PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 17447416-7 2006 MAO B inhibitors such as L-(-)-deprenyl (selegiline) and rasagiline are effective for the treatment of PD. Selegiline 25-39 monoamine oxidase B Homo sapiens 0-5 17447416-7 2006 MAO B inhibitors such as L-(-)-deprenyl (selegiline) and rasagiline are effective for the treatment of PD. Selegiline 41-51 monoamine oxidase B Homo sapiens 0-5 17447416-9 2006 As another mechanism of clinical efficacy, MAO B inhibitors such as selegiline are speculated to have neuroprotective effects to prevent progress of PD. Selegiline 68-78 monoamine oxidase B Homo sapiens 43-48 16274328-1 2005 Selegiline orally disintegrating tablet is a potent, selective and irreversible inhibitor of monoamine oxidase type B. Selegiline 0-10 monoamine oxidase B Homo sapiens 93-117 16413604-1 2005 Selegiline (L-deprenyl) is a selective irreversible monoamine oxidase B inhibitor shown to be effective in the treatment of Parkinson"s and Alzheimer"s diseases. Selegiline 0-10 monoamine oxidase B Homo sapiens 52-71 16413604-1 2005 Selegiline (L-deprenyl) is a selective irreversible monoamine oxidase B inhibitor shown to be effective in the treatment of Parkinson"s and Alzheimer"s diseases. Selegiline 12-22 monoamine oxidase B Homo sapiens 52-71 16274338-2 2005 Selegiline is currently the most widely used monoamine oxidase-B inhibitor for Parkinson"s disease, but has a low and variable bioavailability, and is metabolized to L-methamphetamine and L-amphetamine that carry a risk for potential neurotoxicity. Selegiline 0-10 monoamine oxidase B Homo sapiens 45-64 16296809-4 2005 Preventing the breakdown of dopamine has also been achieved by monoamine oxidase-B inhibition; this approach now having been formulated for sublingual use (Zelapar, Valeant Pharmaceuticals). Selegiline 156-163 monoamine oxidase B Homo sapiens 63-82 16099847-1 2005 Through the inhibition of monoamine oxidase type B (MAO-B), (-)-deprenyl (selegiline) prevents the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the toxic metabolite 1-methyl-4-phenylpyridinium ion (MPP+) and also prevents the neurotoxicity in the dopaminergic neurons in animal models. Selegiline 60-72 monoamine oxidase B Homo sapiens 26-50 16099847-1 2005 Through the inhibition of monoamine oxidase type B (MAO-B), (-)-deprenyl (selegiline) prevents the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the toxic metabolite 1-methyl-4-phenylpyridinium ion (MPP+) and also prevents the neurotoxicity in the dopaminergic neurons in animal models. Selegiline 60-72 monoamine oxidase B Homo sapiens 52-57 16099847-1 2005 Through the inhibition of monoamine oxidase type B (MAO-B), (-)-deprenyl (selegiline) prevents the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the toxic metabolite 1-methyl-4-phenylpyridinium ion (MPP+) and also prevents the neurotoxicity in the dopaminergic neurons in animal models. Selegiline 74-84 monoamine oxidase B Homo sapiens 26-50 16099847-1 2005 Through the inhibition of monoamine oxidase type B (MAO-B), (-)-deprenyl (selegiline) prevents the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the toxic metabolite 1-methyl-4-phenylpyridinium ion (MPP+) and also prevents the neurotoxicity in the dopaminergic neurons in animal models. Selegiline 74-84 monoamine oxidase B Homo sapiens 52-57 16139174-1 2005 Although selegiline, a monoamine oxidase (MAO)-B inhibitor, is reported to exert antidepressant effects in depressant patients, evidence in rodents for effects of selegiline is quite limited. Selegiline 9-19 monoamine oxidase B Homo sapiens 23-48 16139174-8 2005 Selegiline at 1 and 3 mg/kg, which failed to decrease immobility time, markedly inhibited brain total-MAO and MAO-B activities. Selegiline 0-10 monoamine oxidase B Homo sapiens 110-115 15308297-5 2004 Incubation of MDMA treated cells with the SERT inhibitor, fluoxetine (500 nM) or the MAO-B inhibitor, L-deprenyl (0.1 mM) for 30 min prior to DA, significantly blocked free radical production and cell death. Selegiline 102-112 monoamine oxidase B Homo sapiens 85-90 16062100-0 2005 Remarkable effect of selegiline (L-deprenyl), a selective monoamine oxidase type-B inhibitor, in a patient with severe refractory depression: a case report. Selegiline 21-31 monoamine oxidase B Homo sapiens 58-82 16156677-9 2005 Concern has been expressed about the potential of the MAO-B inhibitor selegiline (deprenyl) to induce cardiovascular adverse effects (orthostatic hypotension), either directly or through its amphetamine catabolites. Selegiline 70-80 monoamine oxidase B Homo sapiens 54-59 16156677-9 2005 Concern has been expressed about the potential of the MAO-B inhibitor selegiline (deprenyl) to induce cardiovascular adverse effects (orthostatic hypotension), either directly or through its amphetamine catabolites. Selegiline 82-90 monoamine oxidase B Homo sapiens 54-59 16062100-0 2005 Remarkable effect of selegiline (L-deprenyl), a selective monoamine oxidase type-B inhibitor, in a patient with severe refractory depression: a case report. Selegiline 33-43 monoamine oxidase B Homo sapiens 58-82 16062100-3 2005 Switching from amoxapine 150 mg/day to selegiline 7.5 mg/day, a selective monoamine oxidase type-B inhibitor, produced a dramatic reduction in hypobulia and lassitude, leading to a complete remission of all depressive symptoms. Selegiline 39-49 monoamine oxidase B Homo sapiens 74-98 14696044-3 2004 Selegiline is a selective and irreversible propargylamine type B monoamine oxidase (MAO-B) inhibitor. Selegiline 0-10 monoamine oxidase B Homo sapiens 84-89 15279565-1 2004 Deprenyl, the selective irreversible inhibitor of monoamine oxidase-B (MAO-B), has been synthesised as a potential antidepressant, however, due to its dopamine potentiating capacity, became a registered drug in the treatment of Parkinson"s disease. Selegiline 0-8 monoamine oxidase B Homo sapiens 50-69 15279565-1 2004 Deprenyl, the selective irreversible inhibitor of monoamine oxidase-B (MAO-B), has been synthesised as a potential antidepressant, however, due to its dopamine potentiating capacity, became a registered drug in the treatment of Parkinson"s disease. Selegiline 0-8 monoamine oxidase B Homo sapiens 71-76 14605792-2 2004 Selegiline, a selective monoamine oxidase B inhibitor, indirectly modulates dopamine levels, and research suggests selegiline may modify subjective effects of cocaine. Selegiline 0-10 monoamine oxidase B Homo sapiens 24-43 14697876-3 2004 MAO-A is inhibited by clorgyline; and MAO-B, by deprenyl. Selegiline 48-56 monoamine oxidase B Homo sapiens 38-43 15233592-12 2004 Disulfiram and selegiline increase brain dopamine concentrations by inhibition of dopamine-catabolising enzymes (dopamine-beta-hydroxylase and monoamine oxidase B, respectively). Selegiline 15-25 monoamine oxidase B Homo sapiens 143-162 14697895-2 2004 Selegiline [(-)-deprenil] was developed as a MAO-B inhibitor more than 30 years ago and widely used in the treatment of Parkinson"s disease. Selegiline 0-10 monoamine oxidase B Homo sapiens 45-50 14697895-2 2004 Selegiline [(-)-deprenil] was developed as a MAO-B inhibitor more than 30 years ago and widely used in the treatment of Parkinson"s disease. Selegiline 12-24 monoamine oxidase B Homo sapiens 45-50 14697896-3 2004 The selective monoamine oxidase-B inhibitor selegiline and the selective and reversible inhibitor of monoamine oxidase-A (RIMA) moclobemide are free from the hypertensive crisis, the so-called "cheese effect." Selegiline 44-54 monoamine oxidase B Homo sapiens 14-33 14697898-0 2004 (-)-Deprenyl, a selective MAO-B inhibitor, with apoptotic and anti-apoptotic properties. Selegiline 0-12 monoamine oxidase B Homo sapiens 26-31 14697898-1 2004 (-)-Deprenyl (selegiline) is an irreversible inhibitor of monoamine oxidase (MAO) B, which was discovered in 1962 and become the "golden standard" of MAO research. Selegiline 0-12 monoamine oxidase B Homo sapiens 58-83 14697898-1 2004 (-)-Deprenyl (selegiline) is an irreversible inhibitor of monoamine oxidase (MAO) B, which was discovered in 1962 and become the "golden standard" of MAO research. Selegiline 14-24 monoamine oxidase B Homo sapiens 58-83 14697898-6 2004 (-)-Deprenyl in much lower concentrations needed to induce MAO-B inhibition (10(-9) to 10(-13) M) potently inhibits MPTP or serum withdrawal induced apoptosis in tissue cultures of neuro-ectodermal origin (PC12, M1, M2058). Selegiline 0-12 monoamine oxidase B Homo sapiens 59-64 14697899-4 2004 However irreversible MAO-A inhibitors continue to induce a cheese reaction, whereas MAO-B inhibitors at their selective dosage did not and led to introduction of L-deprenyl (selegiline) as an anti-Parkinson drug, since dopamine is equally well metabolized by both enzyme forms. Selegiline 162-172 monoamine oxidase B Homo sapiens 84-89 14697899-4 2004 However irreversible MAO-A inhibitors continue to induce a cheese reaction, whereas MAO-B inhibitors at their selective dosage did not and led to introduction of L-deprenyl (selegiline) as an anti-Parkinson drug, since dopamine is equally well metabolized by both enzyme forms. Selegiline 174-184 monoamine oxidase B Homo sapiens 84-89 14628189-19 2003 Thus, the lower but equally MAO-B inhibitory dose of selegiline in Zydis Selegiline 1.25 mg, which is associated with lower concentrations of potentially harmful metabolites, could offer a safer and more predictable treatment in the management of patients with Parkinson"s disease. Selegiline 53-63 monoamine oxidase B Homo sapiens 28-33 14636968-1 2003 Selegiline is a specific MAO-B inhibitor. Selegiline 0-10 monoamine oxidase B Homo sapiens 25-30 14636968-2 2003 As MAO-B has been shown to