009	NAA significantly reduced total radical-trapping antioxidant potential, catalase and glucose 6-phosphate dehydrogenase activities, whereas protein carbonyl content and superoxide dismutase activity were significantly enhanced.	N-acetylaspartate	0-3	glucose-6-phosphate dehydrogenase	Rattus norvegicus	85-118
17943458-4	2009	Incubation of rat stomach tissue with NAA 1.5 mM, 1.5 microM and 1.5 nM induced inflammatory agents TNFalpha, p38MAPK, iNOS, PKC, COX2 and ICAM3; transcription factors phospho-NF-kBp65, cjun and cfos; contractile proteins MLCK and phospho MLC; and calcium channel alpha1C and calcium channel, voltage-dependent, beta 3 subunit compared to their respective control.	N-acetylaspartate	38-41	nitric oxide synthase 2	Rattus norvegicus	119-123
19489242-8	2009	The NAA/Cr ratio was positively correlated with the MMSE score (r = 0.731, P = 0.000), and negatively correlated with the ADAS-cog score (r = -0.541, P = 0.011).	N-acetylaspartate	4-7	alkylglycerone phosphate synthase	Homo sapiens	122-126
19489242-9	2009	CONCLUSIONS: The NAA/Cr ratio decreases in the posterior portion cingulate gyrus of AD patients, and has statistical significant correlations with the score of MMSE and ADAS-cog.	N-acetylaspartate	17-20	alkylglycerone phosphate synthase	Homo sapiens	169-173
19022862-4	2009	Our findings suggest that DRB1*1501 increases disease severity in MS by facilitating the development of more T2-foci, thereby increasing the potential for irreversible axonal compromise and subsequent neuronal degeneration, as suggested by the reduction of NAA concentrations in NAWM, ultimately leading to a decline in brain volume.	N-acetylaspartate	257-260	major histocompatibility complex, class II, DR beta 1	Homo sapiens	26-30
19091459-4	2009	Antioxidant N-acetyl-l-aspartate (NAC) decreased vessels number in tumors formed by cells with inactivated p53 and inhibited their growth.	N-acetylaspartate	12-32	tumor protein p53	Homo sapiens	107-110
19091459-4	2009	Antioxidant N-acetyl-l-aspartate (NAC) decreased vessels number in tumors formed by cells with inactivated p53 and inhibited their growth.	N-acetylaspartate	34-37	tumor protein p53	Homo sapiens	107-110
17943458-4	2009	Incubation of rat stomach tissue with NAA 1.5 mM, 1.5 microM and 1.5 nM induced inflammatory agents TNFalpha, p38MAPK, iNOS, PKC, COX2 and ICAM3; transcription factors phospho-NF-kBp65, cjun and cfos; contractile proteins MLCK and phospho MLC; and calcium channel alpha1C and calcium channel, voltage-dependent, beta 3 subunit compared to their respective control.	N-acetylaspartate	38-41	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	130-134
17943458-4	2009	Incubation of rat stomach tissue with NAA 1.5 mM, 1.5 microM and 1.5 nM induced inflammatory agents TNFalpha, p38MAPK, iNOS, PKC, COX2 and ICAM3; transcription factors phospho-NF-kBp65, cjun and cfos; contractile proteins MLCK and phospho MLC; and calcium channel alpha1C and calcium channel, voltage-dependent, beta 3 subunit compared to their respective control.	N-acetylaspartate	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-199
17943458-4	2009	Incubation of rat stomach tissue with NAA 1.5 mM, 1.5 microM and 1.5 nM induced inflammatory agents TNFalpha, p38MAPK, iNOS, PKC, COX2 and ICAM3; transcription factors phospho-NF-kBp65, cjun and cfos; contractile proteins MLCK and phospho MLC; and calcium channel alpha1C and calcium channel, voltage-dependent, beta 3 subunit compared to their respective control.	N-acetylaspartate	38-41	myosin light chain kinase 3	Rattus norvegicus	222-226
18478328-2	2009	The biomedical relevance of such inquiries is highlighted by the myelin-associated pathology of Canavan disease, an inherited childhood disorder resulting from mutation of aspartoacylase (ASPA), the NAA-hydrolyzing enzyme.	N-acetylaspartate	199-202	aspartoacylase	Rattus norvegicus	172-186
18478328-2	2009	The biomedical relevance of such inquiries is highlighted by the myelin-associated pathology of Canavan disease, an inherited childhood disorder resulting from mutation of aspartoacylase (ASPA), the NAA-hydrolyzing enzyme.	N-acetylaspartate	199-202	aspartoacylase	Rattus norvegicus	188-192
18726138-0	2008	SNAP-25 genotype influences NAA/Cho in left hippocampus.	N-acetylaspartate	28-31	synaptosome associated protein 25	Homo sapiens	0-7
17965994-0	2009	Dopamine transporter genotype influences N-acetyl-aspartate in the left putamen.	N-acetylaspartate	41-59	solute carrier family 6 member 3	Homo sapiens	0-20
17965994-3	2009	The aim of this study was to determine whether the DAT1VNTR polymorphism alters the metabolic ratios NAA/Cho, NAA/Cr, Cho/Cr and Ins/Cr in the left dorsolateral prefrontal cortex, anterior cingulate cortex, and putamen in healthy subjects and psychiatric patients irrespective of clinical diagnosis.	N-acetylaspartate	101-104	solute carrier family 6 member 3	Homo sapiens	51-55
17965994-3	2009	The aim of this study was to determine whether the DAT1VNTR polymorphism alters the metabolic ratios NAA/Cho, NAA/Cr, Cho/Cr and Ins/Cr in the left dorsolateral prefrontal cortex, anterior cingulate cortex, and putamen in healthy subjects and psychiatric patients irrespective of clinical diagnosis.	N-acetylaspartate	110-113	solute carrier family 6 member 3	Homo sapiens	51-55
17965994-7	2009	RESULTS: The individuals with the homozygous DAT1 10-repeat genotype presented significantly higher ratios of NAA/Cho and NAA/Cr in the left putamen compared to the group of individuals with the 9/9-repeat or 9/10-repeat genotype.	N-acetylaspartate	110-113	solute carrier family 6 member 3	Homo sapiens	45-49
17965994-7	2009	RESULTS: The individuals with the homozygous DAT1 10-repeat genotype presented significantly higher ratios of NAA/Cho and NAA/Cr in the left putamen compared to the group of individuals with the 9/9-repeat or 9/10-repeat genotype.	N-acetylaspartate	122-125	solute carrier family 6 member 3	Homo sapiens	45-49
17965994-8	2009	CONCLUSION: The VNTR polymorphism of the DAT1-gene modulates NAA/Cho and NAA/Cr in the left putamen independent of psychiatric diagnosis status.	N-acetylaspartate	61-64	solute carrier family 6 member 3	Homo sapiens	41-45
17965994-8	2009	CONCLUSION: The VNTR polymorphism of the DAT1-gene modulates NAA/Cho and NAA/Cr in the left putamen independent of psychiatric diagnosis status.	N-acetylaspartate	73-76	solute carrier family 6 member 3	Homo sapiens	41-45
18707679-0	2008	Impact of the brain-derived neurotrophic factor Val66Met polymorphism on levels of hippocampal N-acetyl-aspartate assessed by magnetic resonance spectroscopic imaging at 3 Tesla.	N-acetylaspartate	95-113	brain derived neurotrophic factor	Homo sapiens	14-47
18707679-1	2008	BACKGROUND: This study was conducted to corroborate prior evidence of an effect of the brain-derived neurotrophic factor (BDNF) valine (val) to methionine (met) amino acid substitution at codon 66 (val66met) polymorphism on measures of N-acetyl-aspartate (NAA) containing compounds in healthy subjects.	N-acetylaspartate	236-254	brain derived neurotrophic factor	Homo sapiens	87-120
18707679-1	2008	BACKGROUND: This study was conducted to corroborate prior evidence of an effect of the brain-derived neurotrophic factor (BDNF) valine (val) to methionine (met) amino acid substitution at codon 66 (val66met) polymorphism on measures of N-acetyl-aspartate (NAA) containing compounds in healthy subjects.	N-acetylaspartate	236-254	brain derived neurotrophic factor	Homo sapiens	122-126
18707679-1	2008	BACKGROUND: This study was conducted to corroborate prior evidence of an effect of the brain-derived neurotrophic factor (BDNF) valine (val) to methionine (met) amino acid substitution at codon 66 (val66met) polymorphism on measures of N-acetyl-aspartate (NAA) containing compounds in healthy subjects.	N-acetylaspartate	256-259	brain derived neurotrophic factor	Homo sapiens	87-120
18707679-1	2008	BACKGROUND: This study was conducted to corroborate prior evidence of an effect of the brain-derived neurotrophic factor (BDNF) valine (val) to methionine (met) amino acid substitution at codon 66 (val66met) polymorphism on measures of N-acetyl-aspartate (NAA) containing compounds in healthy subjects.	N-acetylaspartate	256-259	brain derived neurotrophic factor	Homo sapiens	122-126
18707679-6	2008	CONCLUSIONS: We confirmed the association between the met-BDNF variant and reduced levels of hippocampal NAA found with a similar technique at 1.5T.	N-acetylaspartate	105-108	brain derived neurotrophic factor	Homo sapiens	58-62
18987190-1	2008	Aspartoacylase (ASPA) is an oligodendrocyte-restricted enzyme that catalyzes the hydrolysis of neuronally derived N-acetylaspartate (NAA) to acetate and aspartic acid.	N-acetylaspartate	114-131	aspartoacylase	Mus musculus	0-14
18987190-1	2008	Aspartoacylase (ASPA) is an oligodendrocyte-restricted enzyme that catalyzes the hydrolysis of neuronally derived N-acetylaspartate (NAA) to acetate and aspartic acid.	N-acetylaspartate	114-131	aspartoacylase	Mus musculus	16-20
18987190-1	2008	Aspartoacylase (ASPA) is an oligodendrocyte-restricted enzyme that catalyzes the hydrolysis of neuronally derived N-acetylaspartate (NAA) to acetate and aspartic acid.	N-acetylaspartate	133-136	aspartoacylase	Mus musculus	0-14
18987190-1	2008	Aspartoacylase (ASPA) is an oligodendrocyte-restricted enzyme that catalyzes the hydrolysis of neuronally derived N-acetylaspartate (NAA) to acetate and aspartic acid.	N-acetylaspartate	133-136	aspartoacylase	Mus musculus	16-20
18987190-4	2008	Homozygous Aspa(nur7nur7) mice do not express detectable Aspa protein and display an early-onset spongy degeneration of CNS myelin with increased NAA levels similar to that observed in CD patients.	N-acetylaspartate	146-149	aspartoacylase	Mus musculus	11-15
18987190-4	2008	Homozygous Aspa(nur7nur7) mice do not express detectable Aspa protein and display an early-onset spongy degeneration of CNS myelin with increased NAA levels similar to that observed in CD patients.	N-acetylaspartate	146-149	aspartoacylase	Mus musculus	16-24
19156487-8	2008	RESULTS: We observed that two plasma proteins previously shown to be differentially expressed in AD, complement factor-H (CFH) and alpha-2-macroglobulin (A2M) showed significant positive correlations with hippocampal NAA/mI ratio in AD.	N-acetylaspartate	217-220	complement factor H	Homo sapiens	101-120
19156487-8	2008	RESULTS: We observed that two plasma proteins previously shown to be differentially expressed in AD, complement factor-H (CFH) and alpha-2-macroglobulin (A2M) showed significant positive correlations with hippocampal NAA/mI ratio in AD.	N-acetylaspartate	217-220	complement factor H	Homo sapiens	122-125
19156487-8	2008	RESULTS: We observed that two plasma proteins previously shown to be differentially expressed in AD, complement factor-H (CFH) and alpha-2-macroglobulin (A2M) showed significant positive correlations with hippocampal NAA/mI ratio in AD.	N-acetylaspartate	217-220	alpha-2-macroglobulin	Homo sapiens	131-152
19156487-9	2008	CONCLUSIONS: The association of plasma CFH and A2M with hippocampal NAA/mI in this cohort of AD subjects suggests that these proteins may reflect disease progression in early AD.	N-acetylaspartate	68-71	complement factor H	Homo sapiens	39-42
18319316-5	2008	RESULTS: Compared with controls, young children with MCT8 show choline and myoinositol level increases and N-acetyl aspartate decreases in supraventricular gray and white matter, phenomena associated with the degree of dysmyelinization according to MRI.	N-acetylaspartate	107-125	solute carrier family 16 member 2	Homo sapiens	53-57
18035849-4	2008	Positive correlation was found between total N-Acetylaspartate (tNAA) reduction and neuronal density in hippocampal CA1 (P &lt; 0.001), CA3 (P = 0.015), and CA4 subfields (P = 0.031) and the dentate gyrus (P = 0.006).	N-acetylaspartate	45-62	carbonic anhydrase 1	Homo sapiens	116-119
18035849-4	2008	Positive correlation was found between total N-Acetylaspartate (tNAA) reduction and neuronal density in hippocampal CA1 (P &lt; 0.001), CA3 (P = 0.015), and CA4 subfields (P = 0.031) and the dentate gyrus (P = 0.006).	N-acetylaspartate	45-62	carbonic anhydrase 3	Homo sapiens	136-139
18035849-4	2008	Positive correlation was found between total N-Acetylaspartate (tNAA) reduction and neuronal density in hippocampal CA1 (P &lt; 0.001), CA3 (P = 0.015), and CA4 subfields (P = 0.031) and the dentate gyrus (P = 0.006).	N-acetylaspartate	45-62	carbonic anhydrase 4	Homo sapiens	157-160
17822430-4	2008	Specifically, in subfield CA3 of AHS patients despite of a moderate preservation of neuronal cell densities the concentration of NAA was significantly lowered, while the concentrations of lactate, glucose, and succinate were elevated.	N-acetylaspartate	129-132	carbonic anhydrase 3	Homo sapiens	26-29
18355643-0	2008	N-acetyl-L-aspartate activates hippocampal CA3 neurons in rodent slice preparations.	N-acetylaspartate	0-20	carbonic anhydrase 3	Rattus norvegicus	43-46
18355643-6	2008	NAA activated the hippocampal CA3 neurons of Wistar rats via the metabotropic glutamate receptor (mGluR) in acutely dissociated hippocampal CA3 neurons.	N-acetylaspartate	0-3	carbonic anhydrase 3	Rattus norvegicus	30-33
18355643-6	2008	NAA activated the hippocampal CA3 neurons of Wistar rats via the metabotropic glutamate receptor (mGluR) in acutely dissociated hippocampal CA3 neurons.	N-acetylaspartate	0-3	carbonic anhydrase 3	Rattus norvegicus	140-143
18355643-7	2008	The mechanism of NAA action on CA3 neurons was examined with intracellular recording of Wistar and tremor rat hippocampal slices to evaluate the role of NAA in neuronal networks.	N-acetylaspartate	17-20	carbonic anhydrase 3	Rattus norvegicus	31-34
18355643-8	2008	Bath application of NAA (10 microM-1mM) dose-dependently induced depolarization in CA3 neurons of Wistar and tremor rats.	N-acetylaspartate	20-23	carbonic anhydrase 3	Rattus norvegicus	83-86
18355643-11	2008	These results suggest that NAA probably activates hippocampal CA3 neurons via the mGluR in a neuronal network.	N-acetylaspartate	27-30	carbonic anhydrase 3	Rattus norvegicus	62-65
18164911-1	2008	The objective of this study was to determine whether cerebrospinal fluid(CSF)-corrected concentrations of N-acetylaspartate are lower in several brain regions of drug- and medication-free subjects with bipolar disorder as compared with matched healthy controls.	N-acetylaspartate	106-123	colony stimulating factor 2	Homo sapiens	73-76
24299942-7	2007	In the patients treated with IFNbeta-1b there was a significant increase in the ratio of NAA/Cr in NAWM (p=0.028) at 24 months after the initiation of treatment.	N-acetylaspartate	89-92	interferon beta 1	Homo sapiens	29-36
17913561-5	2008	CONCLUSIONS: after STN DBS cortical NAA/Cho, NAA/Cr ratios increased significantly, which were highly correlated with the significant improvements of the UPDRS scores.	N-acetylaspartate	36-39	eukaryotic translation elongation factor 1 alpha 2	Homo sapiens	19-22
17913561-5	2008	CONCLUSIONS: after STN DBS cortical NAA/Cho, NAA/Cr ratios increased significantly, which were highly correlated with the significant improvements of the UPDRS scores.	N-acetylaspartate	45-48	eukaryotic translation elongation factor 1 alpha 2	Homo sapiens	19-22
17763847-11	2007	There were strong positive correlations between Cho/NAA ratio and MMP-2 COD (r = 0.669, P = 0.002), and between Cho/Cr ratio and MMP-2 COD (r = 0.689, P = 0.001).	N-acetylaspartate	52-55	matrix metallopeptidase 2	Homo sapiens	66-71
17693006-2	2007	Studies have shown that the brain N-acetyl aspartate (NAA) levels are greatly decreased in aralar-deficient mice, suggesting that aralar plays an important role in the synthesis of NAA in neuronal cells.	N-acetylaspartate	34-52	solute carrier family 25 member 12	Homo sapiens	91-97
17560556-2	2007	In the present study we hypothesized that serum BDNF concentration is associated with in vivo level of cerebral N-acetylaspartate (NAA), a well established marker of neuronal integrity.	N-acetylaspartate	112-129	brain derived neurotrophic factor	Homo sapiens	48-52
17560556-2	2007	In the present study we hypothesized that serum BDNF concentration is associated with in vivo level of cerebral N-acetylaspartate (NAA), a well established marker of neuronal integrity.	N-acetylaspartate	131-134	brain derived neurotrophic factor	Homo sapiens	48-52
17560556-5	2007	RESULTS: The BDNF serum concentrations were positively associated with the concentrations of NAA (T = 2.193, p = .037) and total choline (T = 1.997, p = .055; trend) but not total creatine or glutamate in the ACC.	N-acetylaspartate	93-96	brain derived neurotrophic factor	Homo sapiens	13-17
17560556-7	2007	CONCLUSIONS: The preliminary data might indicate that BDNF serum concentration reflects some aspects of neuronal plasticity as indicated by its association with NAA level in the cerebral cortex.	N-acetylaspartate	161-164	brain derived neurotrophic factor	Homo sapiens	54-58
17707174-4	2007	Relative to the creatine/phosphocreatine peak, BCS lesions displayed decreases of N-acetyl aspartate and increases of choline, myo-inositol (mI), glutamine/glutamate (Glx), lactate and lipid+macromolecule signals, in agreement with previous reports.	N-acetylaspartate	82-100	BCS1 homolog, ubiquinol-cytochrome c reductase complex chaperone	Homo sapiens	47-50
17693006-2	2007	Studies have shown that the brain N-acetyl aspartate (NAA) levels are greatly decreased in aralar-deficient mice, suggesting that aralar plays an important role in the synthesis of NAA in neuronal cells.	N-acetylaspartate	54-57	solute carrier family 25 member 12	Homo sapiens	91-97
17693006-2	2007	Studies have shown that the brain N-acetyl aspartate (NAA) levels are greatly decreased in aralar-deficient mice, suggesting that aralar plays an important role in the synthesis of NAA in neuronal cells.	N-acetylaspartate	181-184	solute carrier family 25 member 12	Homo sapiens	91-97
17693006-3	2007	Since magnetic resonance spectroscopy studies have revealed consistently reduced NAA levels in various brain regions of schizophrenic patients and their unaffected relatives, genes that affect aralar levels or NAA metabolism in the brain may be implicated in the pathogenesis of schizophrenia.	N-acetylaspartate	81-84	solute carrier family 25 member 12	Homo sapiens	193-199
17693006-9	2007	Further studies with SLC25A12 variants relating to brain NAA levels in patients with schizophrenia are suggested.	N-acetylaspartate	57-60	solute carrier family 25 member 12	Homo sapiens	21-29
17432958-6	2007	In the spinal cord of G93A-SOD1 mice significantly decreased levels of N-acetyl aspartate were already detected 34 days postpartum, i.e. about 60 days before the average disease onset caused by motor neuron decline.	N-acetylaspartate	71-89	superoxide dismutase 1, soluble	Mus musculus	27-31
17679670-1	2007	BACKGROUND: On proton magnetic resonance spectroscopic imaging ((1)H MRSI), there is a decrease in cerebellar N-acetylaspartate/total creatine (NAA/tCr) in essential tremor (ET), signifying cerebellar neuronal dysfunction or degeneration.	N-acetylaspartate	110-127	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	148-151
17386946-3	2007	In this work we evaluated the use of the monomethyl ester of NAA (NAA MME) to increase the relatively low level of NAA in cultured hippocampal slices.	N-acetylaspartate	61-64	membrane metallo-endopeptidase	Rattus norvegicus	70-73
17386946-3	2007	In this work we evaluated the use of the monomethyl ester of NAA (NAA MME) to increase the relatively low level of NAA in cultured hippocampal slices.	N-acetylaspartate	66-69	membrane metallo-endopeptidase	Rattus norvegicus	70-73
17386946-4	2007	When slices were treated with 30 mM NAA MME for 3 days the NAA concentration increased from 31.6 to 185.3 nmol/mg protein.	N-acetylaspartate	36-39	membrane metallo-endopeptidase	Rattus norvegicus	40-43
17386946-4	2007	When slices were treated with 30 mM NAA MME for 3 days the NAA concentration increased from 31.6 to 185.3 nmol/mg protein.	N-acetylaspartate	59-62	membrane metallo-endopeptidase	Rattus norvegicus	40-43
17386946-6	2007	NAA MME treatment increased NAA in neurons and the increase was non-toxic as determined by the low uptake of propidium iodide, a dye that only enters damaged cells.	N-acetylaspartate	0-3	membrane metallo-endopeptidase	Rattus norvegicus	4-7
17386946-6	2007	NAA MME treatment increased NAA in neurons and the increase was non-toxic as determined by the low uptake of propidium iodide, a dye that only enters damaged cells.	N-acetylaspartate	28-31	membrane metallo-endopeptidase	Rattus norvegicus	4-7
17239356-3	2007	RESULTS: A significantly diminished N-acetylaspartate/total creatine (NAA/tCr) ratio in the dorsolateral prefrontal cortex (DLPFC) was observed in cannabis users (p = .0003).	N-acetylaspartate	36-53	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	74-77
17291773-0	2007	Carbamazepine treatment recovered low N-acetylaspartate+N-acetylaspartylglutamate (tNAA) levels in the megencephaly mouse BALB/cByJ-Kv1.1(mceph/mceph).	N-acetylaspartate	38-55	potassium voltage-gated channel, shaker-related subfamily, member 1	Mus musculus	132-137
17291773-7	2007	mceph/mceph mice had lower levels of N-acetylaspartate+N-acetylaspartylglutamate (tNAA) and choline-containing (tCho) compounds compared to wt mice.	N-acetylaspartate	37-54	potassium voltage-gated channel, shaker-related subfamily, member 1	Mus musculus	0-5
17291773-7	2007	mceph/mceph mice had lower levels of N-acetylaspartate+N-acetylaspartylglutamate (tNAA) and choline-containing (tCho) compounds compared to wt mice.	N-acetylaspartate	37-54	potassium voltage-gated channel, shaker-related subfamily, member 1	Mus musculus	6-11
17425226-10	2007	Before CPAP treatment cortical [NAA] in OSAS (11.86 mM +/- 0.80, mean +/- SD) was significantly lower than in controls (12.85 +/- 0.93; P = 0.01) and positively correlated with minimum SpO2 during sleep (r = 0.69; P = 0.006) and MSLT scores (r = 0.62; P = 0.01).	N-acetylaspartate	32-35	centromere protein J	Homo sapiens	7-11
17189705-3	2007	We recruited 28 healthy adults and employed a multi-modal neuroimaging approach combined with a task designed to specifically activate the human dACC and statistical path analysis to demonstrate clear roles for intelligence, personality and concentrations of neuronal N-acetylaspartate in determining dACC activation.	N-acetylaspartate	268-285	Acetyl-CoA carboxylase	Drosophila melanogaster	301-305
16935940-1	2006	Mutations in the gene for aspartoacylase (ASPA), which catalyzes deacetylation of N-acetyl-L-aspartate in the central nervous system (CNS), result in Canavan Disease, a fatal dysmyelinating disease.	N-acetylaspartate	82-102	aspartoacylase	Rattus norvegicus	26-40
17249194-10	2006	The results of 1H MRS for the subjects with susceptible genes ApoE epsilon3/epsilon4 (HRT group 12 cases, control group 11 cases) showed that the N-acetylaspartate/total creatine at the area of hippocampus in HRT group (1.54 +/- 0.08) were significantly higher than control group (1.45 +/- 0.13, P < 0.05).	N-acetylaspartate	146-163	apolipoprotein E	Homo sapiens	62-66
17275978-3	2007	During early postnatal central nervous system (CNS) development, the expression of lipogenic enzymes in oligodendrocytes, including the NAA-degrading enzyme aspartoacylase (ASPA), is increased along with increased NAA production in neurons.	N-acetylaspartate	136-139	aspartoacylase	Homo sapiens	173-177
17275978-3	2007	During early postnatal central nervous system (CNS) development, the expression of lipogenic enzymes in oligodendrocytes, including the NAA-degrading enzyme aspartoacylase (ASPA), is increased along with increased NAA production in neurons.	N-acetylaspartate	214-217	aspartoacylase	Homo sapiens	173-177
17275978-4	2007	NAA is transported from neurons to the cytoplasm of oligodendrocytes, where ASPA cleaves the acetate moiety for use in fatty acid and steroid synthesis.	N-acetylaspartate	0-3	aspartoacylase	Homo sapiens	76-80
16926034-1	2006	N-acetylated-alpha-linked-acidic peptidase (NAAG peptidase) converts N-acetyl-aspartyl-glutamate (NAAG, mGluR3 agonist) into N-acetyl-aspartate and glutamate.	N-acetylaspartate	125-143	glutamate receptor, ionotropic, AMPA3 (alpha 3)	Mus musculus	104-110
16935940-1	2006	Mutations in the gene for aspartoacylase (ASPA), which catalyzes deacetylation of N-acetyl-L-aspartate in the central nervous system (CNS), result in Canavan Disease, a fatal dysmyelinating disease.	N-acetylaspartate	82-102	aspartoacylase	Rattus norvegicus	42-46
18040781-8	2006	The rapid decline in NAA/Cr with SIV infection/CD8 depletion and its rapid recovery with HAART suggest that: (1) infected monocyte turnover in the CNS is rapid, occurring in days to weeks; (2) there are endogenous mechanisms that reverse neuronal injury; and (3) a threshold level of infected monocytes/macrophages in the CNS is required to overcome the neuronal recovery processes.	N-acetylaspartate	21-24	CD8a molecule	Homo sapiens	47-50
17177147-1	2006	Canavan disease is a childhood leukodystrophy caused by mutations in the gene for human aspartoacylase ( ASPA), which leads to an abnormal accumulation of the substrate molecule N-acetyl-aspartate (NAA) in the brain.	N-acetylaspartate	178-196	aspartoacylase	Homo sapiens	88-102
17177147-1	2006	Canavan disease is a childhood leukodystrophy caused by mutations in the gene for human aspartoacylase ( ASPA), which leads to an abnormal accumulation of the substrate molecule N-acetyl-aspartate (NAA) in the brain.	N-acetylaspartate	178-196	aspartoacylase	Homo sapiens	105-109
17177147-1	2006	Canavan disease is a childhood leukodystrophy caused by mutations in the gene for human aspartoacylase ( ASPA), which leads to an abnormal accumulation of the substrate molecule N-acetyl-aspartate (NAA) in the brain.	N-acetylaspartate	198-201	aspartoacylase	Homo sapiens	88-102
17177147-1	2006	Canavan disease is a childhood leukodystrophy caused by mutations in the gene for human aspartoacylase ( ASPA), which leads to an abnormal accumulation of the substrate molecule N-acetyl-aspartate (NAA) in the brain.	N-acetylaspartate	198-201	aspartoacylase	Homo sapiens	105-109
16530227-9	2006	1H-MRSI showed N-acetylaspartate to creatine ratio (NAA/Cr) decreases in the central brain VOI in all TTR-FAP patients (p < 0.005).	N-acetylaspartate	15-32	transthyretin	Homo sapiens	102-105
16530227-9	2006	1H-MRSI showed N-acetylaspartate to creatine ratio (NAA/Cr) decreases in the central brain VOI in all TTR-FAP patients (p < 0.005).	N-acetylaspartate	52-55	transthyretin	Homo sapiens	102-105
16707098-1	2006	Aspartoacylase (ASPA) hydrolyzes N-acetylaspartic acid (NAA) into aspartate and acetate.	N-acetylaspartate	33-54	aspartoacylase	Mus musculus	0-14
16707098-1	2006	Aspartoacylase (ASPA) hydrolyzes N-acetylaspartic acid (NAA) into aspartate and acetate.	N-acetylaspartate	33-54	aspartoacylase	Mus musculus	16-20
16707098-1	2006	Aspartoacylase (ASPA) hydrolyzes N-acetylaspartic acid (NAA) into aspartate and acetate.	N-acetylaspartate	56-59	aspartoacylase	Mus musculus	0-14
16707098-1	2006	Aspartoacylase (ASPA) hydrolyzes N-acetylaspartic acid (NAA) into aspartate and acetate.	N-acetylaspartate	56-59	aspartoacylase	Mus musculus	16-20
16707098-8	2006	These data suggest that normal hydrolysis of NAA is affected by ASPA activity seen in the type 2 diabetes model mouse and this change is likely to contribute to neuropathy seen in diabetes, if documented also in patients with type 2 diabetes.	N-acetylaspartate	45-48	aspartoacylase	Mus musculus	64-68
16647192-2	2006	ASPA releases acetate by deacetylation of N-acetylaspartate (NAA), a highly abundant amino acid derivative in the central nervous system.	N-acetylaspartate	42-59	aspartoacylase	Homo sapiens	0-4
16647192-2	2006	ASPA releases acetate by deacetylation of N-acetylaspartate (NAA), a highly abundant amino acid derivative in the central nervous system.	N-acetylaspartate	61-64	aspartoacylase	Homo sapiens	0-4
16647192-5	2006	Our hypothesis is that ASPA actively participates in myelin synthesis by providing NAA-derived acetate for acetyl CoA synthesis, which in turn is used for synthesis of the lipid portion of myelin.	N-acetylaspartate	83-86	aspartoacylase	Homo sapiens	23-27
16585454-0	2006	Effect of metabotropic glutamate receptor 3 genotype on N-acetylaspartate measures in the dorsolateral prefrontal cortex.	N-acetylaspartate	56-73	glutamate metabotropic receptor 3	Homo sapiens	10-43
18040781-2	2006	SIV infection and CD8 depletion resulted in a rapid decline in cerebral N-acetylaspartate (NAA) levels, a sensitive marker of neuronal health.	N-acetylaspartate	72-89	CD8a molecule	Homo sapiens	18-21
18040781-2	2006	SIV infection and CD8 depletion resulted in a rapid decline in cerebral N-acetylaspartate (NAA) levels, a sensitive marker of neuronal health.	N-acetylaspartate	91-94	CD8a molecule	Homo sapiens	18-21
16467855-1	2006	Membrane-bound glutamate carboxypeptidase II (GCPII) is a zinc metalloenzyme that catalyzes the hydrolysis of the neurotransmitter N-acetyl-L-aspartyl-L-glutamate (NAAG) to N-acetyl-L-aspartate and L-glutamate (which is itself a neurotransmitter).	N-acetylaspartate	173-193	folate hydrolase 1	Homo sapiens	15-44
16467855-1	2006	Membrane-bound glutamate carboxypeptidase II (GCPII) is a zinc metalloenzyme that catalyzes the hydrolysis of the neurotransmitter N-acetyl-L-aspartyl-L-glutamate (NAAG) to N-acetyl-L-aspartate and L-glutamate (which is itself a neurotransmitter).	N-acetylaspartate	173-193	folate hydrolase 1	Homo sapiens	46-51
16514368-3	2006	N-acetylaspartate/creatine+phosphocreatine ratio was reduced in the posterior cingulate cortex in the Alzheimer"s disease and frontotemporal dementia/Pick complex patients.	N-acetylaspartate	0-17	protein interacting with PRKCA 1	Homo sapiens	150-154
16585454-1	2006	OBJECTIVE: This study was carried out to confirm prior evidence of an effect of a single nucleotide polymorphism (SNP) in the metabotropic glutamate receptor 3 (GRM3) gene (a putative risk factor for schizophrenia) on measures of N-acetylaspartate in healthy comparison subjects.	N-acetylaspartate	230-247	glutamate metabotropic receptor 3	Homo sapiens	126-159
16585454-1	2006	OBJECTIVE: This study was carried out to confirm prior evidence of an effect of a single nucleotide polymorphism (SNP) in the metabotropic glutamate receptor 3 (GRM3) gene (a putative risk factor for schizophrenia) on measures of N-acetylaspartate in healthy comparison subjects.	N-acetylaspartate	230-247	glutamate metabotropic receptor 3	Homo sapiens	161-165
16802706-2	2006	Patients with CD have aspartoacylase (ASPA) deficiency, which results accumulation of N-acetylaspartic acid (NAA) in the brain and elevated excretion of urinary NAA.	N-acetylaspartate	86-107	aspartoacylase	Homo sapiens	38-42
16802706-2	2006	Patients with CD have aspartoacylase (ASPA) deficiency, which results accumulation of N-acetylaspartic acid (NAA) in the brain and elevated excretion of urinary NAA.	N-acetylaspartate	109-112	aspartoacylase	Homo sapiens	38-42
16802706-2	2006	Patients with CD have aspartoacylase (ASPA) deficiency, which results accumulation of N-acetylaspartic acid (NAA) in the brain and elevated excretion of urinary NAA.	N-acetylaspartate	161-164	aspartoacylase	Homo sapiens	38-42
15668429-10	2005	Regionally, NAA/Cho was lowered in the internal capsule (AMN 1.30 +/- 0.20 vs controls 1.69 +/- 0.37; p = 0.002) and in parieto-occipital white matter (AMN 1.45 +/- 0.19 vs controls 1.78 +/- 0.55; p = 0.04).	N-acetylaspartate	12-15	antagonist of mitotic exit network 1 homolog	Homo sapiens	57-62
16403497-1	2006	This study examined the effect of 2-(phosphonomethyl)-pentanedioic acid (2-PMPA), a potent and selective inhibitor of glutamate carboxypeptidase II (GCP II), an enzyme releasing glutamate and N-acetyl-aspartate from synaptical terminals, on the electroconvulsive threshold in mice.	N-acetylaspartate	192-210	folate hydrolase 1	Mus musculus	149-155
16807907-16	2006	ASPA gene delivery attempts in animal models have shown a lowering of N-acetyl L-aspartate and a change in motor functions, while sponginess of the WM, a characteristic of CD remained unchanged (Matalon et al.	N-acetylaspartate	70-90	aspartoacylase	Homo sapiens	0-4
16091461-6	2005	A reduction in the levels of N-acetylaspartate and glutamate, compared with total creatine levels, was found in APP-PS1 mice with advancing age.	N-acetylaspartate	29-46	presenilin 1	Mus musculus	116-119
16190866-3	2005	GCP II is believed to mediate the hydrolysis of N-acetyl-aspartyl-glutamate (NAAG) to glutamate and N-acetyl-aspartate, and inhibition of NAAG peptidase activity (by GCP II and other peptidases) is neuroprotective.	N-acetylaspartate	100-118	folate hydrolase 1	Mus musculus	0-6
16217711-4	2005	The altered NAA metabolism has been traced to mutations in the gene encoding ASPA, located on chromosome 17 (17p13-ter).	N-acetylaspartate	12-15	aspartoacylase	Homo sapiens	77-81
15836629-0	2005	Transport characteristics of N-acetyl-L-aspartate in rat astrocytes: involvement of sodium-coupled high-affinity carboxylate transporter NaC3/NaDC3-mediated transport system.	N-acetylaspartate	29-49	solute carrier family 13 member 3	Rattus norvegicus	137-141
15836629-0	2005	Transport characteristics of N-acetyl-L-aspartate in rat astrocytes: involvement of sodium-coupled high-affinity carboxylate transporter NaC3/NaDC3-mediated transport system.	N-acetylaspartate	29-49	solute carrier family 13 member 3	Rattus norvegicus	142-147