be significantly involved in the metabolism of dopamine in certain regions of the primate brain, selegiline has been proposed for use in the treatment of drug addiction. Selegiline 124-134 monoamine oxidase B Homo sapiens 3-8 14612913-1 2003 l-Deprenyl (R-(-)-deprenyl, selegiline) is an inhibitor of monoamine oxidase-B (MAO-B) that is known to protect nerve cells from a variety of chemical and physical insults. Selegiline 0-10 monoamine oxidase B Homo sapiens 59-78 14612913-1 2003 l-Deprenyl (R-(-)-deprenyl, selegiline) is an inhibitor of monoamine oxidase-B (MAO-B) that is known to protect nerve cells from a variety of chemical and physical insults. Selegiline 0-10 monoamine oxidase B Homo sapiens 80-85 14612913-1 2003 l-Deprenyl (R-(-)-deprenyl, selegiline) is an inhibitor of monoamine oxidase-B (MAO-B) that is known to protect nerve cells from a variety of chemical and physical insults. Selegiline 28-38 monoamine oxidase B Homo sapiens 59-78 14612913-1 2003 l-Deprenyl (R-(-)-deprenyl, selegiline) is an inhibitor of monoamine oxidase-B (MAO-B) that is known to protect nerve cells from a variety of chemical and physical insults. Selegiline 28-38 monoamine oxidase B Homo sapiens 80-85 14563485-1 2003 L-Deprenyl, an inhibitor of mitochondrial monoamine oxidase B (MAO B), inhibits the swelling of liver mitochondria induced by the pro-oxidant 2-methyl-1,4-naphtoquinone with a K(i) dependent on quinone concentration. Selegiline 0-10 monoamine oxidase B Homo sapiens 42-61 14563485-1 2003 L-Deprenyl, an inhibitor of mitochondrial monoamine oxidase B (MAO B), inhibits the swelling of liver mitochondria induced by the pro-oxidant 2-methyl-1,4-naphtoquinone with a K(i) dependent on quinone concentration. Selegiline 0-10 monoamine oxidase B Homo sapiens 63-68 14563485-6 2003 These results indicate a more generalized protective effect of L-deprenyl on mitochondrial functions, involving the inhibition of membrane permeability transition induced not only by the oxidation of substrates of MAO B, but also by pro-oxidant agents such as 2-methyl-1,4-naphtoquinone, which does not involve MAO B activity. Selegiline 63-73 monoamine oxidase B Homo sapiens 214-219 14563485-6 2003 These results indicate a more generalized protective effect of L-deprenyl on mitochondrial functions, involving the inhibition of membrane permeability transition induced not only by the oxidation of substrates of MAO B, but also by pro-oxidant agents such as 2-methyl-1,4-naphtoquinone, which does not involve MAO B activity. Selegiline 63-73 monoamine oxidase B Homo sapiens 311-316 14628189-0 2003 A new formulation of selegiline: improved bioavailability and selectivity for MAO-B inhibition. Selegiline 21-31 monoamine oxidase B Homo sapiens 78-83 14628189-12 2003 A significant (r=0.0001) correlation between daily PEA excretion (a measure of brain MAO-B inhibition) and the log-transformed AUC((0-t)) for selegiline was demonstrated. Selegiline 142-152 monoamine oxidase B Homo sapiens 85-90 14628190-0 2003 A new low-dose formulation of selegiline: clinical efficacy, patient preference and selectivity for MAO-B inhibition. Selegiline 30-40 monoamine oxidase B Homo sapiens 100-105 12200198-2 2002 An inhibitor of type B monoamine oxidase (MAO-B), (-)deprenyl (selegiline), was reported to have neuroprotective activity, but clinical trials failed to confirm it. Selegiline 53-61 monoamine oxidase B Homo sapiens 42-47 12633131-2 2003 A selegiline transdermal system (STS) has been developed with unique pharmacokinetic and pharmacodynamic properties that allow inhibition of central nervous system MAO-A and MAO-B enzymes while substantially avoiding inhibition of intestinal and liver MAO-A enzyme. Selegiline 2-12 monoamine oxidase B Homo sapiens 174-179 12547469-1 2003 BACKGROUND: Since dopaminergic mechanisms appear to be involved in nicotine dependence, we studied the safety and efficacy of the monoamine oxidase B inhibitor selegiline hydrochloride compared with placebo for smoking cessation in nicotine-dependent cigarette smokers. Selegiline 160-184 monoamine oxidase B Homo sapiens 130-149 12873156-7 2003 Although the negative studies obtained with the MAO-B inhibitor selegiline (deprenyl) and the antioxidant tocopherol (vitamin E) may have resulted from an inappropriate choice of drug (selegiline) or an inadequate dose (tocopherol), the niggling problem that still remains is why these drugs, and others, do work in animals while they fail in the clinic. Selegiline 64-74 monoamine oxidase B Homo sapiens 48-53 15035819-1 2003 In Parkinson"s disease and other neurodegenerative diseases, (-)deprenyl, an inhibitor of type B monoamine oxidase (MAO-B), has been proposed to protect or rescue declining neurons. Selegiline 64-72 monoamine oxidase B Homo sapiens 116-121 12946055-2 2003 This hypothesis is, for many clinicians, the rationale for postponing the employment of and reducing the applied dosage of L-DOPA and for beginning therapy with dopamine receptor agonists or the monoamine oxidase type B (MAO-B) inhibitor selegiline. Selegiline 238-248 monoamine oxidase B Homo sapiens 195-219 12946055-2 2003 This hypothesis is, for many clinicians, the rationale for postponing the employment of and reducing the applied dosage of L-DOPA and for beginning therapy with dopamine receptor agonists or the monoamine oxidase type B (MAO-B) inhibitor selegiline. Selegiline 238-248 monoamine oxidase B Homo sapiens 221-226 12202968-3 2002 OBJECTIVES: To examine the effects of the selective MAO-B inhibitor selegiline on withdrawal symptoms, smoking behavior and smoking satisfaction ratings. Selegiline 68-78 monoamine oxidase B Homo sapiens 52-57 14521485-12 2003 Monoamine oxidase-B inhibitors, specifically selegiline, may provide symptomatic improvement; the question as to whether a neuroprotective benefit is present remains unanswered. Selegiline 45-55 monoamine oxidase B Homo sapiens 0-19 12200198-2 2002 An inhibitor of type B monoamine oxidase (MAO-B), (-)deprenyl (selegiline), was reported to have neuroprotective activity, but clinical trials failed to confirm it. Selegiline 63-73 monoamine oxidase B Homo sapiens 42-47 11134050-5 2001 Mutant MAO A-I335Y became like MAO B, which exhibits a higher preference for beta-phenylethylamine than for the MAO A preferred substrate serotonin (5-hydroxytryptamine), and became more sensitive to deprenyl (MAO B-specific inhibitor) than to clorgyline (MAO A-specific inhibitor). Selegiline 200-208 monoamine oxidase B Homo sapiens 31-36 12473970-4 2002 Selegiline, a selective inhibitor of MAO-B has been shown to be effective in the treatment of depression at higher oral doses where selectivity for MAO-B is lost. Selegiline 0-10 monoamine oxidase B Homo sapiens 37-42 12473970-4 2002 Selegiline, a selective inhibitor of MAO-B has been shown to be effective in the treatment of depression at higher oral doses where selectivity for MAO-B is lost. Selegiline 0-10 monoamine oxidase B Homo sapiens 148-153 12036014-6 2002 A selective interaction of [125I]2-IBPO with MAO-B was confirmed by the pretreatment experiment with well known MAO specific inhibitors, l-deprenyl, Ro-16-6491, clorgyline, and Ro-41-1049. Selegiline 137-147 monoamine oxidase B Homo sapiens 45-50 11877901-3 2002 The reported association between vascular dysfunction and neurodegenerative diseases prompted us to investigate the effect of l-deprenyl, a MAO-B inhibitor, on low density lipoprotein (LDL) oxidation. Selegiline 126-136 monoamine oxidase B Homo sapiens 140-145 11813232-1 2002 Selegiline, a selective inhibitor of monoamine oxidase-B (MAO-B), was one of the first adjunct therapies in clinical neurology. Selegiline 0-10 monoamine oxidase B Homo sapiens 37-56 11813232-1 2002 Selegiline, a selective inhibitor of monoamine oxidase-B (MAO-B), was one of the first adjunct therapies in clinical neurology. Selegiline 0-10 monoamine oxidase B Homo sapiens 58-63 11813232-3 2002 The mechanism of action of selegiline is complex and cannot be explained solely by its MAO-B inhibitory action. Selegiline 27-37 monoamine oxidase B Homo sapiens 87-92 11813232-9 2002 Most of the aforementioned properties occur independently of selegiline"s efficacy to inhibit MAO-B. Selegiline 61-71 monoamine oxidase B Homo sapiens 94-99 11978145-3 2002 Drugs for which there is at least some evidence for neuroprotective effect are certain dopamine agonists, amantadine and MAO-B inhibitors (selegiline). Selegiline 139-149 monoamine oxidase B Homo sapiens 121-126 11978145-18 2002 The MAO-B inhibitor selegiline may have a dual effect: reducing the catabolism of dopamine and limiting the formation of neurotoxic free radicals. Selegiline 20-30 monoamine oxidase B Homo sapiens 4-9 11797065-2 2001 The present experiments were conducted to study how the discriminative-stimulus (S(D)) and reinforcing-stimulus (S(R)) effects of beta-PEA in monkeys are modified by treatment with inhibitors of MAO-B [R-(-)-deprenyl and MDL 72974]. Selegiline 204-216 monoamine oxidase B Homo sapiens 195-200 11442353-7 2001 l-Dopa and apomorphine (dopaminergic agonists), ropinirole (selective D2 agonist), and selegiline (an monoamino-oxidase B [MAO-B] inhibitor) improve their clinical status. Selegiline 87-97 monoamine oxidase B Homo sapiens 102-121 11400918-1 2001 In this study, we investigated whether treatment with L-deprenyl, a selective monoamine oxidase B (MAO B) inhibitor, also inhibits MAO A or the dopamine transporter in the human brain. Selegiline 54-64 monoamine oxidase B Homo sapiens 78-97 11400918-1 2001 In this study, we investigated whether treatment with L-deprenyl, a selective monoamine oxidase B (MAO B) inhibitor, also inhibits MAO A or the