15836629-1	2005	We investigated in the present study the transport characteristics of N-acetyl-L-aspartate in primary cultures of astrocytes from rat cerebral cortex and the involvement of NA+-coupled high-affinity carboxylate transporter NaC3 (formerly known as NaDC3) responsible for N-acetyl-L-aspartate transport.	N-acetylaspartate	70-90	solute carrier family 13 member 3	Rattus norvegicus	247-252
15836629-1	2005	We investigated in the present study the transport characteristics of N-acetyl-L-aspartate in primary cultures of astrocytes from rat cerebral cortex and the involvement of NA+-coupled high-affinity carboxylate transporter NaC3 (formerly known as NaDC3) responsible for N-acetyl-L-aspartate transport.	N-acetylaspartate	270-290	solute carrier family 13 member 3	Rattus norvegicus	223-227
15836629-1	2005	We investigated in the present study the transport characteristics of N-acetyl-L-aspartate in primary cultures of astrocytes from rat cerebral cortex and the involvement of NA+-coupled high-affinity carboxylate transporter NaC3 (formerly known as NaDC3) responsible for N-acetyl-L-aspartate transport.	N-acetylaspartate	270-290	solute carrier family 13 member 3	Rattus norvegicus	247-252
15836629-8	2005	Taken collectively, these results indicate that NaC3 expressed in rat cerebrocortical astrocytes is responsible for NA+-dependent N-acetyl-L-aspartate transport.	N-acetylaspartate	130-150	solute carrier family 13 member 3	Rattus norvegicus	48-52
15851013-3	2005	Normally, ASPA is enriched in oligodendrocytes and ASPA deficiency results in elevated levels of its substrate molecule, N-acetylaspartate (NAA), brain edema, and dysmyelination.	N-acetylaspartate	121-138	aspartoacylase	Rattus norvegicus	10-14
15851013-3	2005	Normally, ASPA is enriched in oligodendrocytes and ASPA deficiency results in elevated levels of its substrate molecule, N-acetylaspartate (NAA), brain edema, and dysmyelination.	N-acetylaspartate	121-138	aspartoacylase	Rattus norvegicus	51-55
15851013-3	2005	Normally, ASPA is enriched in oligodendrocytes and ASPA deficiency results in elevated levels of its substrate molecule, N-acetylaspartate (NAA), brain edema, and dysmyelination.	N-acetylaspartate	140-143	aspartoacylase	Rattus norvegicus	10-14
15851013-3	2005	Normally, ASPA is enriched in oligodendrocytes and ASPA deficiency results in elevated levels of its substrate molecule, N-acetylaspartate (NAA), brain edema, and dysmyelination.	N-acetylaspartate	140-143	aspartoacylase	Rattus norvegicus	51-55
15851013-9	2005	Our data suggest that NAA-mediated neuronal hyperexcitation but not oligodendrocyte dysfunction can be compensated for by neuronal ASPA expression.	N-acetylaspartate	22-25	aspartoacylase	Rattus norvegicus	131-135
15798152-13	2005	With the Spearman rank test, a significant direct correlation was detected between synaptophysin and ex vivo NAA/Cr (r(s) = 0.72, P &lt; .013).	N-acetylaspartate	109-112	synaptophysin	Homo sapiens	83-96
15798152-15	2005	CONCLUSION: NAA/Cr is a sensitive marker of neuronal injury, not necessarily neuronal loss, and best correlates with synaptophysin, a marker of synaptodendritic dysfunction.	N-acetylaspartate	12-15	synaptophysin	Homo sapiens	117-130
15857674-2	2005	The absence of ASPA expression in these animals results in undetectable levels of enzyme activity and the accumulation of the substrate N-acetyl-aspartate (NAA) in brain, leading to generalized myelin vacuolation and severe motor and cognitive impairment.	N-acetylaspartate	136-154	aspartoacylase	Rattus norvegicus	15-19
15857674-2	2005	The absence of ASPA expression in these animals results in undetectable levels of enzyme activity and the accumulation of the substrate N-acetyl-aspartate (NAA) in brain, leading to generalized myelin vacuolation and severe motor and cognitive impairment.	N-acetylaspartate	156-159	aspartoacylase	Rattus norvegicus	15-19
15857674-4	2005	AAV-ASPA gene transfer resulted in elevated aspartoacylase bioactivity compared to untreated mutant animals and elicited a significant decrease in the pathologically elevated whole-brain NAA levels.	N-acetylaspartate	187-190	aspartoacylase	Rattus norvegicus	4-8
15784740-2	2005	ASPA acts to hydrolyze N-acetylaspartate (NAA) into l-aspartate and acetate, but the connection between ASPA deficiency and the failure of proper CNS development is unclear.	N-acetylaspartate	23-40	aspartoacylase	Homo sapiens	0-4
15784740-2	2005	ASPA acts to hydrolyze N-acetylaspartate (NAA) into l-aspartate and acetate, but the connection between ASPA deficiency and the failure of proper CNS development is unclear.	N-acetylaspartate	42-45	aspartoacylase	Homo sapiens	0-4
15680261-1	2005	Glutamate carboxypeptidase (GCP) II (EC 3.4.17.21), which is also known as N-acetylated-alpha-linked acidic dipeptidase (NAALADase), hydrolyses the endogenous acidic dipeptide N-acetylaspartylglutamate (NAAG), yielding N-acetyl-aspartate and glutamate.	N-acetylaspartate	219-237	folate hydrolase 1	Rattus norvegicus	0-35
15680261-1	2005	Glutamate carboxypeptidase (GCP) II (EC 3.4.17.21), which is also known as N-acetylated-alpha-linked acidic dipeptidase (NAALADase), hydrolyses the endogenous acidic dipeptide N-acetylaspartylglutamate (NAAG), yielding N-acetyl-aspartate and glutamate.	N-acetylaspartate	219-237	folate hydrolase 1	Rattus norvegicus	75-119
15680261-1	2005	Glutamate carboxypeptidase (GCP) II (EC 3.4.17.21), which is also known as N-acetylated-alpha-linked acidic dipeptidase (NAALADase), hydrolyses the endogenous acidic dipeptide N-acetylaspartylglutamate (NAAG), yielding N-acetyl-aspartate and glutamate.	N-acetylaspartate	219-237	folate hydrolase 1	Rattus norvegicus	121-130
15668429-10	2005	Regionally, NAA/Cho was lowered in the internal capsule (AMN 1.30 +/- 0.20 vs controls 1.69 +/- 0.37; p = 0.002) and in parieto-occipital white matter (AMN 1.45 +/- 0.19 vs controls 1.78 +/- 0.55; p = 0.04).	N-acetylaspartate	12-15	antagonist of mitotic exit network 1 homolog	Homo sapiens	152-157
15481715-4	2004	The authors correlated the NAA/Cr ratio with neuropathological findings in resected hippocampi, specifically glial fibrillary acidic protein (GFAP) immunoreactivity and pyramidal neuronal loss.	N-acetylaspartate	27-30	glial fibrillary acidic protein	Homo sapiens	109-140
15483355-6	2004	The NAA/Cr ratios of the M-1 and SMA in AH, and the SMA in UH were significantly lower than those of normal volunteers.	N-acetylaspartate	4-7	myoregulin	Homo sapiens	25-28
15483355-6	2004	The NAA/Cr ratios of the M-1 and SMA in AH, and the SMA in UH were significantly lower than those of normal volunteers.	N-acetylaspartate	4-7	survival of motor neuron 1, telomeric	Homo sapiens	33-36
15716405-7	2005	MPTP-intoxicated animals that received Cop-1 immune cells showed NAA levels, in the SNpc and striatum, nearly equivalent to PBS-treated animals.	N-acetylaspartate	65-68	COP1, E3 ubiquitin ligase	Mus musculus	39-44
15481715-5	2004	A linear regression analysis of the ipsilateral NAA/Cr ratio revealed a statistically significant relation to the extent of hippocampal neuronal loss in only the CA2 sector (correlation coefficient [r] = -0.66, p &lt; 0.03).	N-acetylaspartate	48-51	carbonic anhydrase 2	Homo sapiens	162-165
15481715-6	2004	The ipsilateral NAA/Cr ratio displayed significant regressions with GFAP immunoreactivity from all the CA sectors (r values ranged from -0.69 and p &lt; 0.01 for the CA4 sector to -0.88 and p &lt; 0.001 for the CA2 sector) except for the CA1.	N-acetylaspartate	16-19	glial fibrillary acidic protein	Homo sapiens	68-72
15481715-6	2004	The ipsilateral NAA/Cr ratio displayed significant regressions with GFAP immunoreactivity from all the CA sectors (r values ranged from -0.69 and p &lt; 0.01 for the CA4 sector to -0.88 and p &lt; 0.001 for the CA2 sector) except for the CA1.	N-acetylaspartate	16-19	carbonic anhydrase 4	Homo sapiens	166-169
15481715-6	2004	The ipsilateral NAA/Cr ratio displayed significant regressions with GFAP immunoreactivity from all the CA sectors (r values ranged from -0.69 and p &lt; 0.01 for the CA4 sector to -0.88 and p &lt; 0.001 for the CA2 sector) except for the CA1.	N-acetylaspartate	16-19	carbonic anhydrase 2	Homo sapiens	211-214
15481715-6	2004	The ipsilateral NAA/Cr ratio displayed significant regressions with GFAP immunoreactivity from all the CA sectors (r values ranged from -0.69 and p &lt; 0.01 for the CA4 sector to -0.88 and p &lt; 0.001 for the CA2 sector) except for the CA1.	N-acetylaspartate	16-19	carbonic anhydrase 1	Homo sapiens	238-241
15481715-10	2004	The significant association of the NAA/Cr ratio with the GFAP immunoreactivity of most CA sectors indicates that the NAA/Cr ratio may provide a more accurate measurement of recent neuronal injury caused by epileptic activity.	N-acetylaspartate	35-38	glial fibrillary acidic protein	Homo sapiens	57-61
15481715-10	2004	The significant association of the NAA/Cr ratio with the GFAP immunoreactivity of most CA sectors indicates that the NAA/Cr ratio may provide a more accurate measurement of recent neuronal injury caused by epileptic activity.	N-acetylaspartate	117-120	glial fibrillary acidic protein	Homo sapiens	57-61
15337171-0	2004	Transport of N-acetylaspartate via murine sodium/dicarboxylate cotransporter NaDC3 and expression of this transporter and aspartoacylase II in ocular tissues in mouse.	N-acetylaspartate	13-30	solute carrier family 13 (sodium-dependent dicarboxylate transporter), member 3	Mus musculus	77-82
15337171-2	2004	Here we show that the plasma membrane transporter NaDC3, a Na+-coupled transporter for dicarboxylates, is able to transport N-acetylaspartate, suggesting that the transporter may function in concert with aspartoacylase II in the metabolism of N-acetylaspartate.	N-acetylaspartate	124-141	solute carrier family 13 (sodium-dependent dicarboxylate transporter), member 3	Mus musculus	50-55
15352223-4	2004	Principal component analysis of ex vivo data showed that decreased levels of N-acetylaspartate (NAA), gamma-aminobutyric acid (GABA), glutamine, and glutamate as well as increased levels of inositols characterized the CLN1 spectra.	N-acetylaspartate	77-94	palmitoyl-protein thioesterase 1	Homo sapiens	218-222
15337171-2	2004	Here we show that the plasma membrane transporter NaDC3, a Na+-coupled transporter for dicarboxylates, is able to transport N-acetylaspartate, suggesting that the transporter may function in concert with aspartoacylase II in the metabolism of N-acetylaspartate.	N-acetylaspartate	243-260	solute carrier family 13 (sodium-dependent dicarboxylate transporter), member 3	Mus musculus	50-55
15337171-6	2004	We conclude that transport of N-acetylaspartate into ocular tissues via NaDC3 and its subsequent hydrolysis by aspartoacylase II play an essential role in the maintenance of visual function.	N-acetylaspartate	30-47	solute carrier family 13 (sodium-dependent dicarboxylate transporter), member 3	Mus musculus	72-77
14634711-3	2004	The enzyme N-acetylated-alpha-linked acidic dipeptidase (NAALADase) hydrolyzes the neurotransmitter N-acetylaspartylglutamate (NAAG) to form glutamate and N-acetylaspartate; NAAG acts as a partial NMDA agonist as well as a full agonist at the presynaptic metabotropic glutamate receptor 3 (mGluR3), where it acts to reduce glutamate release.	N-acetylaspartate	155-172	glutamate receptor, metabotropic 3	Mus musculus	255-288
15240431-2	2004	Magnetic resonance (MR) techniques enable in vivo measurement of the atrophy of the brainstem and cerebellum in spinocerebellar ataxia type 1 (SCA1) and 2 (SCA2) patients, which is accompanied by a decrease in the concentration of N-acetyl aspartate (NAA) or of the NAA/creatine ratio in the pons and cerebellum.	N-acetylaspartate	231-249	ataxin 1	Homo sapiens	143-147
15240431-2	2004	Magnetic resonance (MR) techniques enable in vivo measurement of the atrophy of the brainstem and cerebellum in spinocerebellar ataxia type 1 (SCA1) and 2 (SCA2) patients, which is accompanied by a decrease in the concentration of N-acetyl aspartate (NAA) or of the NAA/creatine ratio in the pons and cerebellum.	N-acetylaspartate	231-249	ataxin 2	Homo sapiens	156-160
15240431-2	2004	Magnetic resonance (MR) techniques enable in vivo measurement of the atrophy of the brainstem and cerebellum in spinocerebellar ataxia type 1 (SCA1) and 2 (SCA2) patients, which is accompanied by a decrease in the concentration of N-acetyl aspartate (NAA) or of the NAA/creatine ratio in the pons and cerebellum.	N-acetylaspartate	251-254	ataxin 1	Homo sapiens	143-147
15240431-2	2004	Magnetic resonance (MR) techniques enable in vivo measurement of the atrophy of the brainstem and cerebellum in spinocerebellar ataxia type 1 (SCA1) and 2 (SCA2) patients, which is accompanied by a decrease in the concentration of N-acetyl aspartate (NAA) or of the NAA/creatine ratio in the pons and cerebellum.	N-acetylaspartate	251-254	ataxin 2	Homo sapiens	156-160
15240431-2	2004	Magnetic resonance (MR) techniques enable in vivo measurement of the atrophy of the brainstem and cerebellum in spinocerebellar ataxia type 1 (SCA1) and 2 (SCA2) patients, which is accompanied by a decrease in the concentration of N-acetyl aspartate (NAA) or of the NAA/creatine ratio in the pons and cerebellum.	N-acetylaspartate	266-269	ataxin 1	Homo sapiens	143-147
15240431-2	2004	Magnetic resonance (MR) techniques enable in vivo measurement of the atrophy of the brainstem and cerebellum in spinocerebellar ataxia type 1 (SCA1) and 2 (SCA2) patients, which is accompanied by a decrease in the concentration of N-acetyl aspartate (NAA) or of the NAA/creatine ratio in the pons and cerebellum.	N-acetylaspartate	266-269	ataxin 2	Homo sapiens	156-160
15240431-7	2004	Compared with control subjects, the SCA1 and SCA2 patients showed a decrease (P &lt; 0.01) in the volume of the brainstem and cerebellum and in the concentration of NAA in the pons and cerebellar hemisphere, whereas D of the brainstem and cerebellum was increased.	N-acetylaspartate	165-168	ataxin 1	Homo sapiens	36-40
15240431-7	2004	Compared with control subjects, the SCA1 and SCA2 patients showed a decrease (P &lt; 0.01) in the volume of the brainstem and cerebellum and in the concentration of NAA in the pons and cerebellar hemisphere, whereas D of the brainstem and cerebellum was increased.	N-acetylaspartate	165-168	ataxin 2	Homo sapiens	45-49
15240431-10	2004	The volume of the brainstem, D of the brainstem and cerebellum and the concentration of NAA in the pons were correlated (P &lt; 0.05) with the IACRS score in SCA1 but not in SCA2.	N-acetylaspartate	88-91	ataxin 1	Homo sapiens	158-162
15136672-5	2004	The coding sequence of the gene coding for glutamate carboxypeptidase II, which converts NAAG to N-acetylaspartate (NAA) and glutamate, was entirely sequenced but revealed no mutations.	N-acetylaspartate	97-114	folate hydrolase 1	Homo sapiens	43-72
15136672-5	2004	The coding sequence of the gene coding for glutamate carboxypeptidase II, which converts NAAG to N-acetylaspartate (NAA) and glutamate, was entirely sequenced but revealed no mutations.	N-acetylaspartate	89-92	folate hydrolase 1	Homo sapiens	43-72
15065127-1	2004	Aspartoacylase (ASPA; EC 3.5.1.15) catalyzes deacetylation of N-acetylaspartate (NAA) to generate free acetate in the central nervous system (CNS).	N-acetylaspartate	62-79	aspartoacylase	Rattus norvegicus	0-14
15065127-1	2004	Aspartoacylase (ASPA; EC 3.5.1.15) catalyzes deacetylation of N-acetylaspartate (NAA) to generate free acetate in the central nervous system (CNS).	N-acetylaspartate	62-79	aspartoacylase	Rattus norvegicus	16-20
15065127-1	2004	Aspartoacylase (ASPA; EC 3.5.1.15) catalyzes deacetylation of N-acetylaspartate (NAA) to generate free acetate in the central nervous system (CNS).	N-acetylaspartate	81-84	aspartoacylase	Rattus norvegicus	0-14
15065127-1	2004	Aspartoacylase (ASPA; EC 3.5.1.15) catalyzes deacetylation of N-acetylaspartate (NAA) to generate free acetate in the central nervous system (CNS).	N-acetylaspartate	81-84	aspartoacylase	Rattus norvegicus	16-20
15352223-6	2004	In concordance with the ex vivo data, the in vivo spectra of late-stage patients with CLN1 (n = 3) revealed a dramatic decrease of NAA and a proportional increase of myo-inositol and lipids compared with control subjects.	N-acetylaspartate	131-134	palmitoyl-protein thioesterase 1	Homo sapiens	86-90
15184060-4	2004	NAA also decreased the levels of COX-2 protein and activated NF-kappaB in IL-1beta-stimulated STTG cells but had little effect on unstimulated cells.	N-acetylaspartate	0-3	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	33-38
15184060-4	2004	NAA also decreased the levels of COX-2 protein and activated NF-kappaB in IL-1beta-stimulated STTG cells but had little effect on unstimulated cells.	N-acetylaspartate	0-3	interleukin 1 beta	Homo sapiens	74-82
15027864-1	2004	The neuropeptidase glutamate carboxypeptidase II (GCPII) hydrolyzes N-acetyl-L-aspartyl-L-glutamate (NAAG) to liberate N-acetylaspartate and glutamate.	N-acetylaspartate	119-136	folate hydrolase 1	Homo sapiens	19-48
15027864-1	2004	The neuropeptidase glutamate carboxypeptidase II (GCPII) hydrolyzes N-acetyl-L-aspartyl-L-glutamate (NAAG) to liberate N-acetylaspartate and glutamate.	N-acetylaspartate	119-136	folate hydrolase 1	Homo sapiens	50-55
14634711-3	2004	The enzyme N-acetylated-alpha-linked acidic dipeptidase (NAALADase) hydrolyzes the neurotransmitter N-acetylaspartylglutamate (NAAG) to form glutamate and N-acetylaspartate; NAAG acts as a partial NMDA agonist as well as a full agonist at the presynaptic metabotropic glutamate receptor 3 (mGluR3), where it acts to reduce glutamate release.	N-acetylaspartate	155-172	glutamate receptor, ionotropic, AMPA3 (alpha 3)	Mus musculus	290-296
12700705-3	2003	NAAG is catabolized to glutamate and N-acetyl-aspartate by the astrocytic enzyme glutamate carboxypeptidase II (GCP II).	N-acetylaspartate	37-55	folate hydrolase 1	Rattus norvegicus	81-110
14556233-1	2003	Glutamate carboxypeptidase II (EC 3.4.17.21) catalyzes the hydrolysis (Km = 0.2 microM) of the neuropeptide N-acetylaspartylglutamate to yield N-acetylaspartate and glutamate and also serves as a high-affinity folate hydrolase in the gut, cleaving the polyglutamate chain to permit the absorption of folate.	N-acetylaspartate	143-160	folate hydrolase 1	Mus musculus	0-29
12917384-2	2004	For this purpose, we made use of 2-(3-mercaptopropyl)pentanedioic acid (2-MPPA), an inhibitor of glutamate carboxypeptidase II [GCP II; also known as N-acetylated alpha-linked acidic dipeptidase (NAALADase)], the enzyme that hydrolyzes NAAG into N-acetylaspartate and glutamate.	N-acetylaspartate	246-263	folate hydrolase 1	Homo sapiens	97-126
12917384-2	2004	For this purpose, we made use of 2-(3-mercaptopropyl)pentanedioic acid (2-MPPA), an inhibitor of glutamate carboxypeptidase II [GCP II; also known as N-acetylated alpha-linked acidic dipeptidase (NAALADase)], the enzyme that hydrolyzes NAAG into N-acetylaspartate and glutamate.	N-acetylaspartate	246-263	folate hydrolase 1	Homo sapiens	128-134
12917384-2	2004	For this purpose, we made use of 2-(3-mercaptopropyl)pentanedioic acid (2-MPPA), an inhibitor of glutamate carboxypeptidase II [GCP II; also known as N-acetylated alpha-linked acidic dipeptidase (NAALADase)], the enzyme that hydrolyzes NAAG into N-acetylaspartate and glutamate.	N-acetylaspartate	246-263	folate hydrolase 1B (pseudogene)	Homo sapiens	150-194
14636347-7	2003	RESULTS: Group analysis showed that thalami NAA/Cr ratios were significantly decreased in JME patients (left side, 1.58 +/- 0.26; right side, 1.5 +/- 0.15) as compared with controls (left side, 1.98 +/- 0.18; right side, 1.88 +/- 0.15; p = 0.001 and p = 0.007, respectively).	N-acetylaspartate	44-47	myoclonic epilepsy, juvenile, 2	Homo sapiens	90-93
14567959-1	2003	Canavan disease (CD) is an inherited leukodystrophy, caused by aspartoacylase (ASPA) deficiency, and accumulation of N-acetylaspartic acid (NAA) in the brain.	N-acetylaspartate	117-138	cathepsin D	Mus musculus	17-19
14567959-1	2003	Canavan disease (CD) is an inherited leukodystrophy, caused by aspartoacylase (ASPA) deficiency, and accumulation of N-acetylaspartic acid (NAA) in the brain.	N-acetylaspartate	140-143	cathepsin D	Mus musculus	17-19
12700705-3	2003	NAAG is catabolized to glutamate and N-acetyl-aspartate by the astrocytic enzyme glutamate carboxypeptidase II (GCP II).	N-acetylaspartate	37-55	folate hydrolase 1	Rattus norvegicus	112-118
12826236-3	2003	N-acetylated-alpha-linked acidic dipeptidase (NAALADase; also termed glutamate carboxypeptidase II) yields N-acetyl aspartate (NAA) and glutamate.	N-acetylaspartate	107-125	folate hydrolase 1B (pseudogene)	Homo sapiens	0-44
12826236-3	2003	N-acetylated-alpha-linked acidic dipeptidase (NAALADase; also termed glutamate carboxypeptidase II) yields N-acetyl aspartate (NAA) and glutamate.	N-acetylaspartate	107-125	folate hydrolase 1B (pseudogene)	Homo sapiens	46-55
12826236-3	2003	N-acetylated-alpha-linked acidic dipeptidase (NAALADase; also termed glutamate carboxypeptidase II) yields N-acetyl aspartate (NAA) and glutamate.	N-acetylaspartate	107-125	folate hydrolase 1	Homo sapiens	69-98
12826236-3	2003	N-acetylated-alpha-linked acidic dipeptidase (NAALADase; also termed glutamate carboxypeptidase II) yields N-acetyl aspartate (NAA) and glutamate.	N-acetylaspartate	46-49	folate hydrolase 1B (pseudogene)	Homo sapiens	0-44
12826236-3	2003	N-acetylated-alpha-linked acidic dipeptidase (NAALADase; also termed glutamate carboxypeptidase II) yields N-acetyl aspartate (NAA) and glutamate.	N-acetylaspartate	46-49	folate hydrolase 1	Homo sapiens	69-98
12533090-0	2003	Lower levels of N-acetylaspartate in multiple sclerosis patients with the apolipoprotein E epsilon4 allele.	N-acetylaspartate	16-33	apolipoprotein E	Homo sapiens	74-99
12796718-0	2003	N-acetylaspartate to total creatine ratio in the hippocampal CA1 sector after transient cerebral ischemia in gerbils: influence of neuronal elements, reactive gliosis, and tissue atrophy.	N-acetylaspartate	0-17	carbonic anhydrase 1	Homo sapiens	61-64
12718900-2	2003	Deficiency of ASPA leads to elevation of N-acetyl-L-aspartic acid (NAA) in the brain and urine.	N-acetylaspartate	41-65	aspartoacylase	Mus musculus	14-18
12718900-2	2003	Deficiency of ASPA leads to elevation of N-acetyl-L-aspartic acid (NAA) in the brain and urine.	N-acetylaspartate	67-70	aspartoacylase	Mus musculus	14-18
12682335-1	2003	The MRS brain metabolite ratio N-acetylaspartate (NAA)/myo-inositol (mI) is reported to be decreased in AD.	N-acetylaspartate	31-48	MROS	Homo sapiens	4-7
12682335-1	2003	The MRS brain metabolite ratio N-acetylaspartate (NAA)/myo-inositol (mI) is reported to be decreased in AD.	N-acetylaspartate	50-53	MROS	Homo sapiens	4-7
12569314-6	2002	CONCLUSIONS: Correlations between NAA/Cr and Lac/Cr ratios, general movements and outcome at 6 months are stronger in the basal ganglia regions than in the frontal border zone.	N-acetylaspartate	34-37	lactase	Homo sapiens	45-48
12694109-6	2003	For the immune status there was a statistically significant correlation (r=0.47, p&lt;0.05) between CD4 counts and NAA/H2O ratio.	N-acetylaspartate	115-118	CD4 molecule	Homo sapiens	100-103
12413472-1	2002	Glutamate carboxypeptidase II (GCPII or prostate-specific membrane antigen or NAALADase) is an enzyme that catalyzes the hydrolysis of the neuropeptide N-acetylaspartylglutamate (NAAG) to N-acetylaspartate (NAA) and glutamate (G).	N-acetylaspartate	188-205	folate hydrolase 1	Homo sapiens	0-29
12413472-1	2002	Glutamate carboxypeptidase II (GCPII or prostate-specific membrane antigen or NAALADase) is an enzyme that catalyzes the hydrolysis of the neuropeptide N-acetylaspartylglutamate (NAAG) to N-acetylaspartate (NAA) and glutamate (G).	N-acetylaspartate	188-205	folate hydrolase 1	Homo sapiens	31-36
12413472-1	2002	Glutamate carboxypeptidase II (GCPII or prostate-specific membrane antigen or NAALADase) is an enzyme that catalyzes the hydrolysis of the neuropeptide N-acetylaspartylglutamate (NAAG) to N-acetylaspartate (NAA) and glutamate (G).	N-acetylaspartate	188-205	folate hydrolase 1	Homo sapiens	78-87
12413472-1	2002	Glutamate carboxypeptidase II (GCPII or prostate-specific membrane antigen or NAALADase) is an enzyme that catalyzes the hydrolysis of the neuropeptide N-acetylaspartylglutamate (NAAG) to N-acetylaspartate (NAA) and glutamate (G).	N-acetylaspartate	78-81	folate hydrolase 1	Homo sapiens	0-29
12413472-1	2002	Glutamate carboxypeptidase II (GCPII or prostate-specific membrane antigen or NAALADase) is an enzyme that catalyzes the hydrolysis of the neuropeptide N-acetylaspartylglutamate (NAAG) to N-acetylaspartate (NAA) and glutamate (G).	N-acetylaspartate	78-81	folate hydrolase 1	Homo sapiens	31-36
12147318-2	2002	A deletion of the aspartoacylase (ASPA) gene and resultant high levels of N-acetyl-aspartate (NAA) in the brain have been found in tremor rats.	N-acetylaspartate	74-92	aspartoacylase	Rattus norvegicus	18-32
12147318-2	2002	A deletion of the aspartoacylase (ASPA) gene and resultant high levels of N-acetyl-aspartate (NAA) in the brain have been found in tremor rats.	N-acetylaspartate	74-92	aspartoacylase	Rattus norvegicus	34-38
12147318-2	2002	A deletion of the aspartoacylase (ASPA) gene and resultant high levels of N-acetyl-aspartate (NAA) in the brain have been found in tremor rats.	N-acetylaspartate	94-97	aspartoacylase	Rattus norvegicus	18-32
12147318-2	2002	A deletion of the aspartoacylase (ASPA) gene and resultant high levels of N-acetyl-aspartate (NAA) in the brain have been found in tremor rats.	N-acetylaspartate	94-97	aspartoacylase	Rattus norvegicus	34-38
12147318-8	2002	These results suggest that gene transfer of ASPA is effective in inhibiting the generation of absence-like seizures, probably by reducing the NAA level.	N-acetylaspartate	142-145	aspartoacylase	Rattus norvegicus	44-48
12098564-9	2002	This stability of the metabolite concentrations over time might result from IFN therapy as for the spontaneous course of relapsing-remitting MS decreasing metabolite (NAA/tCr) ratios have been reported.	N-acetylaspartate	167-170	interferon alpha 1	Homo sapiens	76-79
11969317-0	2002	A fully automated method for tissue segmentation and CSF-correction of proton MRSI metabolites corroborates abnormal hippocampal NAA in schizophrenia.	N-acetylaspartate	129-132	colony stimulating factor 2	Homo sapiens	53-56
11988598-8	2002	There was a tendency for larger rCBF defect size to be associated with greater increases in Cr/NAA values in the same diaschitic cerebral hemisphere, ipsilateral to the infarction.	N-acetylaspartate	95-98	CCAAT/enhancer binding protein zeta	Rattus norvegicus	32-36
11988598-10	2002	The tendency for greater reductions in cortical rCBF values to be associated with increased Cr/NAA values in the same diaschitic cerebral hemisphere implies that a relationship exists between rCBF reductions in gray matter and abnormal changes in white matter subservient to it.	N-acetylaspartate	95-98	CCAAT/enhancer binding protein zeta	Rattus norvegicus	48-52
11988598-10	2002	The tendency for greater reductions in cortical rCBF values to be associated with increased Cr/NAA values in the same diaschitic cerebral hemisphere implies that a relationship exists between rCBF reductions in gray matter and abnormal changes in white matter subservient to it.	N-acetylaspartate	95-98	CCAAT/enhancer binding protein zeta	Rattus norvegicus	192-196
11805250-0	2002	Brain N-acetylaspartate is elevated in Pelizaeus-Merzbacher disease with PLP1 duplication.	N-acetylaspartate	6-23	proteolipid protein 1	Homo sapiens	73-77
11889764-6	2002	Lac peak without other peaks such as NAA, Cr, Cho is a unique finding of proton MRS for epidermoid and this could be useful in the differential diagnosis.	N-acetylaspartate	37-40	MROS	Homo sapiens	80-83
12373553-3	2002	In the MND group we found a significant reduction of NAA/tCr metabolite ratios in the motor cortex, which correlates with the disease severity and the clinical lateralization of neurological symptoms and further decreases in the time course of the disease.	N-acetylaspartate	53-56	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	57-60
11782984-10	2002	After transection at postnatal day 4, total N-acetylaspartate decreased by 80% (P14; p = 0.002) and 94% (P20; p = 0.003).	N-acetylaspartate	44-61	S100 calcium binding protein A9	Rattus norvegicus	80-83
11557259-2	2001	In the brain, glutamate carboxypeptidase II (GCPII) (EC3.4.17.21) hydrolyzes the neuropeptide N-acetylaspartylglutamate (NAAG) to glutamate and N-acetylaspartate.	N-acetylaspartate	144-161	folate hydrolase 1	Rattus norvegicus	14-43
11706094-4	2001	Previously they had demonstrated a reduction in N-acetyl aspartate/creatine + phosphocreatine (NAA/[Cr + PCr]) measured by (1)H-MRS in the subcortical white matter in the motor cortex region in the patients with bulbar-onset ALS.	N-acetylaspartate	48-66	superoxide dismutase 1	Homo sapiens	225-228
11706094-4	2001	Previously they had demonstrated a reduction in N-acetyl aspartate/creatine + phosphocreatine (NAA/[Cr + PCr]) measured by (1)H-MRS in the subcortical white matter in the motor cortex region in the patients with bulbar-onset ALS.	N-acetylaspartate	95-98	superoxide dismutase 1	Homo sapiens	225-228
11557259-2	2001	In the brain, glutamate carboxypeptidase II (GCPII) (EC3.4.17.21) hydrolyzes the neuropeptide N-acetylaspartylglutamate (NAAG) to glutamate and N-acetylaspartate.	N-acetylaspartate	144-161	folate hydrolase 1	Rattus norvegicus	45-50
11589513-0	2001	A potent AMPA/kainate receptor antagonist, YM90K, attenuates the loss of N-acetylaspartate in the hippocampal CA1 area after transient unilateral forebrain ischemia in gerbils.	N-acetylaspartate	73-90	carbonic anhydrase 1	Homo sapiens	110-113
11525768-1	2001	N-acetylated-alpha-linked-acidic-dipeptidase (NAALADase or glutamate carboxypeptidase II) cleaves the neuropeptide N-acetyl-aspartyl-glutamate (NAAG) to glutamate and N-acetyl-aspartate (NAA).	N-acetylaspartate	167-185	folate hydrolase 1	Homo sapiens	46-55
11525768-1	2001	N-acetylated-alpha-linked-acidic-dipeptidase (NAALADase or glutamate carboxypeptidase II) cleaves the neuropeptide N-acetyl-aspartyl-glutamate (NAAG) to glutamate and N-acetyl-aspartate (NAA).	N-acetylaspartate	167-185	folate hydrolase 1	Homo sapiens	59-88
11525768-1	2001	N-acetylated-alpha-linked-acidic-dipeptidase (NAALADase or glutamate carboxypeptidase II) cleaves the neuropeptide N-acetyl-aspartyl-glutamate (NAAG) to glutamate and N-acetyl-aspartate (NAA).	N-acetylaspartate	46-49	folate hydrolase 1	Homo sapiens	59-88
11478930-1	2001	N-Acetylated-alpha-linked acidic dipeptidase (NAALADase) hydrolyzes N-acetyl-aspartyl-glutamate (NAAG) to liberate N-acetyl-aspartate and glutamate.	N-acetylaspartate	115-133	folate hydrolase 1	Rattus norvegicus	0-44
11478930-1	2001	N-Acetylated-alpha-linked acidic dipeptidase (NAALADase) hydrolyzes N-acetyl-aspartyl-glutamate (NAAG) to liberate N-acetyl-aspartate and glutamate.	N-acetylaspartate	115-133	folate hydrolase 1	Rattus norvegicus	46-55
11290466-7	2001	When the pattern of MRS metabolites consisted of abnormally increased choline and decreased N-acetyl aspartate (NAA) resonances, histologic findings of the biopsy specimen invariably was positive for tumor.	N-acetylaspartate	92-110	sterile alpha motif domain containing 11	Homo sapiens	20-23
11375762-3	2001	N-acetylated-a-linked acidic dipeptidase (NAALADase, EC 3.4.17.21) is responsible for the hydrolysis of NAAG into N-acetylaspartate (NAA) and glutamate.	N-acetylaspartate	114-131	folate hydrolase 1	Homo sapiens	0-40
11375762-3	2001	N-acetylated-a-linked acidic dipeptidase (NAALADase, EC 3.4.17.21) is responsible for the hydrolysis of NAAG into N-acetylaspartate (NAA) and glutamate.	N-acetylaspartate	114-131	folate hydrolase 1	Homo sapiens	42-51
11375762-3	2001	N-acetylated-a-linked acidic dipeptidase (NAALADase, EC 3.4.17.21) is responsible for the hydrolysis of NAAG into N-acetylaspartate (NAA) and glutamate.	N-acetylaspartate	42-45	folate hydrolase 1	Homo sapiens	0-40
11290466-7	2001	When the pattern of MRS metabolites consisted of abnormally increased choline and decreased N-acetyl aspartate (NAA) resonances, histologic findings of the biopsy specimen invariably was positive for tumor.	N-acetylaspartate	112-115	sterile alpha motif domain containing 11	Homo sapiens	20-23
11274318-2	2001	When compared with 16 age-matched control participants, patients with PLP mutations had significant and widespread decreased brain N-acetyl aspartate, a neuronal marker.	N-acetylaspartate	131-149	proteolipid protein 1	Homo sapiens	70-73
10751574-11	2000	In addition, NAA applied to the bath rapidly induced a long-lasting depolarization concomitantly with repetitive firings in hippocampal CA3 neurons of normal rat brain slice preparations.	N-acetylaspartate	13-16	carbonic anhydrase 3	Rattus norvegicus	136-139
11172761-8	2001	There was also a significant correlation between 1H-MRS [NAA] and the corresponding reduction in CA1 neuronal density (P&lt;0.004).	N-acetylaspartate	57-60	carbonic anhydrase 1	Homo sapiens	97-100
11133792-12	2001	Proton MR spectroscopy data demonstrated widespread axonal damage (as shown by the decrease in N -acetylaspartate) and diffuse brain mitochondrial dysfunction (as shown by the increase in brain parenchymal lactate) in patients with CTX.	N-acetylaspartate	95-113	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	232-235