dopamine transporter in the human brain. Selegiline 54-64 monoamine oxidase B Homo sapiens 99-104 11400918-8 2001 These results confirm that L-deprenyl after one week of treatment at doses typically used clinically is selective for MAO B and that it does not produce a measurable affect on the dopamine transporter, suggesting that MAO A inhibition and dopamine transporter blockade do not contribute to its pharmacological effects. Selegiline 27-37 monoamine oxidase B Homo sapiens 118-123 11481866-8 2001 In vivo microdialysis studies showed that the irreversible monoamine oxidase A inhibitor clorgyline and the irreversible monoamine oxidase B inhibitor selegiline induced a mild increase and no increase in extracellular serotonin, respectively. Selegiline 151-161 monoamine oxidase B Homo sapiens 121-140 12136372-1 2002 OBJECTIVE: The aim of this study was to investigate the effect of hormone-replacement therapy (HRT) on the pharmacokinetics of the selective monoamine oxidase B inhibitor selegiline and its primary metabolites desmethylselegiline and l-metamphetamine. Selegiline 171-181 monoamine oxidase B Homo sapiens 141-160 12111469-1 2002 Deprenyl, an irreversible MAO-B inhibitor, is known to have a symptomatic effect in de novo patients with Parkinson"s disease (PD). Selegiline 0-8 monoamine oxidase B Homo sapiens 26-31 12044957-1 2002 A number of studies have shown that the selective monoamine oxidase (MAO)-B inhibitor l-selegiline has neuroprotective activities in several cell culture systems and in vivo. Selegiline 86-98 monoamine oxidase B Homo sapiens 50-75 11753429-4 2002 The electron density shows that pargyline, an analog of the clinically used MAO B inhibitor, deprenyl, binds covalently to the flavin N5 atom. Selegiline 93-101 monoamine oxidase B Homo sapiens 76-81 11134050-6 2001 The reciprocal mutant MAO B-Y326I exhibited an increased preference for 5-hydroxytryptamine, a decreased preference for beta-phenylethylamine, and, similar to MAO A, was more sensitive to clorgyline than to deprenyl. Selegiline 207-215 monoamine oxidase B Homo sapiens 22-27 11008487-11 2001 Deprenyl, an inhibitor of MAO B, has been used for the treatment of early-stage Parkinson"s disease and provides protection of neurons from age-related decay. Selegiline 0-8 monoamine oxidase B Homo sapiens 26-31 11226815-3 2001 S-CITPROP production was 5.6 times higher than R-CITPROP production and in incubations containing the MAO-B inhibitor deprenyl, racemic CITPROP production was diminished to 9.1%. Selegiline 118-126 monoamine oxidase B Homo sapiens 102-107 11160474-7 2001 CONCLUSIONS: The increase in platelet MAO-B activity and decrease in plasma PEA concentrations in patients with Parkinson"s disease may be involved in the pathophysiological processes of the disease, and these changes are reversed by treatment with selegiline. Selegiline 249-259 monoamine oxidase B Homo sapiens 38-43 11314774-2 2001 Following a two-months of placebo-controlled withdrawal, the MAO-B inhibitor selegiline was found to maintain a long term significant mild to moderate symptomatic effect on bradykinesia and tremor at rest in nine patients with Parkinson"s disease (stage II and III of H&Y), whose functional impairment had also required a dopaminergic therapy with low-dose bromocriptine. Selegiline 77-87 monoamine oxidase B Homo sapiens 61-66 11944739-1 2001 OBJECTIVE: Selegiline (L-deprenyl) is a selective monoamine oxidase B (MAO-B) inhibitor used in the treatment of Parkinson"s disease. Selegiline 11-21 monoamine oxidase B Homo sapiens 50-69 11944739-1 2001 OBJECTIVE: Selegiline (L-deprenyl) is a selective monoamine oxidase B (MAO-B) inhibitor used in the treatment of Parkinson"s disease. Selegiline 11-21 monoamine oxidase B Homo sapiens 71-76 11944739-1 2001 OBJECTIVE: Selegiline (L-deprenyl) is a selective monoamine oxidase B (MAO-B) inhibitor used in the treatment of Parkinson"s disease. Selegiline 23-33 monoamine oxidase B Homo sapiens 50-69 11944739-1 2001 OBJECTIVE: Selegiline (L-deprenyl) is a selective monoamine oxidase B (MAO-B) inhibitor used in the treatment of Parkinson"s disease. Selegiline 23-33 monoamine oxidase B Homo sapiens 71-76 10867219-1 2000 The monoamine oxidase-B (MAO-B) inhibitor L-deprenyl (Selegiline) is effective in treating Parkinson"s disease and possibly Alzheimer"s disease, with a concomitant extension of life span. Selegiline 42-52 monoamine oxidase B Homo sapiens 4-23 11085911-1 2000 R-(-)-Deprenyl (deprenyl, selegiline), a monoamine oxidase B (MAO-B) inhibitor, delays progression of Parkinson"s disease. Selegiline 16-24 monoamine oxidase B Homo sapiens 41-60 11085911-1 2000 R-(-)-Deprenyl (deprenyl, selegiline), a monoamine oxidase B (MAO-B) inhibitor, delays progression of Parkinson"s disease. Selegiline 16-24 monoamine oxidase B Homo sapiens 62-67 11085911-1 2000 R-(-)-Deprenyl (deprenyl, selegiline), a monoamine oxidase B (MAO-B) inhibitor, delays progression of Parkinson"s disease. Selegiline 26-36 monoamine oxidase B Homo sapiens 41-60 11085911-1 2000 R-(-)-Deprenyl (deprenyl, selegiline), a monoamine oxidase B (MAO-B) inhibitor, delays progression of Parkinson"s disease. Selegiline 26-36 monoamine oxidase B Homo sapiens 62-67 10981823-2 2000 Inhibitors of monoamine oxidase B (MAO-B) have been used in the treatment of PD and at least one of them, i.e., deprenyl, also displays antioxidant activity. Selegiline 112-120 monoamine oxidase B Homo sapiens 14-33 10981823-2 2000 Inhibitors of monoamine oxidase B (MAO-B) have been used in the treatment of PD and at least one of them, i.e., deprenyl, also displays antioxidant activity. Selegiline 112-120 monoamine oxidase B Homo sapiens 35-40 11068448-15 2000 Monoamine oxidase B inhibitor, Selegiline, is useful as an economizer effect to levodopa. Selegiline 31-41 monoamine oxidase B Homo sapiens 0-19 10900396-1 2000 Both the catechol-O-methyltransferase (COMT) inhibitor entacapone and the monoamine oxidase B (MAO-B) inhibitor selegiline are L-dopa extenders. Selegiline 112-122 monoamine oxidase B Homo sapiens 74-93 10900396-1 2000 Both the catechol-O-methyltransferase (COMT) inhibitor entacapone and the monoamine oxidase B (MAO-B) inhibitor selegiline are L-dopa extenders. Selegiline 112-122 monoamine oxidase B Homo sapiens 95-100 10927030-6 2000 The antioxidant activity of lazabemide was significantly more effective than that of either vitamin E or the MAO-B inhibitor, selegiline. Selegiline 126-136 monoamine oxidase B Homo sapiens 109-114 11154095-1 2000 The present pharmacoepidemiologic study was performed to characterize the profile of adverse drug reactions (ADRs) reported with selegiline, a monoamine oxidase B (MAO-B) inhibitor used in the treatment of Parkinson"s disease and previously reported to induce an excess of mortality. Selegiline 129-139 monoamine oxidase B Homo sapiens 143-162 11154095-1 2000 The present pharmacoepidemiologic study was performed to characterize the profile of adverse drug reactions (ADRs) reported with selegiline, a monoamine oxidase B (MAO-B) inhibitor used in the treatment of Parkinson"s disease and previously reported to induce an excess of mortality. Selegiline 129-139 monoamine oxidase B Homo sapiens 164-169 10753262-2 2000 L-dopa therapy was unsuccessful, whereas a combination with selegiline, a selective monoamine oxidase-beta inhibitor, with low-dose L-dopa markedly improved the severe clinical picture. Selegiline 60-70 monoamine oxidase B Homo sapiens 84-106 10727736-4 2000 This result is not due to poor crossing of the placental and blood-brain barriers, since deprenyl caused a dose-dependent inhibition of brain MAO-B activity in pups at birth. Selegiline 89-97 monoamine oxidase B Homo sapiens 142-147 10867219-1 2000 The monoamine oxidase-B (MAO-B) inhibitor L-deprenyl (Selegiline) is effective in treating Parkinson"s disease and possibly Alzheimer"s disease, with a concomitant extension of life span. Selegiline 42-52 monoamine oxidase B Homo sapiens 25-30 10867219-1 2000 The monoamine oxidase-B (MAO-B) inhibitor L-deprenyl (Selegiline) is effective in treating Parkinson"s disease and possibly Alzheimer"s disease, with a concomitant extension of life span. Selegiline 54-64 monoamine oxidase B Homo sapiens 4-23 10867219-1 2000 The monoamine oxidase-B (MAO-B) inhibitor L-deprenyl (Selegiline) is effective in treating Parkinson"s disease and possibly Alzheimer"s disease, with a concomitant extension of life span. Selegiline 54-64 monoamine oxidase B Homo sapiens 25-30 10867219-2 2000 It has been suggested that the therapeutic efficacy of L-deprenyl may involve actions other than the inhibition of the enzyme MAO-B. Selegiline 55-65 monoamine oxidase B Homo sapiens 126-131 10682227-9 2000 We suggest that the most likely explanation for the apparent accumulation of selegiline and desmethylselegiline was the saturation of the MAO-B binding sites in tissues, although decreased first-pass metabolism of selegiline cannot be ruled out. Selegiline 77-87 monoamine oxidase B Homo sapiens 138-143 10682227-9 2000 We suggest that the most likely explanation for the apparent accumulation of selegiline and desmethylselegiline was the saturation of the MAO-B binding sites in tissues, although decreased first-pass metabolism of selegiline cannot be ruled out. Selegiline 101-111 monoamine oxidase B Homo sapiens 138-143 9749568-6 1998 By contrast, monoamine oxidase (MAO) B inhibition by deprenyl monotherapy in early PD was shown to delay the need for levodopa by around 9 months. Selegiline 53-61 monoamine oxidase B Homo sapiens 13-38 11200788-12 2000 L-deprenyl, a MAO-B inhibitor, is significantly more effective in reducing prolactin levels in migraineurs