11133792-13	2001	The close correlation seen between values of the putative axonal marker N-acetylaspartate and patients" disability scores suggests that proton MR spectroscopy can provide a useful measure of disease outcome in CTX.	N-acetylaspartate	72-89	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	210-213
11166133-3	2001	N-acetyl-aspartyl-glutamate is hydrolyzed by N-acetylated-alpha-linked acidic dipeptidase to liberate N-acetyl-aspartate and glutamate.	N-acetylaspartate	102-120	folate hydrolase 1	Rattus norvegicus	45-89
11053229-6	2000	Third, the magnitude of the abnormal dorsal PFC fMRI response was predicted by an assay of N-acetylaspartate concentrations (NAA) in dorsal PFC, a measure of neuronal pathology obtained using proton magnetic resonance spectroscopy.	N-acetylaspartate	91-108	complement factor properdin	Homo sapiens	44-52
11053229-6	2000	Third, the magnitude of the abnormal dorsal PFC fMRI response was predicted by an assay of N-acetylaspartate concentrations (NAA) in dorsal PFC, a measure of neuronal pathology obtained using proton magnetic resonance spectroscopy.	N-acetylaspartate	91-108	complement factor properdin	Homo sapiens	44-47
10913502-0	2000	Lithium increases N-acetyl-aspartate in the human brain: in vivo evidence in support of bcl-2"s neurotrophic effects?	N-acetylaspartate	18-36	BCL2 apoptosis regulator	Homo sapiens	88-93
10837925-7	2000	Our success in preparing the recombinant ASPA in high purity should permit multiple lines of investigations to understand the pathogenic mechanisms of Canavan disease and the functional roles of NAA.	N-acetylaspartate	195-198	aspartoacylase	Homo sapiens	41-45
10992006-0	2000	Transport of N-acetylaspartate by the Na(+)-dependent high-affinity dicarboxylate transporter NaDC3 and its relevance to the expression of the transporter in the brain.	N-acetylaspartate	13-30	solute carrier family 13 member 3	Rattus norvegicus	94-99
10992006-6	2000	We investigated in the present study the ability of NaDC3, a Na(+)-coupled high-affinity dicarboxylate transporter, to transport N-acetylaspartate.	N-acetylaspartate	129-146	solute carrier family 13 member 3	Rattus norvegicus	52-57
10992006-7	2000	The cloned rat and human NaDC3s were found to transport N-acetylaspartate in a Na(+)-coupled manner in two different heterologous expression systems.	N-acetylaspartate	56-73	solute carrier family 13 member 3	Homo sapiens	25-30
10992006-8	2000	The Michaelis-Menten constant for N-acetylaspartate was approximately 60 microM for rat NaDC3 and approximately 250 microM for human NaDC3.	N-acetylaspartate	34-51	solute carrier family 13 member 3	Rattus norvegicus	88-93
10992006-8	2000	The Michaelis-Menten constant for N-acetylaspartate was approximately 60 microM for rat NaDC3 and approximately 250 microM for human NaDC3.	N-acetylaspartate	34-51	solute carrier family 13 member 3	Homo sapiens	133-138
10992006-12	2000	These studies establish NaDC3 as the transporter responsible for the Na(+)-coupled transport of N-acetylaspartate in the brain.	N-acetylaspartate	96-113	solute carrier family 13 member 3	Rattus norvegicus	24-29
10672584-6	2000	At P21, the cells are severely damaged and further intracellular changes include a decrease in N-acetylaspartate (NAA) and loss of amino acids and many organic osmolytes.	N-acetylaspartate	95-112	H3 histone pseudogene 16	Homo sapiens	3-6
10718292-3	2000	The ratio of ml over total creatine (Cr), ml/Cr, was significantly elevated (mean change +38%), while NAA/Cr was significantly decreased (mean change -18%) in Ts65Dn mice (n=5) compared with control mice (n= 7).	N-acetylaspartate	102-105	reciprocal translocation, Chr 16, cytogenetic band C3-4; and Chr 17, cytogenetic band A2, Davisson 65	Mus musculus	159-165
10714400-8	2000	RESULTS: Patients with JME had significantly reduced prefrontal concentrations of NAA in relation to controls (9.1 +/- 1.0 vs. 10.2 +/- 0.8 mM; p = 0.031 after Bonferroni correction).	N-acetylaspartate	82-85	myoclonic epilepsy, juvenile, 2	Homo sapiens	23-26
10714400-10	2000	CONCLUSIONS: The observed reduction in NAA levels suggests a prefrontal neuronal lesion in patients with JME.	N-acetylaspartate	39-42	myoclonic epilepsy, juvenile, 2	Homo sapiens	105-108
10672584-6	2000	At P21, the cells are severely damaged and further intracellular changes include a decrease in N-acetylaspartate (NAA) and loss of amino acids and many organic osmolytes.	N-acetylaspartate	114-117	H3 histone pseudogene 16	Homo sapiens	3-6
9882712-1	1999	Glutamate carboxypeptidase II (GCP II) catalyzes the extracellular hydrolysis of the neuromodulator N-acetyl-aspartylglutamate to N-acetyl-aspartate and glutamate.	N-acetylaspartate	130-148	folate hydrolase 1	Homo sapiens	0-29
10092982-3	1999	N-acetyl-aspartate levels were determined in the blood of stroke patients and related to clinical outcome, volume of infarction and to serum neurone-specific enolase.	N-acetylaspartate	0-18	enolase 2	Homo sapiens	141-165
10092982-8	1999	Serum N-acetyl-aspartate at 24 h and neurone-specific enolase at 72 h were negatively correlated, suggesting that more N-acetyl-aspartate reaches the blood when brain tissue is less irreversibly affected.	N-acetylaspartate	119-137	enolase 2	Homo sapiens	37-61
10092982-9	1999	CONCLUSION: Serum N-acetyl-aspartate appears to be an early peripheral marker of ischaemically affected brain neurones, and the ratio of N-acetyl-aspartate to a protein marker, such as NSE, may serve as an index of irreversibility.	N-acetylaspartate	137-155	enolase 2	Homo sapiens	185-188
10581082-1	1999	We describe here a new strategy for the treatment of stroke, through the inhibition of NAALADase (N-acetylated-alpha-linked-acidic dipeptidase), an enzyme responsible for the hydrolysis of the neuropeptide NAAG (N-acetyl-aspartyl-glutamate) to N-acetyl-aspartate and glutamate.	N-acetylaspartate	244-262	folate hydrolase 1	Rattus norvegicus	87-96
10581082-1	1999	We describe here a new strategy for the treatment of stroke, through the inhibition of NAALADase (N-acetylated-alpha-linked-acidic dipeptidase), an enzyme responsible for the hydrolysis of the neuropeptide NAAG (N-acetyl-aspartyl-glutamate) to N-acetyl-aspartate and glutamate.	N-acetylaspartate	244-262	folate hydrolase 1	Rattus norvegicus	98-142
10534142-5	1999	A negative correlation between NAA and CD4 lymphocyte count was seen in the FIV-14 group only.	N-acetylaspartate	31-34	CD4 molecule	Felis catus	39-42
9882712-1	1999	Glutamate carboxypeptidase II (GCP II) catalyzes the extracellular hydrolysis of the neuromodulator N-acetyl-aspartylglutamate to N-acetyl-aspartate and glutamate.	N-acetylaspartate	130-148	folate hydrolase 1	Homo sapiens	31-37
9413005-0	1997	Decrease of N-acetylaspartate after ACTH therapy in patients with infantile spasms.	N-acetylaspartate	12-29	proopiomelanocortin	Homo sapiens	36-40
9576546-6	1998	However, the NAA/Cr ratio was significantly lower in PML and lymphomas than in HIV encephalopathies (p&lt;0.02) and toxoplasmosis (p&lt;0.05).	N-acetylaspartate	13-16	PML nuclear body scaffold	Homo sapiens	53-56
9485066-4	1998	The N-acetylaspartate/creatine ratio and the choline/creatine ratio in the basis pontis were markedly decreased in 2 symptomatic SCA1 carriers and moderately decreased in 2 asymptomatic SCA1 carriers, compared with the unaffected family members and a control group of 10 healthy volunteers.	N-acetylaspartate	4-21	ataxin 1	Homo sapiens	129-133
9485066-5	1998	Minor decreases in the N-acetylaspartate/creatine ratio and the normal choline/creatine ratio were observed in the cerebellar hemisphere of the SCA1 carriers.	N-acetylaspartate	23-40	ataxin 1	Homo sapiens	144-148
9485066-6	1998	Reduction of the N-acetylaspartate/creatine ratio, demonstrated by MR spectroscopy in the pons, is likely to reflect a loss of neuronal viability and might represent a biochemical marker of SCA1 more sensitive than brainstem and cerebellum atrophy and signal changes shown by MR imaging.	N-acetylaspartate	17-34	ataxin 1	Homo sapiens	190-194
9749599-1	1998	We investigated the correlation between N-acetylaspartate (NAA) level and neuronal density in the hippocampal CA1 region of the brain after occlusion of both common carotid arteries for 5 minutes and reperfusion for 3 hours to 4 weeks in gerbils with and without ischemic preconditioning (tolerance).	N-acetylaspartate	40-57	carbonic anhydrase 1	Homo sapiens	110-113
9749599-1	1998	We investigated the correlation between N-acetylaspartate (NAA) level and neuronal density in the hippocampal CA1 region of the brain after occlusion of both common carotid arteries for 5 minutes and reperfusion for 3 hours to 4 weeks in gerbils with and without ischemic preconditioning (tolerance).	N-acetylaspartate	59-62	carbonic anhydrase 1	Homo sapiens	110-113
9749599-3	1998	The CA1 region was dissected out from freeze-dried sections for high-performance liquid chromatographic assay of NAA, and adjacent sections were stained with cresyl violet for measurement of the neuronal density.	N-acetylaspartate	113-116	carbonic anhydrase 1	Homo sapiens	4-7
17895107-8	1998	However, on MRS, the N-acetyl aspartate signal was significantly higher in the MCI-186 group than in the conventionally treated patients.	N-acetylaspartate	21-39	sterile alpha motif domain containing 11	Homo sapiens	12-15
9413005-7	1997	These data suggest catabolic effects of ACTH on brain tissue, such as cell loss, decrease in NAA synthesis in mitochondria, and leakage of NAA from cell membrane.	N-acetylaspartate	93-96	proopiomelanocortin	Homo sapiens	40-44
9413005-7	1997	These data suggest catabolic effects of ACTH on brain tissue, such as cell loss, decrease in NAA synthesis in mitochondria, and leakage of NAA from cell membrane.	N-acetylaspartate	139-142	proopiomelanocortin	Homo sapiens	40-44
9220406-3	1996	The change in NAA/Cho (for TE = 270 ms: 2.52 in patients vs. 1.96 in controls, p270 &lt; 0.0001) can be explained by a significant difference in T2 values of choline compounds between patients and controls.	N-acetylaspartate	14-17	AT-rich interaction domain 1A	Homo sapiens	79-83
9361299-3	1997	NAAG is catabolized to N-acetylaspartate and glutamate primarily by glutamate carboxypeptidase II, which is expressed on the extracellular surface of astrocytes.	N-acetylaspartate	23-40	folate hydrolase 1	Homo sapiens	68-97
8910796-1	1996	N-Acetylated alpha-linked acidic dipeptidase is a membrane-bound peptidase that cleaves the neuropeptide N-acetyl-aspartyl-glutamate to N-acetyl-aspartate and glutamate.	N-acetylaspartate	136-154	folate hydrolase 1	Rattus norvegicus	0-44
7575102-4	1995	Moreover, NAAG is cleaved to glutamate and N-acetylaspartate by a specific peptidase, N-acetyl-alpha-linked acidic dipeptidase (NAALADase).	N-acetylaspartate	43-60	folate hydrolase 1	Homo sapiens	86-126
8724989-4	1996	Systemic administration of bFGF had significant neuroprotective effects as assessed by T2-weighted magnetic resonance imaging and measurements of n-acetylaspartate and lactate using chemical shift magnetic resonance imaging.	N-acetylaspartate	146-163	fibroblast growth factor 2	Rattus norvegicus	27-31
8618683-4	1996	We found a significant reduction in N-acetyl aspartate/creatine only in patients who had advanced dementia and CD4 counts less that 200/microliter.	N-acetylaspartate	36-54	CD4 molecule	Homo sapiens	111-114
8570628-2	1996	NAALADase is a membrane hydrolase that has been characterized in the mammalian nervous system on the basis of its catabolism of the neuropeptide N-acetylaspartylglutamate (NAAG) to yield glutamate and N-acetylaspartate and that has been hypothesized to influence glutamatergic signaling processes.	N-acetylaspartate	201-218	folate hydrolase 1B (pseudogene)	Homo sapiens	0-9
8558536-4	1996	NAALADase is responsible for the catabolism of the abundant neuropeptide N-acetyl-aspartylglutamate (NAAG) into N-acetylaspartate and glutamate.	N-acetylaspartate	112-129	folate hydrolase 1B (pseudogene)	Homo sapiens	0-9
7575102-4	1995	Moreover, NAAG is cleaved to glutamate and N-acetylaspartate by a specific peptidase, N-acetyl-alpha-linked acidic dipeptidase (NAALADase).	N-acetylaspartate	43-60	folate hydrolase 1	Homo sapiens	128-137
7798941-8	1995	In the extracts 3-4% of the C-6 of N-acetyl-aspartate (NAA; CH3 of the acetyl group) contained label as determined by both NMR and mass spectrometry, which indicated that there was no significant labeling to other carbons in NAA.	N-acetylaspartate	35-53	complement C6	Rattus norvegicus	28-31
8532851-2	1995	NAA is synthesized by L-aspartate N-acetyl transferase or by cleavage from N-acetyl aspartyl glutamate by N-acylated alpha-linked L-amino dipeptidase (NAALADase); and it is catabolized to acetate and aspartate by N-acetyl aspartate amino hydrolase (amino acylase II).	N-acetylaspartate	0-3	folate hydrolase 1	Homo sapiens	151-160
7745446-1	1995	N-acetylated alpha-linked acidic dipeptidase is a membrane-bound brain peptidase which cleaves the neuropeptide N-acetyl-aspartyl-glutamate to N-acetyl-aspartate and glutamate.	N-acetylaspartate	143-161	folate hydrolase 1B (pseudogene)	Homo sapiens	0-44
7798941-8	1995	In the extracts 3-4% of the C-6 of N-acetyl-aspartate (NAA; CH3 of the acetyl group) contained label as determined by both NMR and mass spectrometry, which indicated that there was no significant labeling to other carbons in NAA.	N-acetylaspartate	55-58	complement C6	Rattus norvegicus	28-31
8474556-9	1993	The endogenous amino acids, glycine, taurine and N-acetylaspartic acid, also significantly inhibited PAG activity in the 5-10 mM range.	N-acetylaspartate	49-70	glutaminase 2	Homo sapiens	101-104
8355209-6	1993	The effects observed were caused by the intact dipeptide and not the degradation artifacts produced by the enzyme N-acetylated-alpha-linked-acidic dipeptidase because N-acetyl-L-aspartate had no significant effect on the release and L-glutamate was stimulatory.	N-acetylaspartate	167-187	folate hydrolase 1	Rattus norvegicus	114-158
2355230-2	1990	NAAG inactivation may proceed through enzymatic hydrolysis into N-acetyl-L-aspartate and glutamate by an N-acetylated-alpha-linked acidic dipeptidase (NAALADase).	N-acetylaspartate	64-84	folate hydrolase 1	Rattus norvegicus	105-149
1360862-1	1992	N-Acetylated-alpha-linked acidic dipeptidase (NAALADase) is a membrane-bound peptidase which hydrolyzes the endogenous neuropeptide N-acetylaspartylglutamate (NAAG) to N-acetylaspartate (NAA) and the excitatory amino acid, glutamate (Glu).	N-acetylaspartate	168-185	folate hydrolase 1	Rattus norvegicus	0-44
1360862-1	1992	N-Acetylated-alpha-linked acidic dipeptidase (NAALADase) is a membrane-bound peptidase which hydrolyzes the endogenous neuropeptide N-acetylaspartylglutamate (NAAG) to N-acetylaspartate (NAA) and the excitatory amino acid, glutamate (Glu).	N-acetylaspartate	168-185	folate hydrolase 1	Rattus norvegicus	46-55
1360862-1	1992	N-Acetylated-alpha-linked acidic dipeptidase (NAALADase) is a membrane-bound peptidase which hydrolyzes the endogenous neuropeptide N-acetylaspartylglutamate (NAAG) to N-acetylaspartate (NAA) and the excitatory amino acid, glutamate (Glu).	N-acetylaspartate	46-49	folate hydrolase 1	Rattus norvegicus	0-44
1754068-3	1991	Clones were selected which secrete IgG2a(k) antibodies highly specific for conjugated N-acetyl-aspartate.	N-acetylaspartate	86-104	immunoglobulin heavy variable V1-9	Mus musculus	35-40
2355230-2	1990	NAAG inactivation may proceed through enzymatic hydrolysis into N-acetyl-L-aspartate and glutamate by an N-acetylated-alpha-linked acidic dipeptidase (NAALADase).	N-acetylaspartate	64-84	folate hydrolase 1	Rattus norvegicus	151-160
28364102-5	2017	:  Results: The NAA/Cr in the pons and cerebellar dentate nucleus from the onset patients with SCA3/MJD was significantly reduced compared to that in the normal control group.	N-acetylaspartate	16-19	ataxin 3	Homo sapiens	95-99
33779415-1	2021	Canavan disease is an autosomal recessive leukodystrophy caused by mutations in the gene encoding aspartoacylase (ASPA), which hydrolyses N-acetylaspartate (NAA) to acetate and aspartate.	N-acetylaspartate	138-155	aspartoacylase	Felis catus	98-112
33779415-1	2021	Canavan disease is an autosomal recessive leukodystrophy caused by mutations in the gene encoding aspartoacylase (ASPA), which hydrolyses N-acetylaspartate (NAA) to acetate and aspartate.	N-acetylaspartate	138-155	aspartoacylase	Felis catus	114-118
33779415-1	2021	Canavan disease is an autosomal recessive leukodystrophy caused by mutations in the gene encoding aspartoacylase (ASPA), which hydrolyses N-acetylaspartate (NAA) to acetate and aspartate.	N-acetylaspartate	157-160	aspartoacylase	Felis catus	98-112
33779415-1	2021	Canavan disease is an autosomal recessive leukodystrophy caused by mutations in the gene encoding aspartoacylase (ASPA), which hydrolyses N-acetylaspartate (NAA) to acetate and aspartate.	N-acetylaspartate	157-160	aspartoacylase	Felis catus	114-118