than in controls. Selegiline 0-10 monoamine oxidase B Homo sapiens 14-19 10641793-2 1999 Clorgyline and deprenyl in fact represent archetypal MAO-A and MAO-B inhibitors respectively. Selegiline 15-23 monoamine oxidase B Homo sapiens 63-68 10641793-3 1999 In the present study several ring-substituted deprenyl structural analogues were synthesized and alterations of selectivity and potency towards MAO-A and MAO-B activities were found. Selegiline 46-54 monoamine oxidase B Homo sapiens 154-159 10579543-1 1999 We studied the effects of selegiline, a monoamine oxidase B inhibitor, on the subjective effects of experimentally administered cocaine in chronically cocaine-dependent subjects. Selegiline 26-36 monoamine oxidase B Homo sapiens 40-59 11281991-4 1999 Subnormal phenylethylamine levels have been linked to disorders such as attention deficit and depression; the use of selegiline (Deprenyl) in Parkinson"s disease may conceivably favour recovery from deficient dopaminergic neurotransmission by a monoamine oxidase-B inhibitory action that increases central phenylethylamine. Selegiline 117-127 monoamine oxidase B Homo sapiens 245-264 10778622-1 1999 BACKGROUND: Selegiline hydrochloride, a selective MAO-B inhibitor is known to improve motor functions in Parkinson"s disease (PD). Selegiline 12-36 monoamine oxidase B Homo sapiens 50-55 10433493-9 1999 These data represent a selectivity value of 1066 for MAO-B, being 48 times more selective than L-deprenyl (Ki values of 376+/-0.032 and 16.8+/-0.1 nM for MAO A and MAO-B, respectively). Selegiline 95-105 monoamine oxidase B Homo sapiens 164-169 10047935-3 1999 To assess the effect of deprenyl, a monoamine oxidase type B inhibitor, on VMC in the early stages of parkinsonism. Selegiline 24-32 monoamine oxidase B Homo sapiens 36-60 11005543-1 2000 (-)Deprenyl (selegeline) is a monoamine oxidase B (MAO-B) inhibitor, but it also exerts several effects independent of MAO-B inhibition. Selegiline 0-11 monoamine oxidase B Homo sapiens 30-49 11005543-1 2000 (-)Deprenyl (selegeline) is a monoamine oxidase B (MAO-B) inhibitor, but it also exerts several effects independent of MAO-B inhibition. Selegiline 0-11 monoamine oxidase B Homo sapiens 51-56 16787846-9 2000 Similar to selegiline, 7-nitroindazole is a MAO-B inhibitor, which blocks the bio-activation of MPTP and oxidative stress. Selegiline 11-21 monoamine oxidase B Homo sapiens 44-49 11281991-4 1999 Subnormal phenylethylamine levels have been linked to disorders such as attention deficit and depression; the use of selegiline (Deprenyl) in Parkinson"s disease may conceivably favour recovery from deficient dopaminergic neurotransmission by a monoamine oxidase-B inhibitory action that increases central phenylethylamine. Selegiline 129-137 monoamine oxidase B Homo sapiens 245-264 9974121-4 1999 Using in vivo microdialysis, we investigated the pharmacological activity of selegiline, a selective irreversible inhibitor of MAO B, in the striatum of marmosets. Selegiline 77-87 monoamine oxidase B Homo sapiens 127-132 10599872-1 1999 This study examined the potential of L-Deprenyl, a selective monoamine oxidase-B (MAO-B) inhibitor, for the treatment of neuroleptic-induced parkinsonism (NIP). Selegiline 37-47 monoamine oxidase B Homo sapiens 82-87 9853994-3 1998 This study, based on monoamine oxidase-B (MAO-B) inhibition, investigates whether a reduction in selegiline dose can provide the same beneficial effects seen with a 10-mg dose. Selegiline 97-107 monoamine oxidase B Homo sapiens 21-40 9853994-3 1998 This study, based on monoamine oxidase-B (MAO-B) inhibition, investigates whether a reduction in selegiline dose can provide the same beneficial effects seen with a 10-mg dose. Selegiline 97-107 monoamine oxidase B Homo sapiens 42-47 9853994-4 1998 The inhibition of platelet MAO-B activity against multiple dosing of selegiline (2.5, 5, and 7.5 mg) was predicted from the data obtained from literature (0.5, 1.0, 1.5, and 10 mg). Selegiline 69-79 monoamine oxidase B Homo sapiens 27-32 9853994-6 1998 The data suggested that by 96 hours (four doses) the inhibition of platelet MAO-B activity is approximately 95% after a daily dose of 2.5 mg selegiline, whereas it takes only 48 hours (two doses) for doses of 5 mg and 7.5 mg to achieve this degree of inhibition. Selegiline 141-151 monoamine oxidase B Homo sapiens 76-81 9853994-8 1998 Based on the inhibition of MAO-B activity, a reduction in daily oral dose of selegiline appears possible without compromising the therapeutic effect. Selegiline 77-87 monoamine oxidase B Homo sapiens 27-32 9721939-1 1998 The monoamine oxidase-B inhibitor L-deprenyl (Selegiline) is effective in treating Parkinson"s disease and possibly Alzheimer"s disease. Selegiline 34-44 monoamine oxidase B Homo sapiens 4-23 9726430-8 1998 Together, these results suggest that both (-)-deprenyl and melatonin up-regulate GDNF gene expression at threshold doses lower than that needed for altering MAOB activity and/or the antioxidant enzyme systems, respectively. Selegiline 42-54 monoamine oxidase B Homo sapiens 157-161 9721939-1 1998 The monoamine oxidase-B inhibitor L-deprenyl (Selegiline) is effective in treating Parkinson"s disease and possibly Alzheimer"s disease. Selegiline 46-56 monoamine oxidase B Homo sapiens 4-23 9833630-1 1998 Selegiline is an irreversible inhibitor of monoamine oxidase B with trophic and neuroprotective effects. Selegiline 0-10 monoamine oxidase B Homo sapiens 43-62 9673855-1 1998 Selegiline (deprenyl), a selective, irreversible inhibitor of monoamine oxidase type B (MAO-B) is widely used in the treatment of Parkinson"s disease. Selegiline 0-10 monoamine oxidase B Homo sapiens 62-86 9698084-9 1998 Indeed, the irreversible monoamine oxidase type A inhibitor clorgyline and the irreversible monoamine oxidase type B inhibitor selegiline (both at 0.5 microM in the incubation mixture) inhibited CIT-PROP formation, depending on the substrate, up to 70% and 88%, respectively. Selegiline 127-137 monoamine oxidase B Homo sapiens 92-116 9673855-1 1998 Selegiline (deprenyl), a selective, irreversible inhibitor of monoamine oxidase type B (MAO-B) is widely used in the treatment of Parkinson"s disease. Selegiline 0-10 monoamine oxidase B Homo sapiens 88-93 9673855-1 1998 Selegiline (deprenyl), a selective, irreversible inhibitor of monoamine oxidase type B (MAO-B) is widely used in the treatment of Parkinson"s disease. Selegiline 12-20 monoamine oxidase B Homo sapiens 62-86 9673855-1 1998 Selegiline (deprenyl), a selective, irreversible inhibitor of monoamine oxidase type B (MAO-B) is widely used in the treatment of Parkinson"s disease. Selegiline 12-20 monoamine oxidase B Homo sapiens 88-93 9663810-24 1998 The effects of the two drugs on platelet MAO activity and plasma DHPG concentration are in agreement with previous reports and consistent with the relative selectivity of moclobemide for MAO-A and of selegiline for MAO-B. Selegiline 200-210 monoamine oxidase B Homo sapiens 215-220 9372556-1 1997 The aim was to investigate the effects of inhibition of monoamine oxidase type B (MAO-B) with selegiline alone and the combined inhibition of peripheral catechol-O-methyltransferase (COMT) with entacapone and MAO-B with selegiline on striatal 6-[18F]fluorodopa (FDOPA) accumulation, and whether the effect of entacapone + selegiline on FDOPA uptake differed depending on the severity of the presynaptic dopaminergic dysfunction. Selegiline 94-104 monoamine oxidase B Homo sapiens 82-87 12671304-3 1998 In addition, selegiline in a dosage below the level that inhibits monoamine oxidase B (MAO-B), protects dopaminergic neurons in culture against toxic factor(s) present in the CSF of patients with PD, and the said effect is mediated via elaboration of brain-derived neurotrophic factor (BDNF). Selegiline 13-23 monoamine oxidase B Homo sapiens 66-85 12671304-3 1998 In addition, selegiline in a dosage below the level that inhibits monoamine oxidase B (MAO-B), protects dopaminergic neurons in culture against toxic factor(s) present in the CSF of patients with PD, and the said effect is mediated via elaboration of brain-derived neurotrophic factor (BDNF). Selegiline 13-23 monoamine oxidase B Homo sapiens 87-92 9730267-9 1998 Both clorgyline (a selective MAO-A inhibitor) and selegiline (a selective MAO-B inhibitor) reduced the formation of dihydroxyphenylglycol (DOPEG), DOMA and O-methylated-deaminated metabolites (OMDA), and increased that of normetanephrine (NMN). Selegiline 50-60 monoamine oxidase B Homo sapiens 74-79 9489486-1 1998 Deprenyl, a monoamine oxidase-B (MAO-B) inhibitor, has a wide range of pharmacological properties that are beneficial therapeutically in the treatment of human neurodegenerative diseases. Selegiline 0-8 monoamine oxidase B Homo sapiens 12-31 9489486-1 1998 Deprenyl, a monoamine oxidase-B (MAO-B) inhibitor, has a wide range of pharmacological properties that are beneficial therapeutically in the treatment of human neurodegenerative diseases. Selegiline 0-8 monoamine oxidase B Homo sapiens 33-38 9443715-3 1998 Selegiline hydrochloride (Eldepryl) is a monoamine oxidase-B inhibitor with antioxidant properties. Selegiline 0-24 monoamine oxidase B Homo sapiens 41-60 9443715-3 1998 Selegiline hydrochloride (Eldepryl) is a monoamine oxidase-B inhibitor with antioxidant properties. Selegiline 26-34 monoamine oxidase B Homo sapiens 41-60 9564606-0 1998 Differential trace amine alterations in individuals receiving acetylenic inhibitors of MAO-A (clorgyline) or MAO-B (selegiline and pargyline). Selegiline 116-126 monoamine oxidase B Homo sapiens 109-114 9564606-2 1998 In comparative studies with other, structurally similar acetylenic inhibitors of MAO, pargyline, an MAO-B > MAO-A inhibitor used in doses of 90 mg/day for three or more weeks, produced elevations in these trace amines which were similar to those found with the highest dose of selegiline studied. Selegiline 280-290 monoamine oxidase B Homo sapiens 100-105 9564606-5 1998 Selegiline produced larger changes in trace amines--at least at the higher doses studied--than found in individuals lacking the gene for MAO-B, in agreement with other data suggesting a lesser selectivity for MAO-B inhibition when selegiline was given in doses higher than 10 mg/day. Selegiline 0-10 monoamine oxidase B Homo sapiens 209-214 9564606-5 1998 Selegiline produced larger changes in trace amines--at least at the higher doses studied--than found in individuals lacking the gene for MAO-B, in agreement with other data suggesting a lesser selectivity for MAO-B inhibition when selegiline was given in doses higher than 10 mg/day. Selegiline 231-241 monoamine oxidase B Homo sapiens 137-142 9564606-6 1998 Overall, trace amine elevations in individuals receiving the highest dose of deprenyl or receiving pargyline were approximately three to five-fold lower than the elevations observed in individuals lacking the genes for both MAO-A and MAO-B, suggesting that these drug doses yield incomplete inhibition of MAO-A and MAO-B. Selegiline 77-85 monoamine oxidase B Homo sapiens 234-239 9564606-6 1998 Overall, trace amine elevations in individuals receiving the highest dose of deprenyl or receiving pargyline were approximately three to five-fold lower than the elevations observed in individuals lacking the genes for both MAO-A and MAO-B, suggesting that these drug doses yield incomplete inhibition of MAO-A and MAO-B. Selegiline 77-85 monoamine oxidase B Homo sapiens 315-320 9564608-1 1998 Deprenyl is a potent MAO-B inhibitor which is commonly prescribed for treatment of parkinsonism. Selegiline 0-8 monoamine oxidase B Homo sapiens 21-26 9564614-1 1998 The pharmacological effects of (-)-deprenyl is multi-fold in its nature (dopamine sparing activity, neuroprotective and neuronal rescue effects), which cannot be explained solely by the irreversible MAO-B inhibitory action of the substance. Selegiline 35-43 monoamine oxidase B Homo sapiens 199-204 9564633-1 1998 In clinical studies the MAO-B inhibitor selegiline appears to slow the progression of neurological deficits in Parkinson"s disease (PD) and the cognitive decline in Alzheimer"s disease (AD). Selegiline 40-50 monoamine oxidase B Homo sapiens 24-29 9503561-4 1997 MAO-A preferentially deaminates serotonin (5HT) and is selectively inhibited by harmine and clorgyline, while MAO-B preferentially deaminates phenethylamine and benzylamine, and is selectively inhibited by (-)deprenyl as well as low concentrations of pargyline. Selegiline 206-217 monoamine oxidase B Homo sapiens 110-115 9373724-1 1997 Selegiline is a selective, irreversible inhibitor of MAO-B, used in the treatment of Parkinson"s disease, either alone or as an adjunct to L-DOPA. Selegiline 0-10 monoamine oxidase B Homo sapiens 53-58 9503565-0 1997 [History of deprenyl--the first selective inhibitor of monoamine oxidase type B]. Selegiline 12-20 monoamine oxidase B Homo sapiens 55-79 9503565-6 1997 (-)Deprenyl, the first selective inhibitor of MAO-B described in the literature, has become a universally used research tool for selectively blocking B-type MAO and is still the only selective MAO-B inhibitor in world wide clinical use. Selegiline 3-11 monoamine oxidase B Homo sapiens 46-51 9503565-6 1997 (-)Deprenyl, the first selective inhibitor of MAO-B described in the literature, has become a universally used research tool for selectively blocking B-type MAO and is still the only selective MAO-B inhibitor in world wide clinical use. Selegiline 3-11 monoamine oxidase B Homo sapiens 193-198 9503567-1 1997 The complexity of the pharmacological activity of selegiline cannot be considered only as a result of a simple MAO-B inhibition. Selegiline 50-60 monoamine oxidase B Homo sapiens 111-116 9280684-16 1997 Selegiline, a MAOB inhibitor with a possible neuroprotective effect, should also be considered as initial option for Parkinson"s disease. Selegiline 0-10 monoamine oxidase B Homo sapiens 14-18 9330778-1 1997 Selegiline (SEL) is a selective, irreversible inhibitor of MAO-B, used in the treatment of Parkinson"s disease, either alone or as an adjunct to L-DOPA. Selegiline 0-10 monoamine oxidase B Homo sapiens 59-64 9330778-1 1997 Selegiline (SEL) is a selective, irreversible inhibitor of MAO-B, used in the treatment of Parkinson"s disease, either alone or as an adjunct to L-DOPA. Selegiline 12-15 monoamine oxidase B Homo sapiens 59-64 9331518-1 1997 We have evaluated the risk for pharmacokinetic and/or pharmacodynamic interactions of concomitantly administered selegiline, a selective monoamine oxidase type B inhibitor, and citalopram, a widely used selective serotonin uptake inhibitor antidepressant. Selegiline 113-123 monoamine oxidase B Homo sapiens 137-161 9260033-2 1997 Selegiline is a selective inhibitor of monoamine oxidase-B (MAO-B) at a dose of 10 mg/day and is given to patients with Parkinson"s disease as an adjunct to levodopa therapy. Selegiline 0-10 monoamine oxidase B Homo sapiens 39-58 9260033-2 1997 Selegiline is a selective inhibitor of monoamine oxidase-B (MAO-B) at a dose of 10 mg/day and is given to patients with Parkinson"s disease as an adjunct to levodopa therapy. Selegiline 0-10 monoamine oxidase B Homo sapiens 60-65 9260033-3 1997 By inhibiting MAO-B, selegiline increases the dopamine levels in the substantia nigra. Selegiline 21-31 monoamine oxidase B Homo sapiens 14-19 9260033-15 1997 One of the metabolites of selegiline, desmethylselegiline, is believed to posses some MAO-B inhibitory property, though to a lesser extent than that of selegiline. Selegiline 26-36 monoamine oxidase B Homo sapiens 86-91 9260033-15 1997 One of the metabolites of selegiline, desmethylselegiline, is believed to posses some MAO-B inhibitory property, though to a lesser extent than that of selegiline. Selegiline 47-57 monoamine oxidase B Homo sapiens 86-91 9260033-16 1997 Within 2 to 4 hours of an oral dose of selegiline 10 mg, 86% of the platelet MAO-B activity was inhibited and it took almost 2 weeks for platelet MAO-B activity to return to the baseline values. Selegiline 39-49 monoamine oxidase B Homo sapiens 77-82 9260033-16 1997 Within 2 to 4 hours of an oral dose of selegiline 10 mg, 86% of the platelet MAO-B activity was inhibited and it took almost 2 weeks for platelet MAO-B activity to return to the baseline values. Selegiline 39-49 monoamine oxidase B Homo sapiens 146-151 9258314-3 1997 We describe an uneventful perioperative course in a parkinsonian patient who required urgent coronary artery bypass graft surgery while he was taking selegiline, a selective inhibitor of monoamine oxidase type B. Selegiline 150-160 monoamine oxidase B Homo sapiens 187-211 9109551-7 1997 Treatment with deprenyl, a monoamine oxidase B inhibitor, produced a complete reversal of MPTP-induced uptake inhibition, but was ineffective following exposure of cells to the MPTP metabolite, 1-methyl-4-phenylpyridinium (MPP+). Selegiline 15-23 monoamine oxidase B Homo sapiens 27-46 9251066-13 1997 Entacapone decreased erythrocyte COMT activity by > 35% (p < 0.001), and platelet MAO-B activity was almost completely inhibited by selegiline (p < 0.001). Selegiline 132-142 monoamine oxidase B Homo sapiens 82-87 9432289-12 1997 of MAO-B, at this time mainly selegiline). Selegiline 30-40 monoamine oxidase B Homo sapiens 3-8 9125383-2 1997 This study investigates whether L-deprenyl, an irreversible and selective MAO-B inhibitor, reduces brain damage following global forebrain ischemia in adult gerbils. Selegiline 32-42 monoamine oxidase B Homo sapiens 74-79 9076907-2 1997 We have outlined the successful management of canine PDH patients with l-deprenyl, a selective MAO-B inhibitor. Selegiline 71-81 monoamine oxidase B Homo sapiens 95-100 9159721-6 1997 These results demonstrate that 20 mg weekly is the minimal dosage of selegiline able to induce a maximal and long-lasting inhibition of platelet MAO-B activity in patients with parkinsonism. Selegiline 69-79 monoamine oxidase B Homo sapiens 145-150 9065544-1 1997 Selegiline (L-deprenyl), a selective inhibitor of monoamine oxidase type B, is an established adjuvant to levodopa therapy in Parkinson"s disease (PD). Selegiline 0-10 monoamine oxidase B Homo sapiens 50-74 9065544-1 1997 Selegiline (L-deprenyl), a selective inhibitor of monoamine oxidase type B, is an established adjuvant to levodopa therapy in Parkinson"s disease (PD). Selegiline 12-22 monoamine oxidase B Homo sapiens 50-74 9126147-10 1997 The first agent to be tested as a candidate for neuroprotection was the MAO-B inhibitor deprenyl. Selegiline 88-96 monoamine oxidase B Homo sapiens 72-77 9089426-1 1997 Orally administered selegiline hydrochloride is a selective monoamine oxidase type B inhibitor at the recommended regimen of 10 mg/day, but it loses selectivity at higher doses. Selegiline 20-44 monoamine oxidase B Homo sapiens 60-84 8978707-1 1997 L-Deprenyl is a relatively selective inhibitor of monoamine oxidase (MAO)-B that delays the emergence of disability and the progression of signs and symptoms of Parkinson"s disease. Selegiline 0-10 monoamine oxidase B Homo sapiens 50-75 9013137-1 1997 We have examined in vitro radical trapping by the monoamine oxidase-B (MAO-B) inhibitor deprenyl and compared it to the specific MAO-B inhibitor MDL 72,974A. Selegiline 88-96 monoamine oxidase B Homo sapiens 50-69 9013137-1 1997 We