33763176-10	2021	It was shown that LY379268 concentration remains at a level that is required for activation of mGluR2 for up to 24 h; however, NAAG is quickly metabolized by glutamate carboxypeptidase II (GCPII) into glutamate and N-acetyl-aspartate.	N-acetylaspartate	215-233	folate hydrolase 1	Rattus norvegicus	189-194
28364102-6	2017	The NAA/Cr in the cerebellar dentate nucleus of onset patients with SCA3/MJD was obviously correlated with ICARS.	N-acetylaspartate	4-7	ataxin 3	Homo sapiens	68-72
34920037-2	2022	OCD patients have shown altered concentrations in neurometabolites in the dACC, particularly Glx (glutamate+glutamine) and tNAA (N-acetylaspartate+N-acetyl-aspartyl-glutamate).	N-acetylaspartate	129-146	Acetyl-CoA carboxylase	Drosophila melanogaster	74-78
25633678-6	2015	APOE epsilon4 versus epsilon3 children had a reduced NAA/Cr ratio in the right frontal white matter and decrements on attention, short-term memory, and below-average scores in Verbal and Full Scale IQ (&gt;10 points).	N-acetylaspartate	53-56	apolipoprotein E	Homo sapiens	0-4
34638000-5	2022	Additionally, we found that frontal levels of n-acetylaspartate relative to creatine (tNAA/tCr) were predicted by levels of t-tau.	N-acetylaspartate	46-63	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	91-94
34638000-5	2022	Additionally, we found that frontal levels of n-acetylaspartate relative to creatine (tNAA/tCr) were predicted by levels of t-tau.	N-acetylaspartate	46-63	microtubule associated protein tau	Homo sapiens	126-129
34896001-8	2021	RESULTS: There were significant differences between the TR and RN groups in terms of ADC (p = 0.001), rADC (p < 0.001), FA (p = 0.001), DA (p = 0.003), DR (p = 0.003), rCBV (p < 0.001), rCBF (p < 0.001), Cho/NAA (p < 0.001), Lac/Cr (p < 0.001) and Lip/Cr (p < 0.001).	N-acetylaspartate	208-211	coagulation factor II thrombin receptor	Homo sapiens	56-58
34888674-8	2022	The NAA/Cr ratio was negatively correlated with BMI z-scores (r = -0.25, P = 0.03) and serum insulin (rho = -0.27, P = 0.04), C-peptide (rho = -0.26, P = 0.04), amylin (r = -0.27, P = 0.04), ghrelin (rho = -0.30, P = 0.02) and neuropeptide Y (r = -0.27, P = 0.04).	N-acetylaspartate	4-7	insulin	Homo sapiens	93-100
34888674-8	2022	The NAA/Cr ratio was negatively correlated with BMI z-scores (r = -0.25, P = 0.03) and serum insulin (rho = -0.27, P = 0.04), C-peptide (rho = -0.26, P = 0.04), amylin (r = -0.27, P = 0.04), ghrelin (rho = -0.30, P = 0.02) and neuropeptide Y (r = -0.27, P = 0.04).	N-acetylaspartate	4-7	islet amyloid polypeptide	Homo sapiens	161-167
34888674-9	2022	Also, NAA/Cr ratio was positively correlated with circulating IL-8 levels (rho = 0.26, P = 0.04).	N-acetylaspartate	6-9	C-X-C motif chemokine ligand 8	Homo sapiens	62-66
34899214-11	2021	In DLPFC, only (N-acetyl aspartate + N-acetyl aspartyl-glutamate)/creatine (NAA + NAAG)/tCr was increased in the hyperthyroid patients.	N-acetylaspartate	76-79	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	88-91
34573036-1	2021	Neuronal N-acetylaspartate production appears in the presence of aspartate N-acetyltransferase (NAT8L) and binds acetyl groups from acetyl-CoA with aspartic acid.	N-acetylaspartate	9-26	N-acetyltransferase 8-like	Rattus norvegicus	96-101
34762311-7	2021	Path analyses showed that reduced NAA levels accounted significantly for higher diffusivity and higher rCBF values in ASD compared with TD participants.	N-acetylaspartate	34-37	CCAAT/enhancer binding protein zeta	Rattus norvegicus	103-107
34498299-1	2021	Canavan disease is caused by ASPA mutations that diminish brain aspartoacylase activity, and is characterized by excessive brain storage of the aspartoacylase substrate N-acetyl-L-aspartate (NAA) and by astroglial and intramyelinic vacuolation.	N-acetylaspartate	169-189	aspartoacylase	Mus musculus	29-33
34498299-1	2021	Canavan disease is caused by ASPA mutations that diminish brain aspartoacylase activity, and is characterized by excessive brain storage of the aspartoacylase substrate N-acetyl-L-aspartate (NAA) and by astroglial and intramyelinic vacuolation.	N-acetylaspartate	191-194	aspartoacylase	Mus musculus	29-33
34498299-2	2021	Astroglia and arachnoid mater express NaDC3, encoded by Slc13a3, a sodium-coupled transporter for NAA and other dicarboxylates.	N-acetylaspartate	98-101	solute carrier family 13 (sodium-dependent dicarboxylate transporter), member 3	Mus musculus	38-43
34498299-2	2021	Astroglia and arachnoid mater express NaDC3, encoded by Slc13a3, a sodium-coupled transporter for NAA and other dicarboxylates.	N-acetylaspartate	98-101	solute carrier family 13 (sodium-dependent dicarboxylate transporter), member 3	Mus musculus	56-63
34498299-3	2021	Constitutive Slc13a3 deletion in aspartoacylase-deficient Canavan disease mice prevents brain NAA over-accumulation, ataxia, and brain vacuolation.	N-acetylaspartate	94-97	solute carrier family 13 (sodium-dependent dicarboxylate transporter), member 3	Mus musculus	13-20
34477360-3	2021	Interestingly, genetic deletion of N-acetyltransferase-8-like (NAT8L), which encodes aspartate N-aceyltransferase (ANAT), an enzyme responsible for the synthesis of NAA from l-aspartate and acetyl-CoA, leads to normalization of NAA levels and improvement of symptoms in several genetically engineered mouse models of CD.	N-acetylaspartate	165-168	N-acetyltransferase 8-like	Mus musculus	35-61
34477360-3	2021	Interestingly, genetic deletion of N-acetyltransferase-8-like (NAT8L), which encodes aspartate N-aceyltransferase (ANAT), an enzyme responsible for the synthesis of NAA from l-aspartate and acetyl-CoA, leads to normalization of NAA levels and improvement of symptoms in several genetically engineered mouse models of CD.	N-acetylaspartate	165-168	N-acetyltransferase 8-like	Mus musculus	63-68
34477360-3	2021	Interestingly, genetic deletion of N-acetyltransferase-8-like (NAT8L), which encodes aspartate N-aceyltransferase (ANAT), an enzyme responsible for the synthesis of NAA from l-aspartate and acetyl-CoA, leads to normalization of NAA levels and improvement of symptoms in several genetically engineered mouse models of CD.	N-acetylaspartate	228-231	N-acetyltransferase 8-like	Mus musculus	35-61
34477360-3	2021	Interestingly, genetic deletion of N-acetyltransferase-8-like (NAT8L), which encodes aspartate N-aceyltransferase (ANAT), an enzyme responsible for the synthesis of NAA from l-aspartate and acetyl-CoA, leads to normalization of NAA levels and improvement of symptoms in several genetically engineered mouse models of CD.	N-acetylaspartate	228-231	N-acetyltransferase 8-like	Mus musculus	63-68
35428956-9	2022	Decreased N-acetyl aspartate (NAA) in aged mice was upregulated by Shati/Nat8l overexpression, suggesting that the Shati/Nat8l-NAA pathway determines cognitive function with aging.	N-acetylaspartate	30-33	N-acetyltransferase 8-like	Mus musculus	115-120
35636725-2	2022	ASPA is highly expressed in oligodendrocytes and catalyzes the cleavage of N-acetylaspartate (NAA) to produce aspartate and acetate.	N-acetylaspartate	75-92	aspartoacylase	Homo sapiens	0-4
35636725-2	2022	ASPA is highly expressed in oligodendrocytes and catalyzes the cleavage of N-acetylaspartate (NAA) to produce aspartate and acetate.	N-acetylaspartate	94-97	aspartoacylase	Homo sapiens	0-4
35636725-3	2022	In this review ,we examine the pathologies and clinical presentation in CD, the metabolism and transportation of NAA in the brain, and the hypothetical mechanisms whereby ASPA deficiency results in dysmyelination and a failure of normal brain development.	N-acetylaspartate	113-116	aspartoacylase	Homo sapiens	171-175
34282130-0	2021	The relationship between synaptic density marker SV2A, glutamate and N-acetyl aspartate levels in healthy volunteers and schizophrenia: a multimodal PET and magnetic resonance spectroscopy brain imaging study.	N-acetylaspartate	69-87	synaptic vesicle glycoprotein 2A	Homo sapiens	49-53
34282130-3	2021	Here, we investigated whether synaptic vesicle glycoprotein 2 A (SV2A) levels are related to glutamatergic markers and NAA in healthy volunteers (HV) and schizophrenia patients (SCZ).	N-acetylaspartate	119-122	synaptic vesicle glycoprotein 2A	Homo sapiens	30-63
34282130-3	2021	Here, we investigated whether synaptic vesicle glycoprotein 2 A (SV2A) levels are related to glutamatergic markers and NAA in healthy volunteers (HV) and schizophrenia patients (SCZ).	N-acetylaspartate	119-122	synaptic vesicle glycoprotein 2A	Homo sapiens	65-69
34296219-10	2021	Changes in NAA positively correlated with changes in FM (r=0.63, p=0.2) and FMp (r=0.93, p=0.03), suggesting that patients who show greater neuronal changes have a better chance of recovery.	N-acetylaspartate	11-14	fibromodulin	Homo sapiens	53-55
34296219-10	2021	Changes in NAA positively correlated with changes in FM (r=0.63, p=0.2) and FMp (r=0.93, p=0.03), suggesting that patients who show greater neuronal changes have a better chance of recovery.	N-acetylaspartate	11-14	fibromodulin	Homo sapiens	76-79
35587282-5	2022	Metabolomics analysis of neurotransmitters revealed that glutamic acid and N-acetyl-L-aspartic acid were increased in the striatum of VGF-overexpressing mice.	N-acetylaspartate	75-99	VGF nerve growth factor inducible	Mus musculus	134-137
35428956-9	2022	Decreased N-acetyl aspartate (NAA) in aged mice was upregulated by Shati/Nat8l overexpression, suggesting that the Shati/Nat8l-NAA pathway determines cognitive function with aging.	N-acetylaspartate	10-28	N-acetyltransferase 8-like	Mus musculus	67-72
35428956-9	2022	Decreased N-acetyl aspartate (NAA) in aged mice was upregulated by Shati/Nat8l overexpression, suggesting that the Shati/Nat8l-NAA pathway determines cognitive function with aging.	N-acetylaspartate	10-28	N-acetyltransferase 8-like	Mus musculus	73-78
35428956-9	2022	Decreased N-acetyl aspartate (NAA) in aged mice was upregulated by Shati/Nat8l overexpression, suggesting that the Shati/Nat8l-NAA pathway determines cognitive function with aging.	N-acetylaspartate	127-130	N-acetyltransferase 8-like	Mus musculus	67-72
35428956-9	2022	Decreased N-acetyl aspartate (NAA) in aged mice was upregulated by Shati/Nat8l overexpression, suggesting that the Shati/Nat8l-NAA pathway determines cognitive function with aging.	N-acetylaspartate	10-28	N-acetyltransferase 8-like	Mus musculus	115-120
35428956-9	2022	Decreased N-acetyl aspartate (NAA) in aged mice was upregulated by Shati/Nat8l overexpression, suggesting that the Shati/Nat8l-NAA pathway determines cognitive function with aging.	N-acetylaspartate	10-28	N-acetyltransferase 8-like	Mus musculus	121-126
35428956-9	2022	Decreased N-acetyl aspartate (NAA) in aged mice was upregulated by Shati/Nat8l overexpression, suggesting that the Shati/Nat8l-NAA pathway determines cognitive function with aging.	N-acetylaspartate	30-33	N-acetyltransferase 8-like	Mus musculus	67-72
35428956-9	2022	Decreased N-acetyl aspartate (NAA) in aged mice was upregulated by Shati/Nat8l overexpression, suggesting that the Shati/Nat8l-NAA pathway determines cognitive function with aging.	N-acetylaspartate	30-33	N-acetyltransferase 8-like	Mus musculus	73-78
35428956-9	2022	Decreased N-acetyl aspartate (NAA) in aged mice was upregulated by Shati/Nat8l overexpression, suggesting that the Shati/Nat8l-NAA pathway determines cognitive function with aging.	N-acetylaspartate	127-130	N-acetyltransferase 8-like	Mus musculus	73-78
35428956-9	2022	Decreased N-acetyl aspartate (NAA) in aged mice was upregulated by Shati/Nat8l overexpression, suggesting that the Shati/Nat8l-NAA pathway determines cognitive function with aging.	N-acetylaspartate	127-130	N-acetyltransferase 8-like	Mus musculus	115-120
35428956-9	2022	Decreased N-acetyl aspartate (NAA) in aged mice was upregulated by Shati/Nat8l overexpression, suggesting that the Shati/Nat8l-NAA pathway determines cognitive function with aging.	N-acetylaspartate	127-130	N-acetyltransferase 8-like	Mus musculus	121-126
35418161-9	2022	RESULTS: We found that the levels of choline (Cho) in the basal forebrain were markedly higher compared to other brain regions and that its decrease along with N-acetyl aspartate (NAA) levels in the hippocampus was accompanied by memory deficits in APP/PS1 mice aged 4, 6, and 8 months.	N-acetylaspartate	160-178	presenilin 1	Mus musculus	253-256
35418161-9	2022	RESULTS: We found that the levels of choline (Cho) in the basal forebrain were markedly higher compared to other brain regions and that its decrease along with N-acetyl aspartate (NAA) levels in the hippocampus was accompanied by memory deficits in APP/PS1 mice aged 4, 6, and 8 months.	N-acetylaspartate	180-183	presenilin 1	Mus musculus	253-256
35038671-4	2022	An increase in posterior cingulate gyrus tau deposition, but not elevated Abeta, was associated with lower N-acetylaspartate/total creatine (tCr) and glutamate (Glu)/tCr ratios, and sex by tau interaction was observed in association with Glu/tCr.	N-acetylaspartate	107-124	microtubule associated protein tau	Homo sapiens	41-44
35345457-5	2022	Untargeted metabolomics revealed NAA and NAAG commonly accumulating in CRPC across three independent models and proteomics showed upregulation of related enzymes, namely N-acetylated alpha-linked acidic dipeptidases (FOLH1/NAALADL2).	N-acetylaspartate	33-36	folate hydrolase 1	Mus musculus	217-222
35345457-5	2022	Untargeted metabolomics revealed NAA and NAAG commonly accumulating in CRPC across three independent models and proteomics showed upregulation of related enzymes, namely N-acetylated alpha-linked acidic dipeptidases (FOLH1/NAALADL2).	N-acetylaspartate	33-36	N-acetylated alpha-linked acidic dipeptidase-like 2	Mus musculus	223-231
35197056-6	2022	RESULTS: 1H MRS reliably quantified changes in cerebral metabolites, including glutamate/glutamine, lactate, and N-acetyl aspartate in a neuronal Pank1 and Pank2 double-knockout (SynCre+ Pank1,2 dKO) mouse model of brain CoA deficiency.	N-acetylaspartate	113-131	pantothenate kinase 1	Mus musculus	146-151
35197056-6	2022	RESULTS: 1H MRS reliably quantified changes in cerebral metabolites, including glutamate/glutamine, lactate, and N-acetyl aspartate in a neuronal Pank1 and Pank2 double-knockout (SynCre+ Pank1,2 dKO) mouse model of brain CoA deficiency.	N-acetylaspartate	113-131	pantothenate kinase 2	Mus musculus	156-161
35197056-7	2022	The neuronal SynCre+ Pank1,2 dKO mice had distinct decreases in Glx/tCr, NAA/tCr, and lactate/tCr ratios compared to the wildtype matched control mice that increased in response to BBP-671 treatment.	N-acetylaspartate	73-76	pantothenate kinase 1	Mus musculus	21-26
35157758-8	2022	Among the IDH-mutated subtypes, we observed high levels of amino acids, especially glycine and 2-aminoadipic acid, in grade 4 glioma, and N-acetyl aspartic acid in low-grade astrocytoma and oligodendroglioma.	N-acetylaspartate	138-160	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	10-13
35183218-6	2022	The Glu/GABA ratio, N-acetylaspartate (NAA)/total creatine (tCr) ratio, and tCr level in the prefrontal cortex were significantly different in Cntnap2-/- mice compared to those in wild-type mice, and they significantly correlated with the sociability of mice.	N-acetylaspartate	20-37	contactin associated protein-like 2	Mus musculus	143-150
35183218-6	2022	The Glu/GABA ratio, N-acetylaspartate (NAA)/total creatine (tCr) ratio, and tCr level in the prefrontal cortex were significantly different in Cntnap2-/- mice compared to those in wild-type mice, and they significantly correlated with the sociability of mice.	N-acetylaspartate	39-42	contactin associated protein-like 2	Mus musculus	143-150
2611666-3	1989	NAAG is hydrolyzed into glutamate (Glu) and N-acetyl-aspartate (NAA) by N-acetylated-alpha-linked acidic dipeptidase (NAALADase), a membrane-bound peptidase.	N-acetylaspartate	44-62	folate hydrolase 1	Rattus norvegicus	72-116
35048325-9	2022	Furthermore, there existed a positive correlation between the NAA/Cr ratio and the NeuN protein expression (R = 0.496 p < 0.001 IHC; R = 0.568 p < 0.001 WB), the same results existed in the relationship between the mI/Cr ratio and the GFAP protein expression (R = 0.338 p = 0.019 IHC; R = 0.440 p = 0.002 WB).	N-acetylaspartate	62-65	RNA binding fox-1 homolog 3	Rattus norvegicus	83-87
35048325-9	2022	Furthermore, there existed a positive correlation between the NAA/Cr ratio and the NeuN protein expression (R = 0.496 p < 0.001 IHC; R = 0.568 p < 0.001 WB), the same results existed in the relationship between the mI/Cr ratio and the GFAP protein expression (R = 0.338 p = 0.019 IHC; R = 0.440 p = 0.002 WB).	N-acetylaspartate	62-65	glial fibrillary acidic protein	Rattus norvegicus	235-239