have examined in vitro radical trapping by the monoamine oxidase-B (MAO-B) inhibitor deprenyl and compared it to the specific MAO-B inhibitor MDL 72,974A. Selegiline 88-96 monoamine oxidase B Homo sapiens 71-76 8978757-1 1997 Selegiline [L-(-)-deprenyl], a monoamine oxidase B inhibitor, has been used in the treatment of Parkinson"s disease as a putative neuroprotective agent. Selegiline 0-10 monoamine oxidase B Homo sapiens 31-50 8978757-1 1997 Selegiline [L-(-)-deprenyl], a monoamine oxidase B inhibitor, has been used in the treatment of Parkinson"s disease as a putative neuroprotective agent. Selegiline 12-26 monoamine oxidase B Homo sapiens 31-50 10728198-4 1997 Treatment with a combination of the AADC cofactor pyridoxine, the monoamine oxidase B inhibitor selegiline and bromocriptine was started during the fifth year of life and showed only a moderate clinical improvement in contrast to patients who have been treated since the first year of life. Selegiline 96-106 monoamine oxidase B Homo sapiens 66-85 9266433-5 1997 Our research into the development of small diffusible molecules that reduce apoptosis has grown from studies of the irreversible MAO-B inhibitor (-)-deprenyl. Selegiline 145-157 monoamine oxidase B Homo sapiens 129-134 8959986-1 1996 (-)-Deprenyl has been used to irreversibly inhibit monoamine oxidase B (MAO-B) in Parkinson"s disease (PD) and Alzheimer"s disease (AD) as a possible means of improving dopaminergic neurotransmission or of reducing neuronal necrosis caused by oxidative radical damage. Selegiline 0-12 monoamine oxidase B Homo sapiens 51-70 8959982-7 1996 Although not all features of its anti-PD action are known, studies using brain obtained at autopsy from patients who had been treated with 10 mg of selegiline showed that selective inhibition of MAO-B, with the concomitant increase of phenylethylamine and dopamine (DA) but not of serotonin or noradrenaline, in the basal ganglia may be regarded as its mode of action. Selegiline 148-158 monoamine oxidase B Homo sapiens 195-200 8959985-12 1996 Thus, the inhibition of MAO-B by drugs such as selegiline may protect against activation of some toxins and free radicals formed from the MAO-B oxidation of dopamine. Selegiline 47-57 monoamine oxidase B Homo sapiens 24-29 8959985-12 1996 Thus, the inhibition of MAO-B by drugs such as selegiline may protect against activation of some toxins and free radicals formed from the MAO-B oxidation of dopamine. Selegiline 47-57 monoamine oxidase B Homo sapiens 138-143 8959986-1 1996 (-)-Deprenyl has been used to irreversibly inhibit monoamine oxidase B (MAO-B) in Parkinson"s disease (PD) and Alzheimer"s disease (AD) as a possible means of improving dopaminergic neurotransmission or of reducing neuronal necrosis caused by oxidative radical damage. Selegiline 0-12 monoamine oxidase B Homo sapiens 72-77 9116194-2 1996 In clinical studies the monoamine oxidase-B inhibitor Selegiline appears to slow the progression of neurological deficits in PD and the cognitive decline in AD. Selegiline 54-64 monoamine oxidase B Homo sapiens 24-43 8994331-1 1996 BACKGROUND: To improve dose-related fluctuations in patients with Parkinson"s disease, the efficacy of selegiline, a selective inhibitor of monoamine oxidase B, was determined. Selegiline 103-113 monoamine oxidase B Homo sapiens 140-159 8998375-8 1996 DATA SYNTHESIS: Selegiline is a selective, irreversible inhibitor of monoamine oxidase type B. Selegiline 16-26 monoamine oxidase B Homo sapiens 69-93 8988458-1 1996 There have been many claims that the selective monoamine oxidase type B (MAO-B) inhibitor selegiline may have distinct properties in slowing the progression of Parkinson"s disease (PD). Selegiline 90-100 monoamine oxidase B Homo sapiens 47-71 8800629-10 1996 As a selective monoamine oxidase type B (MAO-B) inhibitor, selegiline (deprenyl) is free of the "cheese-effect" when employed in recommended dosages. Selegiline 59-69 monoamine oxidase B Homo sapiens 15-39 8800629-10 1996 As a selective monoamine oxidase type B (MAO-B) inhibitor, selegiline (deprenyl) is free of the "cheese-effect" when employed in recommended dosages. Selegiline 59-69 monoamine oxidase B Homo sapiens 41-46 8800629-10 1996 As a selective monoamine oxidase type B (MAO-B) inhibitor, selegiline (deprenyl) is free of the "cheese-effect" when employed in recommended dosages. Selegiline 71-79 monoamine oxidase B Homo sapiens 41-46 11862265-17 1996 The prolonged half-lives of selegiline and N-desmethylselegiline with multiple dosing may be the result of binding to the mitochondrial monoamine oxidase type B pool. Selegiline 28-38 monoamine oxidase B Homo sapiens 136-160 8661341-4 1996 As expected, the development of the fluorescence was inhibited by both clorgyline (an MAO-A inhibitor) and deprenyl (an MAO-B inhibitor). Selegiline 107-115 monoamine oxidase B Homo sapiens 120-125 8791022-5 1996 The addition of direct-acting dopamine agonists or the MAO-B inhibitor selegiline is helpful for short-term improvement. Selegiline 71-81 monoamine oxidase B Homo sapiens 55-60 8798928-6 1996 The method was successfully applied to the determination of PEA urinary excretion in Parkinsonian patients after oral administration of the monoamine oxidase B (MAO-B) inhibitor, selegiline. Selegiline 179-189 monoamine oxidase B Homo sapiens 140-159 8798928-6 1996 The method was successfully applied to the determination of PEA urinary excretion in Parkinsonian patients after oral administration of the monoamine oxidase B (MAO-B) inhibitor, selegiline. Selegiline 179-189 monoamine oxidase B Homo sapiens 161-166 8713690-5 1996 Consequently, selegiline (deprenyl), a selective MAO-B inhibitor, was developed for the treatment of idiopathic Parkinson"s disease. Selegiline 14-24 monoamine oxidase B Homo sapiens 49-54 8713690-5 1996 Consequently, selegiline (deprenyl), a selective MAO-B inhibitor, was developed for the treatment of idiopathic Parkinson"s disease. Selegiline 26-34 monoamine oxidase B Homo sapiens 49-54 8618686-6 1996 Chronic treatment with the MAO-B inhibitor, deprenyl (N=16), was not associated with any differences in serum malondialdehyde or plasma 5-S-cysteinyl-dopa concentrations compared with those not treated with deprenyl (N=11). Selegiline 44-52 monoamine oxidase B Homo sapiens 27-32 8632725-7 1996 Furthermore, (AB161-375)A was more sensitive to the MAO-B specific inhibitor deprenyl (IC50 2.7 +/- 0.4 x 10(-8) M) than to the MAO-A specific inhibitor clorgyline (IC50 5.4 +/- 0.8 x 10(-7) M). Selegiline 77-85 monoamine oxidase B Homo sapiens 52-57 8988458-1 1996 There have been many claims that the selective monoamine oxidase type B (MAO-B) inhibitor selegiline may have distinct properties in slowing the progression of Parkinson"s disease (PD). Selegiline 90-100 monoamine oxidase B Homo sapiens 73-78 8988458-12 1996 Under treatment with the MAO-B inhibitor selegiline, the degradation of putrescine via MAO, a key factor in regulating the polyamine metabolism, might be diminished in the Parkinsonian brain, which in turn would suppress the polyamine synthesis. Selegiline 41-51 monoamine oxidase B Homo sapiens 25-30 8988460-1 1996 (-)-deprenyl cannot be considered as a simple, selective inhibitor of MAO-B. Selegiline 0-12 monoamine oxidase B Homo sapiens 70-75 8988460-9 1996 The most widely used MAO-B inhibitor in the therapy is (-)-deprenyl and it lacks the "cheese reaction". Selegiline 55-67 monoamine oxidase B Homo sapiens 21-26 8988461-1 1996 (-)-Deprenyl stereospecifically reduces neuronal death even after neurons have sustained seemingly lethal damage at concentrations too small to cause monoamine oxidase-B (MAO-B) inhibition. Selegiline 0-12 monoamine oxidase B Homo sapiens 150-169 8988461-1 1996 (-)-Deprenyl stereospecifically reduces neuronal death even after neurons have sustained seemingly lethal damage at concentrations too small to cause monoamine oxidase-B (MAO-B) inhibition. Selegiline 0-12 monoamine oxidase B Homo sapiens 171-176 8988463-1 1996 Selegiline is a relatively selective inhibitor of monoamine oxidase type B that has been used in Parkinson"s disease as an adjunct to levodopa and as putative neuroprotective therapy. Selegiline 0-10 monoamine oxidase B Homo sapiens 50-74 8614567-2 1995 Further, selegiline, a monoamine oxidase B (MAO) inhibitor (0.125-0.250 microM) enhanced the number of tyrosine hydroxylase (TH)-positive neurons, augmented the high affinity uptake of dopamine (DA), and averted the neurotoxic effects of CSF of PD patients on rat mesencephalic neurons in culture. Selegiline 9-19 monoamine oxidase B Homo sapiens 23-42 8614567-2 1995 Further, selegiline, a monoamine oxidase B (MAO) inhibitor (0.125-0.250 microM) enhanced the number of tyrosine hydroxylase (TH)-positive neurons, augmented the high affinity uptake of dopamine (DA), and averted the neurotoxic effects of CSF of PD patients on rat mesencephalic neurons in culture. Selegiline 9-19 monoamine oxidase B Homo sapiens 44-47 8614567-3 1995 The neuroprotective effects of selegiline may be related either to its ability to inhibit MAO B, preventing the generation of free radicals, or to neuronal rescue property due to unknown mechanisms. Selegiline 31-41 monoamine oxidase B Homo sapiens 90-95 7872875-2 1995 OBJECTIVES: To determine whether cerebrospinal fluid (CSF) homovanillic acid (HVA) concentration in subjects with early, mild Parkinson"s disease (PD) treated with the monoamine oxidase type B inhibitor selegiline hydrochloride differs from that of control subjects receiving placebo. Selegiline 203-227 monoamine oxidase B Homo sapiens 168-192 7587975-1 1995 Selegiline, an irreversible monoamine oxidase-B (MAO-B) inhibitor, is