35008954-2	2022	The deficiency in AGC1/Aralar leads to the human rare disease named "early infantile epileptic encephalopathy 39" (EIEE 39, OMIM # 612949) characterized by epilepsy, hypotonia, arrested psychomotor neurodevelopment, hypo myelination and a drastic drop in brain aspartate (Asp) and N-acetylaspartate (NAA).	N-acetylaspartate	281-298	solute carrier family 25 member 12	Homo sapiens	18-22
35008954-2	2022	The deficiency in AGC1/Aralar leads to the human rare disease named "early infantile epileptic encephalopathy 39" (EIEE 39, OMIM # 612949) characterized by epilepsy, hypotonia, arrested psychomotor neurodevelopment, hypo myelination and a drastic drop in brain aspartate (Asp) and N-acetylaspartate (NAA).	N-acetylaspartate	281-298	solute carrier family 25 member 12	Homo sapiens	23-29
35008954-2	2022	The deficiency in AGC1/Aralar leads to the human rare disease named "early infantile epileptic encephalopathy 39" (EIEE 39, OMIM # 612949) characterized by epilepsy, hypotonia, arrested psychomotor neurodevelopment, hypo myelination and a drastic drop in brain aspartate (Asp) and N-acetylaspartate (NAA).	N-acetylaspartate	300-303	solute carrier family 25 member 12	Homo sapiens	18-22
35008954-2	2022	The deficiency in AGC1/Aralar leads to the human rare disease named "early infantile epileptic encephalopathy 39" (EIEE 39, OMIM # 612949) characterized by epilepsy, hypotonia, arrested psychomotor neurodevelopment, hypo myelination and a drastic drop in brain aspartate (Asp) and N-acetylaspartate (NAA).	N-acetylaspartate	300-303	solute carrier family 25 member 12	Homo sapiens	23-29
35008954-5	2022	Herein, we discuss the role of the AGC1/Aralar-MAS pathway in neuronal functions such as Asp and NAA synthesis, lactate use, respiration on glucose, glutamate (Glu) oxidation and other neurometabolic aspects.	N-acetylaspartate	97-100	solute carrier family 25 member 12	Homo sapiens	35-39
34976589-2	2022	Reduced brain N-acetylaspartylglutamate (NAAG) levels are linked to impaired cognition in various neurological diseases, including MS. NAAG levels are regulated by glutamate carboxypeptidase II (GCPII), which hydrolyzes the neuropeptide to N-acetyl-aspartate and glutamate.	N-acetylaspartate	240-258	folate hydrolase 1	Mus musculus	164-193
34976589-2	2022	Reduced brain N-acetylaspartylglutamate (NAAG) levels are linked to impaired cognition in various neurological diseases, including MS. NAAG levels are regulated by glutamate carboxypeptidase II (GCPII), which hydrolyzes the neuropeptide to N-acetyl-aspartate and glutamate.	N-acetylaspartate	240-258	folate hydrolase 1	Mus musculus	195-200
35162943-9	2022	In Drosophila melanogaster, DmUCP4A could be involved in the transport of aspartate from mitochondria to the cytosol, in which it could be used for protein and nucleotide synthesis, as well as in the biosynthesis of ss-alanine and N-acetylaspartate, which play key roles in signal transmission in the central nervous system.	N-acetylaspartate	231-248	Ucp4A	Drosophila melanogaster	28-35
2611666-3	1989	NAAG is hydrolyzed into glutamate (Glu) and N-acetyl-aspartate (NAA) by N-acetylated-alpha-linked acidic dipeptidase (NAALADase), a membrane-bound peptidase.	N-acetylaspartate	44-62	folate hydrolase 1	Rattus norvegicus	118-127
2611666-3	1989	NAAG is hydrolyzed into glutamate (Glu) and N-acetyl-aspartate (NAA) by N-acetylated-alpha-linked acidic dipeptidase (NAALADase), a membrane-bound peptidase.	N-acetylaspartate	0-3	folate hydrolase 1	Rattus norvegicus	72-116
2611666-3	1989	NAAG is hydrolyzed into glutamate (Glu) and N-acetyl-aspartate (NAA) by N-acetylated-alpha-linked acidic dipeptidase (NAALADase), a membrane-bound peptidase.	N-acetylaspartate	0-3	folate hydrolase 1	Rattus norvegicus	118-127
3667587-2	1987	High performance liquid chromatography studies documented the presence of an enzyme activity, N-acetylated alpha-linked acidic dipeptidase (NAALA dipeptidase), in rat brain membranes that cleaves the endogenous brain dipeptide, N-acetyl-L-aspartyl-L-glutamate to N-acetyl-aspartate and glutamate.	N-acetylaspartate	263-281	folate hydrolase 1	Rattus norvegicus	94-138
2850921-2	1988	Recently, a membrane-bound metallopeptidase, N-acetylated alpha-linked acidic dipeptidase (NAALADase), which cleaves NAAG to N-acetyl-aspartate (NAA) and glutamate, has been characterized and has been shown to exhibit optimal activity under incubation conditions used to measure NAAG binding sites.	N-acetylaspartate	125-143	endothelin converting enzyme-like 1	Rattus norvegicus	27-43
2850921-2	1988	Recently, a membrane-bound metallopeptidase, N-acetylated alpha-linked acidic dipeptidase (NAALADase), which cleaves NAAG to N-acetyl-aspartate (NAA) and glutamate, has been characterized and has been shown to exhibit optimal activity under incubation conditions used to measure NAAG binding sites.	N-acetylaspartate	125-143	folate hydrolase 1	Rattus norvegicus	45-89
2850921-2	1988	Recently, a membrane-bound metallopeptidase, N-acetylated alpha-linked acidic dipeptidase (NAALADase), which cleaves NAAG to N-acetyl-aspartate (NAA) and glutamate, has been characterized and has been shown to exhibit optimal activity under incubation conditions used to measure NAAG binding sites.	N-acetylaspartate	125-143	folate hydrolase 1	Rattus norvegicus	91-100
2850921-2	1988	Recently, a membrane-bound metallopeptidase, N-acetylated alpha-linked acidic dipeptidase (NAALADase), which cleaves NAAG to N-acetyl-aspartate (NAA) and glutamate, has been characterized and has been shown to exhibit optimal activity under incubation conditions used to measure NAAG binding sites.	N-acetylaspartate	91-94	endothelin converting enzyme-like 1	Rattus norvegicus	27-43
2850921-2	1988	Recently, a membrane-bound metallopeptidase, N-acetylated alpha-linked acidic dipeptidase (NAALADase), which cleaves NAAG to N-acetyl-aspartate (NAA) and glutamate, has been characterized and has been shown to exhibit optimal activity under incubation conditions used to measure NAAG binding sites.	N-acetylaspartate	91-94	folate hydrolase 1	Rattus norvegicus	45-89
3346674-10	1988	Similar to in vitro data documenting the route of NAAG degradation by NAALADase, after intrastriatal injection, NAAG was rapidly cleaved to two major products, N-acetyl-aspartate and Glu, with a t1/2 of approximately 10 min.	N-acetylaspartate	160-178	folate hydrolase 1B (pseudogene)	Homo sapiens	70-79
3116332-2	1987	A high CSF/plasma concentration ratio of N-acetylaspartate indicates that this substance originates in the brain.	N-acetylaspartate	41-58	colony stimulating factor 2	Homo sapiens	7-10
6398119-0	1984	Action of L-aspartic, methyl aspartic and acetyl aspartic acids on GABA transaminase histochemical activity in nervous tissue.	N-acetylaspartate	42-63	4-aminobutyrate aminotransferase	Homo sapiens	67-84
6833238-9	1983	Pulse-chase experiments show that over the course of 1 h, this precursor is transformed first to an actin with a free NH2-terminal aspartic acid and is subsequently converted to mature L-cell actin with an acetylaspartic acid NH2 terminus.	N-acetylaspartate	206-225	actin	Oryctolagus cuniculus	192-197
6131106-4	1983	In the current investigation, HSF-1 was further purified and found to be N-acetyl-L-aspartic acid.	N-acetylaspartate	73-97	heat shock transcription factor 1	Rattus norvegicus	30-35
33063293-7	2021	In SCA14, total N-acetylaspartate (tNAA) was reduced in the vermis by 34%.	N-acetylaspartate	16-33	protein kinase C gamma	Homo sapiens	3-8
214328-0	1978	An electrophysiological study of N-acetyl-L-aspartic acid (NAAA) on the stellate ganglion of the squid.	N-acetylaspartate	33-57	N-acylethanolamine acid amidase	Homo sapiens	59-63
33600886-9	2021	These findings suggested that as early as 1~4 weeks after chronic cerebral ischemia, the metabolism of NAA, Glu, mI and Cho was synchronously impaired in neural circuit of hippocampus-mediodorsal thalamus-mPFC, and the loss of GABA delayed in the hippocampus, and optogenetics modulation of parvalbumin (PV) neurons in the mPFC can improve the neurochemical metabolism of working memory neural circuit and enhance working memory.	N-acetylaspartate	103-106	parvalbumin	Rattus norvegicus	291-302
5878127-0	1964	[Concentration of N-acetylaspartic acid at various levels of the rabbit brain in hypoglycemic coma induced with insulin].	N-acetylaspartate	18-39	insulin	Oryctolagus cuniculus	112-119
32621646-9	2020	Importantly, N-acetylaspartate and total choline correlated with NFL and MPB, respectively, in Q135 mice.	N-acetylaspartate	13-30	neurofilament, light polypeptide	Mus musculus	65-68
33594539-3	2021	This study sought to investigate whether metabolites, including glutamate (Glu), N-acetyl aspartate (NAA), and gamma aminobutyric acid (GABA), in the supplementary motor area (SMA) measured by magnetic resonance spectroscopy (MRS), could be a surrogate biomarker for ALS.	N-acetylaspartate	81-99	survival of motor neuron 1, telomeric	Homo sapiens	176-179
33594539-3	2021	This study sought to investigate whether metabolites, including glutamate (Glu), N-acetyl aspartate (NAA), and gamma aminobutyric acid (GABA), in the supplementary motor area (SMA) measured by magnetic resonance spectroscopy (MRS), could be a surrogate biomarker for ALS.	N-acetylaspartate	101-104	survival of motor neuron 1, telomeric	Homo sapiens	176-179
33594539-9	2021	The present findings might indicate that both the Glu/NAA and the Glu/GABA ratios in the SMA could be potential biomarkers for the diagnosis of ALS.	N-acetylaspartate	54-57	survival of motor neuron 1, telomeric	Homo sapiens	89-92
33120242-8	2021	Exploratory analyses showed that LLD patients had lower NAA levels in the PCC relative to controls.	N-acetylaspartate	56-59	crystallin gamma D	Homo sapiens	74-77
33363485-4	2020	Three cytokines influenced brain metabolite concentrations: IL-9 positively predicts glutamate, IL-1beta positively predicts Myo-inositol, and CCL5 positively predicts N-acetylaspartate concentrations.	N-acetylaspartate	168-185	C-C motif chemokine ligand 5	Homo sapiens	143-147
32507787-5	2020	N-acetyl-aspartate (NAA), a substrate of ASPA, showed accumulation in all brain regions and in the spinal cord.	N-acetylaspartate	0-18	aspartoacylase	Rattus norvegicus	41-45
32507787-5	2020	N-acetyl-aspartate (NAA), a substrate of ASPA, showed accumulation in all brain regions and in the spinal cord.	N-acetylaspartate	20-23	aspartoacylase	Rattus norvegicus	41-45
33304273-10	2020	Notably, ACSS2 can activate acetate released from acetylated metabolites including N-acetylaspartate (NAA), the most concentrated acetylated metabolite in the human brain.	N-acetylaspartate	83-100	acyl-CoA synthetase short chain family member 2	Homo sapiens	9-14
33304273-10	2020	Notably, ACSS2 can activate acetate released from acetylated metabolites including N-acetylaspartate (NAA), the most concentrated acetylated metabolite in the human brain.	N-acetylaspartate	102-105	acyl-CoA synthetase short chain family member 2	Homo sapiens	9-14
33304273-11	2020	NAA has been associated with the metabolic reprograming of cancer cells, where ACSS2 also plays a role.	N-acetylaspartate	0-3	acyl-CoA synthetase short chain family member 2	Homo sapiens	79-84
33304759-1	2020	Canavan disease (CD) is a fatal leukodystrophy caused by mutation of the aspartoacylase (ASPA) gene, which leads to deficiency in ASPA activity, accumulation of the substrate N-acetyl-L-aspartate (NAA), demyelination, and spongy degeneration of the brain.	N-acetylaspartate	175-195	aspartoacylase	Homo sapiens	89-93
33304759-1	2020	Canavan disease (CD) is a fatal leukodystrophy caused by mutation of the aspartoacylase (ASPA) gene, which leads to deficiency in ASPA activity, accumulation of the substrate N-acetyl-L-aspartate (NAA), demyelination, and spongy degeneration of the brain.	N-acetylaspartate	197-200	aspartoacylase	Homo sapiens	89-93
31273671-6	2020	SLC11A1 rs7576974_T was significantly associated with higher frontal gray matter N-acetylaspartate (p = 3.62e-5).	N-acetylaspartate	81-98	solute carrier family 11 member 1	Homo sapiens	0-7
32940938-15	2021	Among 2-HG ratios, the highest AUC for the identification of IDH mutant status was achieved using the 2-HG/NAA (AUC = 0.8, 95% CI 0.67-.89).	N-acetylaspartate	107-110	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	61-64
32621646-11	2020	CONCLUSIONS: N-acetylaspartate, myo-inositol, and total choline levels in the cerebellum are candidate biomarkers of neuroaxonal and oligodendrocyte pathology in SCA3, aspects of pathology that are reversible by RNAi therapy.	N-acetylaspartate	13-30	ataxin 3	Mus musculus	162-166
32651050-9	2021	NAA and glutathione levels are reduced in APOE epsilon4 carriers.	N-acetylaspartate	0-3	apolipoprotein E	Homo sapiens	42-46
32715663-5	2020	Higher insulin resistance was associated with lower prefrontal NAA levels in the T2DM-O group (t = -2.21, P = 0.032) but not in the T2DM-N group (t = -0.72, P = 0.48).	N-acetylaspartate	63-66	insulin	Homo sapiens	7-14
32639720-0	2020	Structure of the Brain N-Acetylaspartate Biosynthetic Enzyme NAT8L Revealed by Computer Modeling.	N-acetylaspartate	23-40	N-acetyltransferase 8 like	Homo sapiens	61-66
32639720-1	2020	We report the results of computational modeling of a three-dimensional all-atom structure of the membrane-associated protein encoded by the NAT8L gene, aspartate N-acetyltransferase, which is essential for brain synthesis of N-acetyl-L-aspartate (NAA).	N-acetylaspartate	225-245	N-acetyltransferase 8 like	Homo sapiens	140-145
32639720-1	2020	We report the results of computational modeling of a three-dimensional all-atom structure of the membrane-associated protein encoded by the NAT8L gene, aspartate N-acetyltransferase, which is essential for brain synthesis of N-acetyl-L-aspartate (NAA).	N-acetylaspartate	247-250	N-acetyltransferase 8 like	Homo sapiens	140-145
32639720-2	2020	The lack of experimentally derived three-dimensional structures of NAT8L poses one of the obstacles in studies of the mechanism of NAA formation and understanding the precise role of NAA in neurological disorders.	N-acetylaspartate	131-134	N-acetyltransferase 8 like	Homo sapiens	67-72
32639720-2	2020	The lack of experimentally derived three-dimensional structures of NAT8L poses one of the obstacles in studies of the mechanism of NAA formation and understanding the precise role of NAA in neurological disorders.	N-acetylaspartate	183-186	N-acetyltransferase 8 like	Homo sapiens	67-72
32035198-8	2020	There was a significant positive correlation between the Cho/NAA ratio and MIB-1 index (r = 0.46, P = 0.04).	N-acetylaspartate	61-64	MIB E3 ubiquitin protein ligase 1	Homo sapiens	75-80
32545833-1	2020	N-acetylaspartate is produced by neuronal aspartate N-acetyltransferase (NAT8L) from acetyl-CoA and aspartate.	N-acetylaspartate	0-17	N-acetyltransferase 8-like	Rattus norvegicus	73-78
32035198-9	2020	Cho level (P = 0.003) and Cho/NAA ratio (P = 0.002) were significantly higher in VOIs that were MIB-1-positive than in those that were MIB-1-negative.	N-acetylaspartate	30-33	MIB E3 ubiquitin protein ligase 1	Homo sapiens	96-101
32035198-10	2020	Detection of a Cho level >1.074 mM and a Cho/NAA ratio >0.48 using iMRS resulted in high diagnostic accuracy for MIB-1-positive remnants (Cho level: sensitivity 86%, specificity 100%; Cho/NAA ratio: sensitivity 79%, specificity 100%).	N-acetylaspartate	45-48	MIB E3 ubiquitin protein ligase 1	Homo sapiens	113-118
32035198-10	2020	Detection of a Cho level >1.074 mM and a Cho/NAA ratio >0.48 using iMRS resulted in high diagnostic accuracy for MIB-1-positive remnants (Cho level: sensitivity 86%, specificity 100%; Cho/NAA ratio: sensitivity 79%, specificity 100%).	N-acetylaspartate	188-191	MIB E3 ubiquitin protein ligase 1	Homo sapiens	113-118
31349070-7	2019	In addition, lower NAA, Glx, and mI levels in the SM1 were found to be correlates of poorer dexterous performance on a bimanual dexterity task.	N-acetylaspartate	19-22	SM1	Homo sapiens	50-53
32033248-1	2020	Because of a decreased sensitivity toward insulin, a key regulator of pyruvate dehydrogenase (PDH), Alzheimer"s patients have lower brain glucose utilization with reductions in Tricarboxylic Acid (TCA) cycle metabolites such as citrate, a precursor to n-acetyl-aspartate.	N-acetylaspartate	252-270	insulin	Homo sapiens	42-49
32033248-1	2020	Because of a decreased sensitivity toward insulin, a key regulator of pyruvate dehydrogenase (PDH), Alzheimer"s patients have lower brain glucose utilization with reductions in Tricarboxylic Acid (TCA) cycle metabolites such as citrate, a precursor to n-acetyl-aspartate.	N-acetylaspartate	252-270	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	70-92
32033248-1	2020	Because of a decreased sensitivity toward insulin, a key regulator of pyruvate dehydrogenase (PDH), Alzheimer"s patients have lower brain glucose utilization with reductions in Tricarboxylic Acid (TCA) cycle metabolites such as citrate, a precursor to n-acetyl-aspartate.	N-acetylaspartate	252-270	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	94-97
31376479-0	2019	Generation of an Atxn2-CAG100 knock-in mouse reveals N-acetylaspartate production deficit due to early Nat8l dysregulation.	N-acetylaspartate	53-70	ataxin 2	Mus musculus	17-22
31376479-8	2019	Novel molecular analyses from stages before the onset of motor deficits revealed a strong selective effect of ATXN2 on Nat8l mRNA which encodes the enzyme responsible for NAA synthesis.	N-acetylaspartate	171-174	ataxin 2	Homo sapiens	110-115
31376479-8	2019	Novel molecular analyses from stages before the onset of motor deficits revealed a strong selective effect of ATXN2 on Nat8l mRNA which encodes the enzyme responsible for NAA synthesis.	N-acetylaspartate	171-174	N-acetyltransferase 8-like	Mus musculus	119-124
32378630-2	2020	Shati/Nat8l is a synthetic enzyme that produces N-acetylaspartate (NAA) from L-aspartate and acetyl-coenzyme NAA is converted into N-acetylaspartylglutamate (NAAG) by NAAG synthetase (NAAGS).	N-acetylaspartate	48-65	N-acetyltransferase 8-like	Mus musculus	0-5
32378630-2	2020	Shati/Nat8l is a synthetic enzyme that produces N-acetylaspartate (NAA) from L-aspartate and acetyl-coenzyme NAA is converted into N-acetylaspartylglutamate (NAAG) by NAAG synthetase (NAAGS).	N-acetylaspartate	48-65	N-acetyltransferase 8-like	Mus musculus	6-11
32378630-2	2020	Shati/Nat8l is a synthetic enzyme that produces N-acetylaspartate (NAA) from L-aspartate and acetyl-coenzyme NAA is converted into N-acetylaspartylglutamate (NAAG) by NAAG synthetase (NAAGS).	N-acetylaspartate	48-65	ribosomal modification protein rimK-like family member A	Mus musculus	167-182
32378630-2	2020	Shati/Nat8l is a synthetic enzyme that produces N-acetylaspartate (NAA) from L-aspartate and acetyl-coenzyme NAA is converted into N-acetylaspartylglutamate (NAAG) by NAAG synthetase (NAAGS).	N-acetylaspartate	48-65	ribosomal modification protein rimK-like family member A	Mus musculus	184-189
32378630-2	2020	Shati/Nat8l is a synthetic enzyme that produces N-acetylaspartate (NAA) from L-aspartate and acetyl-coenzyme NAA is converted into N-acetylaspartylglutamate (NAAG) by NAAG synthetase (NAAGS).	N-acetylaspartate	67-70	N-acetyltransferase 8-like	Mus musculus	0-5
32378630-2	2020	Shati/Nat8l is a synthetic enzyme that produces N-acetylaspartate (NAA) from L-aspartate and acetyl-coenzyme NAA is converted into N-acetylaspartylglutamate (NAAG) by NAAG synthetase (NAAGS).	N-acetylaspartate	67-70	N-acetyltransferase 8-like	Mus musculus	6-11
32378630-2	2020	Shati/Nat8l is a synthetic enzyme that produces N-acetylaspartate (NAA) from L-aspartate and acetyl-coenzyme NAA is converted into N-acetylaspartylglutamate (NAAG) by NAAG synthetase (NAAGS).	N-acetylaspartate	67-70	ribosomal modification protein rimK-like family member A	Mus musculus	167-182
32378630-2	2020	Shati/Nat8l is a synthetic enzyme that produces N-acetylaspartate (NAA) from L-aspartate and acetyl-coenzyme NAA is converted into N-acetylaspartylglutamate (NAAG) by NAAG synthetase (NAAGS).	N-acetylaspartate	67-70	ribosomal modification protein rimK-like family member A	Mus musculus	184-189
32378630-2	2020	Shati/Nat8l is a synthetic enzyme that produces N-acetylaspartate (NAA) from L-aspartate and acetyl-coenzyme NAA is converted into N-acetylaspartylglutamate (NAAG) by NAAG synthetase (NAAGS).	N-acetylaspartate	109-112	N-acetyltransferase 8-like	Mus musculus	0-5
32378630-2	2020	Shati/Nat8l is a synthetic enzyme that produces N-acetylaspartate (NAA) from L-aspartate and acetyl-coenzyme NAA is converted into N-acetylaspartylglutamate (NAAG) by NAAG synthetase (NAAGS).	N-acetylaspartate	109-112	N-acetyltransferase 8-like	Mus musculus	6-11
32378630-2	2020	Shati/Nat8l is a synthetic enzyme that produces N-acetylaspartate (NAA) from L-aspartate and acetyl-coenzyme NAA is converted into N-acetylaspartylglutamate (NAAG) by NAAG synthetase (NAAGS).	N-acetylaspartate	109-112	ribosomal modification protein rimK-like family member A	Mus musculus	167-182
32378630-2	2020	Shati/Nat8l is a synthetic enzyme that produces N-acetylaspartate (NAA) from L-aspartate and acetyl-coenzyme NAA is converted into N-acetylaspartylglutamate (NAAG) by NAAG synthetase (NAAGS).	N-acetylaspartate	109-112	ribosomal modification protein rimK-like family member A	Mus musculus	184-189
31398432-9	2019	The difference in ADC was found to be statistically significant for the creatines, cholines, N-acetylaspartate, myo-inositol, and glutamate.	N-acetylaspartate	93-110	antizyme inhibitor 2	Homo sapiens	18-21
30970252-3	2019	We found that NAAG is more abundant in higher grade cancers and is a source of glutamate in cancers expressing glutamate carboxypeptidase II (GCPII), the enzyme that hydrolyzes NAAG to glutamate and N-acetyl-aspartate (NAA).	N-acetylaspartate	199-217	folate hydrolase 1	Homo sapiens	111-140
31315971-7	2019	RESULTS: Asymptomatic MAPT mutation carriers had lower neuronal marker N-acetylaspartate (NAA)/creatine (Cr) (p = 0.001) and lower NAA/myo-inositol (mI) (p = 0.026) than noncarriers after adjustment for age.	N-acetylaspartate	71-88	microtubule associated protein tau	Homo sapiens	22-26
31315971-7	2019	RESULTS: Asymptomatic MAPT mutation carriers had lower neuronal marker N-acetylaspartate (NAA)/creatine (Cr) (p = 0.001) and lower NAA/myo-inositol (mI) (p = 0.026) than noncarriers after adjustment for age.	N-acetylaspartate	90-93	microtubule associated protein tau	Homo sapiens	22-26
31315971-7	2019	RESULTS: Asymptomatic MAPT mutation carriers had lower neuronal marker N-acetylaspartate (NAA)/creatine (Cr) (p = 0.001) and lower NAA/myo-inositol (mI) (p = 0.026) than noncarriers after adjustment for age.	N-acetylaspartate	131-134	microtubule associated protein tau	Homo sapiens	22-26
31315971-8	2019	Symptomatic MAPT mutation carriers had lower NAA/Cr (p = 0.01) and NAA/mI (p = 0.01) and higher mI/Cr (p = 0.02) compared to noncarriers after adjustment for age.	N-acetylaspartate	45-48	microtubule associated protein tau	Homo sapiens	12-16
31315971-8	2019	Symptomatic MAPT mutation carriers had lower NAA/Cr (p = 0.01) and NAA/mI (p = 0.01) and higher mI/Cr (p = 0.02) compared to noncarriers after adjustment for age.	N-acetylaspartate	67-70	microtubule associated protein tau	Homo sapiens	12-16
31516913-8	2019	Baseline NfL levels were associated with worse pretreatment disease measures (Expanded Disability Status Scale [EDSS], relapses, MRI lesions, and MR spectroscopy (MRS) N-acetylaspartate/creatine).	N-acetylaspartate	168-185	neurofilament light chain	Homo sapiens	9-12
29400109-3	2019	Region-specific neurochemical alterations were detected in asymptomatic G93A-SOD1 mice, particularly in lactate (-19%) and glutamate (+8%) of brainstem, along with gamma-amino-butyric acid (-30%), N-acetyl-aspartate (-5%) and ascorbate (+51%) of motor cortex.	N-acetylaspartate	197-215	superoxide dismutase 1, soluble	Mus musculus	77-81
30431265-2	2019	The hAsp enzyme hydrolyzes one of the most abundant amino acid derivatives in the brain, N-acetyl-aspartate.	N-acetylaspartate	89-107	assembly factor for spindle microtubules	Homo sapiens	4-8
31488434-0	2019	Correction: Cancer-Specific Production of N-Acetylaspartate via NAT8L Overexpression in Non-Small Cell Lung Cancer and Its Potential as a Circulating Biomarker.	N-acetylaspartate	42-59	N-acetyltransferase 8 like	Homo sapiens	64-69
31292734-11	2019	The change in the NAA/Cr ratio in the left DLPFC was negatively correlated with the change in the cognitive scales of the Alzheimer"s Disease Assessment Scale (ADAS-cog).	N-acetylaspartate	18-21	alkylglycerone phosphate synthase	Homo sapiens	160-164
30970252-3	2019	We found that NAAG is more abundant in higher grade cancers and is a source of glutamate in cancers expressing glutamate carboxypeptidase II (GCPII), the enzyme that hydrolyzes NAAG to glutamate and N-acetyl-aspartate (NAA).	N-acetylaspartate	199-217	folate hydrolase 1	Homo sapiens	142-147
30970252-3	2019	We found that NAAG is more abundant in higher grade cancers and is a source of glutamate in cancers expressing glutamate carboxypeptidase II (GCPII), the enzyme that hydrolyzes NAAG to glutamate and N-acetyl-aspartate (NAA).	N-acetylaspartate	14-17	folate hydrolase 1	Homo sapiens	111-140
30970252-3	2019	We found that NAAG is more abundant in higher grade cancers and is a source of glutamate in cancers expressing glutamate carboxypeptidase II (GCPII), the enzyme that hydrolyzes NAAG to glutamate and N-acetyl-aspartate (NAA).	N-acetylaspartate	14-17	folate hydrolase 1	Homo sapiens	142-147
31001069-5	2019	In parallel MR spectroscopy experiments, we found that CNO reduced creatine + phosphcreatine (Cr+PCr) and increased N-acetylaspartate + N-acetylaspartylglutamate (NAA+NAAG) signals in the prefrontal cortex, and also reduced the glutamate signal in dorsal striatum, with peak effect at 2 mg/kg.	N-acetylaspartate	116-133	biogenesis of lysosomal organelles complex 1 subunit 4	Rattus norvegicus	55-58
31001069-5	2019	In parallel MR spectroscopy experiments, we found that CNO reduced creatine + phosphcreatine (Cr+PCr) and increased N-acetylaspartate + N-acetylaspartylglutamate (NAA+NAAG) signals in the prefrontal cortex, and also reduced the glutamate signal in dorsal striatum, with peak effect at 2 mg/kg.	N-acetylaspartate	163-166	biogenesis of lysosomal organelles complex 1 subunit 4	Rattus norvegicus	55-58
30711191-4	2019	We also assessed the moderating influences of participant age, sex, and IQ on our findings and the correlations of rCBF with N-acetylaspartate metabolite levels.	N-acetylaspartate	125-142	CCAAT/enhancer binding protein zeta	Rattus norvegicus	115-119
30711191-8	2019	rCBF in the ASD group correlated inversely with N-acetylaspartate metabolite levels throughout the frontal white matter, with greater rCBF accompanying lower and increasingly abnormal N-acetylaspartate levels relative to those of typically developing control subjects.	N-acetylaspartate	48-65	CCAAT/enhancer binding protein zeta	Rattus norvegicus	0-4
30711191-8	2019	rCBF in the ASD group correlated inversely with N-acetylaspartate metabolite levels throughout the frontal white matter, with greater rCBF accompanying lower and increasingly abnormal N-acetylaspartate levels relative to those of typically developing control subjects.	N-acetylaspartate	184-201	CCAAT/enhancer binding protein zeta	Rattus norvegicus	0-4
29981000-6	2019	CCR2 was associated with neuronal damage, based on the inverse correlation of CCR2 on CD14+CD16+ monocytes with total N-Acetyl Aspartate (tNAA)/total Creatine (tCr) (r2 = 0.348, p = 0.01) and Glutamine-Glutamate (Glx)/tCr (r2 = 0.356, p = 0.01) in the right and left caudate nucleus, respectively.	N-acetylaspartate	118-136	C-C motif chemokine receptor 2	Homo sapiens	0-4
30635937-1	2019	OBJECTIVE: SLC13A3 encodes the plasma membrane Na+ /dicarboxylate cotransporter 3, which imports inside the cell 4 to 6 carbon dicarboxylates as well as N-acetylaspartate (NAA).	N-acetylaspartate	153-170	solute carrier family 13 member 3	Homo sapiens	11-18
30635937-1	2019	OBJECTIVE: SLC13A3 encodes the plasma membrane Na+ /dicarboxylate cotransporter 3, which imports inside the cell 4 to 6 carbon dicarboxylates as well as N-acetylaspartate (NAA).	N-acetylaspartate	172-175	solute carrier family 13 member 3	Homo sapiens	11-18
30635937-13	2019	Functional studies performed on HEK293T cells transiently transfected with wild-type and mutant SLC13A3 indicated that the missense mutations caused a marked reduction in the capacity to transport alphaKG, succinate, and NAA.	N-acetylaspartate	221-224	solute carrier family 13 member 3	Homo sapiens	96-103
30828585-2	2019	Although important in joining tRNAs to their cognate amino acids, AIMP1 has several other functions including axonal growth, cytokine activity, and interactions with N-acetylaspartic acid in ribosomal tRNA synthetase complexes.	N-acetylaspartate	166-187	aminoacyl tRNA synthetase complex interacting multifunctional protein 1	Homo sapiens	66-71
30828585-6	2019	In the absence of whole exome sequencing, we propose that decreased N-acetylaspartic acid peaks on magnetic resonance spectroscopy could act as a biomarker for AIMP1 mutations.	N-acetylaspartate	68-89	aminoacyl tRNA synthetase complex interacting multifunctional protein 1	Homo sapiens	160-165
30595160-3	2019	Aspartate N-acetyltransferase (Asp-NAT, encoded by Nat8l) synthesizes NAA from acetyl-CoA and aspartate and increases energy expenditure in brown adipocytes.	N-acetylaspartate	70-73	N-acetyltransferase 8 like	Homo sapiens	51-56
30595160-7	2019	Overexpression of Nat8l drains glucose-derived acetyl-CoA into the NAA pool at the expense of cellular lipids and certain amino acids.	N-acetylaspartate	67-70	N-acetyltransferase 8 like	Homo sapiens	18-23
29981000-6	2019	CCR2 was associated with neuronal damage, based on the inverse correlation of CCR2 on CD14+CD16+ monocytes with total N-Acetyl Aspartate (tNAA)/total Creatine (tCr) (r2 = 0.348, p = 0.01) and Glutamine-Glutamate (Glx)/tCr (r2 = 0.356, p = 0.01) in the right and left caudate nucleus, respectively.	N-acetylaspartate	118-136	C-C motif chemokine receptor 2	Homo sapiens	78-82
29981000-6	2019	CCR2 was associated with neuronal damage, based on the inverse correlation of CCR2 on CD14+CD16+ monocytes with total N-Acetyl Aspartate (tNAA)/total Creatine (tCr) (r2 = 0.348, p = 0.01) and Glutamine-Glutamate (Glx)/tCr (r2 = 0.356, p = 0.01) in the right and left caudate nucleus, respectively.	N-acetylaspartate	118-136	CD14 molecule	Homo sapiens	86-90
29981000-6	2019	CCR2 was associated with neuronal damage, based on the inverse correlation of CCR2 on CD14+CD16+ monocytes with total N-Acetyl Aspartate (tNAA)/total Creatine (tCr) (r2 = 0.348, p = 0.01) and Glutamine-Glutamate (Glx)/tCr (r2 = 0.356, p = 0.01) in the right and left caudate nucleus, respectively.	N-acetylaspartate	118-136	Fc gamma receptor IIIa	Homo sapiens	91-95
29498007-5	2018	We also found that the neuronal mitochondrial metabolite N-acetylaspartate (NAA), a marker of neuronal mitochondrial activity, was increased with EPO treatment.	N-acetylaspartate	57-74	erythropoietin	Mus musculus	146-149
30458729-7	2018	CONCLUSION: Using two non-invasive methods, 1H-MRS and T2 MR imaging, as well as in vitro brain-water content measurements, we demonstrated that the mechanism underlying the neuroprotective effects of GCP II-KO against brain swelling in TBI involves changes in glutamate and N-acetylaspartate levels.	N-acetylaspartate	275-292	folate hydrolase 1	Mus musculus	201-207
29498007-5	2018	We also found that the neuronal mitochondrial metabolite N-acetylaspartate (NAA), a marker of neuronal mitochondrial activity, was increased with EPO treatment.	N-acetylaspartate	76-79	erythropoietin	Mus musculus	146-149
29498007-6	2018	Further, we measured the effects of EPO on preventing mitochondrial deficits in the cuprizone toxic demyelinating mouse model of MS. We found that EPO prevented cuprizone-mediated decreases in Hbb, complex III, and NAA.	N-acetylaspartate	215-218	erythropoietin	Mus musculus	147-150
30364402-6	2018	Results: NAA/Cr, WMH, and cortical thickness were all correlated with age and CD4 nadir in unadjusted associations.	N-acetylaspartate	9-12	CD4 molecule	Homo sapiens	78-81
30364402-7	2018	Stepwise regression models showed that NAA/Cr alone best predicted CD4 nadir (beta = 40.1 +- 13.3; P = .005), whereas WMH (beta = 2.3 +- .9; P = .02) and mean cortical thickness (beta = -2.7 +- 6.6; P &lt; .0001) together produced the best model fit with age.	N-acetylaspartate	39-42	CD4 molecule	Homo sapiens	67-70
30364402-8	2018	NAA/Cr was higher for HIV stage 1 (CD4 nadir &gt;= 500 cells/ microL; n = 15) compared with stage 2 (200 &gt;= CD4 nadir &lt; 500; n = 13) and stage 3 (CD4 nadir &lt; 200; n = 9; P &lt; .01 for both).	N-acetylaspartate	0-3	CD4 molecule	Homo sapiens	35-38
30364402-8	2018	NAA/Cr was higher for HIV stage 1 (CD4 nadir &gt;= 500 cells/ microL; n = 15) compared with stage 2 (200 &gt;= CD4 nadir &lt; 500; n = 13) and stage 3 (CD4 nadir &lt; 200; n = 9; P &lt; .01 for both).	N-acetylaspartate	0-3	CD4 molecule	Homo sapiens	111-114
30364402-8	2018	NAA/Cr was higher for HIV stage 1 (CD4 nadir &gt;= 500 cells/ microL; n = 15) compared with stage 2 (200 &gt;= CD4 nadir &lt; 500; n = 13) and stage 3 (CD4 nadir &lt; 200; n = 9; P &lt; .01 for both).	N-acetylaspartate	0-3	CD4 molecule	Homo sapiens	111-114
20301412-8	1993	In mild/juvenile Canavan disease NAA may only be slightly elevated; thus, the diagnosis relies on molecular genetic testing of ASPA, the gene encoding the enzyme aspartoacylase.	N-acetylaspartate	33-36	aspartoacylase	Homo sapiens	127-131