under investigation as a treatment for cocaine relapse prevention. Selegiline 0-10 monoamine oxidase B Homo sapiens 28-47 7587975-1 1995 Selegiline, an irreversible monoamine oxidase-B (MAO-B) inhibitor, is under investigation as a treatment for cocaine relapse prevention. Selegiline 0-10 monoamine oxidase B Homo sapiens 49-54 7555990-3 1995 Deprenyl is an irreversible inhibitor of monoamine oxidase type B (MAO-B) with a very high affinity for the enzyme. Selegiline 0-8 monoamine oxidase B Homo sapiens 41-65 7555990-3 1995 Deprenyl is an irreversible inhibitor of monoamine oxidase type B (MAO-B) with a very high affinity for the enzyme. Selegiline 0-8 monoamine oxidase B Homo sapiens 67-72 7790952-1 1995 UNLABELLED: Recent human PET studies with the monoamine oxidase B (MAO B) tracer [11C]L-deprenyl show that the rapid rate of radiotracer trapping relative to transport reduces the sensitivity of the tracer in regions of high MAO B concentration. Selegiline 86-96 monoamine oxidase B Homo sapiens 46-65 7790952-1 1995 UNLABELLED: Recent human PET studies with the monoamine oxidase B (MAO B) tracer [11C]L-deprenyl show that the rapid rate of radiotracer trapping relative to transport reduces the sensitivity of the tracer in regions of high MAO B concentration. Selegiline 86-96 monoamine oxidase B Homo sapiens 67-72 7790952-1 1995 UNLABELLED: Recent human PET studies with the monoamine oxidase B (MAO B) tracer [11C]L-deprenyl show that the rapid rate of radiotracer trapping relative to transport reduces the sensitivity of the tracer in regions of high MAO B concentration. Selegiline 86-96 monoamine oxidase B Homo sapiens 225-230 7790952-11 1995 CONCLUSION: This study demonstrates that deuterium substitution causes a significant reduction in the rate of trapping of labeled deprenyl, providing a direct link between radiotracer uptake and MAO B in the human brain and enhancing tracer sensitivity to changes in MAO B concentration. Selegiline 130-138 monoamine oxidase B Homo sapiens 195-200 7790952-11 1995 CONCLUSION: This study demonstrates that deuterium substitution causes a significant reduction in the rate of trapping of labeled deprenyl, providing a direct link between radiotracer uptake and MAO B in the human brain and enhancing tracer sensitivity to changes in MAO B concentration. Selegiline 130-138 monoamine oxidase B Homo sapiens 267-272 7487655-3 1995 The optimal independent roles of the ergot derivatives bromocriptine and pergolide, and the MAOb inhibitor selegiline, are not yet generally agreed although they are accepted as useful in supplementing the effects of levodopa. Selegiline 107-117 monoamine oxidase B Homo sapiens 92-96 7593732-2 1995 Selegiline (L-deprenyl), a selective inhibitor of MAO-B, ameliorates the "wearing off" akinesia and delays the need for levodopa in mild, previously untreated Parkinson"s disease. Selegiline 0-10 monoamine oxidase B Homo sapiens 50-55 7593732-2 1995 Selegiline (L-deprenyl), a selective inhibitor of MAO-B, ameliorates the "wearing off" akinesia and delays the need for levodopa in mild, previously untreated Parkinson"s disease. Selegiline 12-22 monoamine oxidase B Homo sapiens 50-55 7616414-1 1995 L-Deprenyl (selegiline) is an irreversible inhibitor of monoamine oxidase type B, but also exerts several effects on dopamine and noradrenaline systems independent of monoamine oxidase type B inhibition. Selegiline 0-10 monoamine oxidase B Homo sapiens 56-80 7616414-1 1995 L-Deprenyl (selegiline) is an irreversible inhibitor of monoamine oxidase type B, but also exerts several effects on dopamine and noradrenaline systems independent of monoamine oxidase type B inhibition. Selegiline 12-22 monoamine oxidase B Homo sapiens 56-80 8748635-4 1995 High concentrations of the dopamimetic substances L-DOPA slightly and the monoamine oxidase B inhibitor selegiline more effectively inhibit SOD activity. Selegiline 104-114 monoamine oxidase B Homo sapiens 74-93 7828725-1 1995 The MPTP metabolic activity of porcine FAD-containing monooxygenase (FMO) (EC 1.14.13.8) was inhibited considerably by deprenyl and pargyline, selective MAO-B inhibitors, and they showed typical competitive inhibition. Selegiline 119-127 monoamine oxidase B Homo sapiens 153-158 7669938-4 1995 (-)deprenyl, the first selective inhibitor of MAO-B described in literature, has become the universally used research tool for selectively blocking B-type MAO. Selegiline 3-11 monoamine oxidase B Homo sapiens 46-51 7697377-0 1995 Responses of forebrain neurons to the MAO-B blocker L-deprenyl. Selegiline 52-62 monoamine oxidase B Homo sapiens 38-43 7995014-2 1994 Although not all features of its antiParkinson action are known, studies that used brains obtained at autopsy from patients who took l-deprenyl show that the selective inhibition of MAO-B with a concomitant increase of phenylethylamine and dopamine, but not of serotonin or noradrenaline, in the basal ganglia may be responsible for its mode of action. Selegiline 133-143 monoamine oxidase B Homo sapiens 182-187 7995015-1 1994 l-Deprenyl is a selective, irreversible monoamine oxidase (MAO) type B inhibitor. Selegiline 0-10 monoamine oxidase B Homo sapiens 40-70 7995015-4 1994 MAO-B inhibition explains the clinical efficacy of l-deprenyl in the treatment of Parkinson"s disease and the prevention of the conversion of protoxins such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, which is oxidized by MAO-B and can cause a parkinsonian syndrome, to their active neurotoxin. Selegiline 51-61 monoamine oxidase B Homo sapiens 0-5 7995015-4 1994 MAO-B inhibition explains the clinical efficacy of l-deprenyl in the treatment of Parkinson"s disease and the prevention of the conversion of protoxins such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, which is oxidized by MAO-B and can cause a parkinsonian syndrome, to their active neurotoxin. Selegiline 51-61 monoamine oxidase B Homo sapiens 227-232 7995015-5 1994 In addition, l-deprenyl appears to exhibit other biochemical actions that are independent of its MAO-B activity. Selegiline 13-23 monoamine oxidase B Homo sapiens 97-102 7721026-3 1994 1-Deprenyl (selegiline), an archetypical MAO-B inhibitor, alone does not seem to exert an antidepressive effect, however, it may become useful when administered in combination with amine neurotransmitter precursors. Selegiline 12-22 monoamine oxidase B Homo sapiens 41-46 9358191-5 1994 Selegiline is a monoamine oxidase-B inhibitor; once thought to affect the pathogenesis of idiopathic parkinsonism, it is now known to offer only symptomatic relief. Selegiline 0-10 monoamine oxidase B Homo sapiens 16-35 7839316-0 1994 Slow recovery of human brain MAO B after L-deprenyl (Selegeline) withdrawal. Selegiline 41-51 monoamine oxidase B Homo sapiens 29-34 7839316-1 1994 L-Deprenyl (Selegeline) is an enzyme-activated irreversible inhibitor of monoamine oxidase B (MAO B; EC 1.4.3.4). Selegiline 0-10 monoamine oxidase B Homo sapiens 73-92 7839316-1 1994 L-Deprenyl (Selegeline) is an enzyme-activated irreversible inhibitor of monoamine oxidase B (MAO B; EC 1.4.3.4). Selegiline 0-10 monoamine oxidase B Homo sapiens 94-99 7839316-4 1994 We have measured a 40 day half-time for brain MAO B synthesis in Parkinson"s disease and in normal subjects after withdrawal from L-deprenyl. Selegiline 130-140 monoamine oxidase B Homo sapiens 46-51 7839316-7 1994 The slow turnover of brain MAO B suggests that the current clinical dose of L-deprenyl may be excessive and that the clinical efficacy of reduced dosing should be evaluated. Selegiline 76-86 monoamine oxidase B Homo sapiens 27-32 8000101-1 1994 To confirm the clinical utility of selegiline (L-deprenyl), a selective inhibitor of monoamine oxidase B, as an anti-Parkinson"s disease (PD) agent, the first Japanese multi-center, double-blind comparative study of this drug was conducted. Selegiline 35-45 monoamine oxidase B Homo sapiens 85-104 8000101-1 1994 To confirm the clinical utility of selegiline (L-deprenyl), a selective inhibitor of monoamine oxidase B, as an anti-Parkinson"s disease (PD) agent, the first Japanese multi-center, double-blind comparative study of this drug was conducted. Selegiline 47-57 monoamine oxidase B Homo sapiens 85-104 8000982-1 1994 The use of the combination of fluoxetine, an anti-depressant serotonin uptake inhibitor, and selegiline, a monoamine oxidase -B inhibitor, was reviewed in a large population of patients with Parkinson"s disease. Selegiline 93-103 monoamine oxidase B Homo sapiens 107-127 7953696-0 1994 The MAO-B inhibitor deprenyl, but not the MAO-A inhibitor clorgyline, potentiates the neurotoxicity of p-chloroamphetamine. Selegiline 20-28 monoamine oxidase B Homo sapiens 4-9 7953696-4 1994 However, co-administration of the MAO-B selective inhibitor deprenyl (1 mg/kg) or the non-selective inhibitor pargyline (50 mg/kg) produced significant decreases in radioligand binding. Selegiline 60-68 monoamine oxidase B Homo sapiens 34-39 7953696-9 1994 Administration of deprenyl or pargyline, together with pCA, itself a MAO-A inhibitor, will lead to inhibition of both MAO-A and MAO-B activities. Selegiline 18-26 monoamine oxidase B Homo sapiens 128-133 7981318-0 1994 An enzymatic assay for the MAO-B inhibitor selegiline in plasma. Selegiline 43-53 monoamine oxidase B Homo sapiens 27-32 8161354-4 1994 Incubation with clorgyline and deprenyl, probe inhibitors of MAO-A and MAO-B, respectively, showed that [14C]sumatriptan was metabolized by MAO-A; there was no evidence of P450 involvement in its metabolism. Selegiline 31-39 monoamine oxidase B Homo sapiens 71-76 7931231-1 1994 In this paper we present results from a double blind cross over trial with deprenyl, a selective and irreversible monoamine oxidase-B (MAO-B) inhibitor, in 10 patients suffering from amyotrophic lateral sclerosis. Selegiline 75-83 monoamine oxidase B Homo sapiens 114-133 7884399-1 1994 Attempts to lessen the progression of Parkinson"s Disease (PD) have made use of 2 strategies: inhibition of monoamine oxidase type B with deprenyl (selegiline) and the free radical trapping agent alpha-tocopherol (vitamin E). Selegiline 138-146 monoamine oxidase B Homo sapiens 108-132 7884399-1 1994 Attempts to lessen the progression of Parkinson"s Disease (PD) have made use of 2 strategies: inhibition of monoamine oxidase type B with deprenyl (selegiline) and the free radical trapping agent alpha-tocopherol (vitamin E). Selegiline 148-158 monoamine oxidase B Homo sapiens 108-132 7931245-2 1994 The selectivity of MAO-B inhibition of L, selegiline and MDL 72974 was also measured in vitro in human brain tissue as well as ex vivo in rat brain and liver after acute and subchronic administration. Selegiline 42-52 monoamine oxidase B Homo sapiens 19-24 7931257-7 1994 MAO-B inhibitors, such as MDL 72974A and L-deprenyl, offer the potential of being neuroprotective in Parkinson"s Disease and other neurogenerative disorders. Selegiline 41-51 monoamine oxidase B Homo sapiens 0-5 7931231-1 1994 In this paper we present results from a double blind cross over trial with deprenyl, a selective and irreversible monoamine oxidase-B (MAO-B) inhibitor, in 10 patients suffering from amyotrophic lateral sclerosis. Selegiline 75-83 monoamine oxidase B Homo sapiens 135-140 7931231-6 1994 MAO-B activity in blood platelets was completely inhibited during treatment with deprenyl. Selegiline 81-89 monoamine oxidase B Homo sapiens 0-5 7931233-1 1994 Six months of administration of the selective MAO-B inhibitor, selegiline (l-deprenyl 0.25 mg/kg, s.c.) to aged female Fisher 344N rats suppressed MAO-A as well as MAO-B activity and increased serotonin (substrate for melatonin biosynthesis) and N-acetylserotonin (immediate melatonin precursor) levels in pineal glands taken from the animals during the night. Selegiline 63-73 monoamine oxidase B Homo sapiens 46-51 7931233-1 1994 Six months of administration of the selective MAO-B inhibitor, selegiline (l-deprenyl 0.25 mg/kg, s.c.) to aged female Fisher 344N rats suppressed MAO-A as well as MAO-B activity and increased serotonin (substrate for melatonin biosynthesis) and N-acetylserotonin (immediate melatonin precursor) levels in pineal glands taken from the animals during the night. Selegiline 63-73 monoamine oxidase B Homo sapiens 164-169 7931233-1 1994 Six months of administration of the selective MAO-B inhibitor, selegiline (l-deprenyl 0.25 mg/kg, s.c.) to aged female Fisher 344N rats suppressed MAO-A as well as MAO-B activity and increased serotonin (substrate for melatonin biosynthesis) and N-acetylserotonin (immediate melatonin precursor) levels in pineal glands taken from the animals during the night. Selegiline 75-85 monoamine oxidase B Homo sapiens 46-51 7931233-1 1994 Six months of administration of the selective MAO-B inhibitor, selegiline (l-deprenyl 0.25 mg/kg, s.c.) to aged female Fisher 344N rats suppressed MAO-A as well as MAO-B activity and increased serotonin (substrate for melatonin biosynthesis) and N-acetylserotonin (immediate melatonin precursor) levels in pineal glands taken from the animals during the night. Selegiline 75-85 monoamine oxidase B Homo sapiens 164-169 7931235-2 1994 In addition, the rational for using selegiline as a neuroprotector in Parkinson"s disease may also be applicable in Alzheimer"s disease in which a dramatic increase in the MAO-B activity has been reported. Selegiline 36-46 monoamine oxidase B Homo sapiens 172-177 8293522-4 1993 A selective interaction with MAO-A in the accumulation of [11C]fluorclorgyline was confirmed by a competition experiment performed with the MAO-A specific inhibitor,clorgyline, and MAO-B specific inhibitor, l-deprenyl. Selegiline 207-217 monoamine oxidase B Homo sapiens 181-186 8302308-0 1993 The relevance of glial monoamine oxidase-B and polyamines to the action of selegiline in Parkinson"s disease. Selegiline 75-85 monoamine oxidase B Homo sapiens 23-42 8363632-3 1993 A new parameter, the specificity index is defined and used in a model which describes the specific and non-specific binding of (-)-deprenyl to MAO B and MAO A, respectively. Selegiline 127-139 monoamine oxidase B Homo sapiens 143-148 8102552-1 1993 The goal of this study was to determine whether selegiline (L-deprenyl), a selective monoamine oxidase B inhibitor and antioxidant, would improve neuroleptic-induced tardive dyskinesia (TD). Selegiline 48-58 monoamine oxidase B Homo sapiens 85-104 8102552-1 1993 The goal of this study was to determine whether selegiline (L-deprenyl), a selective monoamine oxidase B inhibitor and antioxidant, would improve neuroleptic-induced tardive dyskinesia (TD). Selegiline 60-70 monoamine oxidase B Homo sapiens 85-104 8302302-6 1993 Initial studies demonstrate that the MAO-B inhibitor L-deprenyl (selegiline) delays the development of disability in otherwise untreated patients with early Parkinson"s disease. Selegiline 53-63 monoamine oxidase B Homo sapiens 37-42 8302302-6 1993 Initial studies demonstrate that the MAO-B inhibitor L-deprenyl (selegiline) delays the development of disability in otherwise untreated patients with early Parkinson"s disease. Selegiline 65-75 monoamine oxidase B Homo sapiens 37-42 8377010-5 1993 (-)-Deprenyl, a specific monoamine oxidase (MAO) B inhibitor, has been used as an effective antiparkinsonian drug, and it has been reported to possess neuroprotective and neurorescue properties. Selegiline 0-12 monoamine oxidase B Homo sapiens 25-50 8377010-7 1993 The effect seems to be specific to MAO B inhibitors because (+)-deprenyl and clorgyline exhibit no effect. Selegiline 60-72 monoamine oxidase B Homo sapiens 35-40 8374913-1 1993 Selegiline (deprenyl) and lazabemide (Ro 19-6327) are inhibitors of monoamine oxidase-B but differ in several other pharmacological properties. Selegiline 0-10 monoamine oxidase B Homo sapiens 68-87 8374913-1 1993 Selegiline (deprenyl) and lazabemide (Ro 19-6327) are inhibitors of monoamine oxidase-B but differ in several other pharmacological properties. Selegiline 12-20 monoamine oxidase B Homo sapiens 68-87 8374913-5 1993 This work confirms that the symptomatic effects of selegiline against Parkinsonism are small and are likely due to its inhibition of monoamine oxidase-B. Selegiline 51-61 monoamine oxidase B Homo sapiens 133-152 8489205-2 1993 The monoamine oxidase type B inhibitor deprenyl (selegiline) has been demonstrated to delay the emergence of disability in early untreated Parkinson"s disease. Selegiline 39-47 monoamine oxidase B Homo sapiens 4-28 8489205-2 1993 The monoamine oxidase type B inhibitor deprenyl (selegiline) has been demonstrated to delay the emergence of disability in early untreated Parkinson"s disease. Selegiline 49-59 monoamine oxidase B Homo sapiens 4-28 8302308-4 1993 Theoretically at least, MAO-B inhibition by selegiline could result in the increase in the levels of polyamines and their N-acetyl derivatives. Selegiline 44-54 monoamine oxidase B Homo sapiens 24-29 1488910-1 1992 The combination of C-11-labelled Selegiline with PET gives the possibility of a non-invasive method for the determination of the distribution, activity and turnover of MAO-B enzyme and all the enzyme-related changes in the brain as well as for the early detection of Parkinson"s disease. Selegiline 33-43 monoamine oxidase B Homo sapiens 168-173 1557063-5 1992 Treatment with deprenyl, an inhibitor of monoamine oxidase type B, partially prevented levodopa neurotoxicity, suggesting that the mechanism of toxicity was, at least in part, related to an increase in the metabolism of dopamine catalyzed by monoamine oxidase. Selegiline 15-23 monoamine oxidase B Homo sapiens 41-65 10146952-1 1992 Selegiline (deprenyl) is a selective, irreversible cerebral monoamine oxidase type B inhibitor (MAO-B) that is used in the treatment of Parkinson"s disease. Selegiline 0-10 monoamine oxidase B Homo sapiens 60-84 10146952-1 1992 Selegiline (deprenyl) is a selective, irreversible cerebral monoamine oxidase type B inhibitor (MAO-B) that is used in the treatment of Parkinson"s disease. Selegiline 0-10 monoamine oxidase B Homo sapiens 96-101 10146952-1 1992 Selegiline (deprenyl) is a selective, irreversible cerebral monoamine oxidase type B inhibitor (MAO-B) that is used in the treatment of Parkinson"s disease. Selegiline 12-20 monoamine oxidase B Homo sapiens 60-84 10146952-1 1992 Selegiline (deprenyl) is a selective, irreversible cerebral monoamine oxidase type B inhibitor (MAO-B) that is used in the treatment of Parkinson"s disease. Selegiline 12-20 monoamine oxidase B Homo sapiens 96-101 1639115-1 1992 L-Deprenyl, the selective inhibitor of monoamine oxidase type B (MAO-B), has gained wide acceptance as a useful form of adjunct therapeutic drug in the treatment of Parkinson"s disease. Selegiline 0-10 monoamine oxidase B Homo sapiens 39-63 1639115-1 1992 L-Deprenyl, the selective inhibitor of monoamine oxidase type B (MAO-B), has gained wide acceptance as a useful form of adjunct therapeutic drug in the treatment of Parkinson"s disease. Selegiline 0-10 monoamine oxidase B Homo sapiens 65-70 1639115-7 1992 The observed in vitro selectivity of L-deprenyl for MAO-B may be accounted for by differences in the affinities of the two MAO subtypes for reversible interaction with L-deprenyl, differences in the rates of reaction within the noncovalent complexes to form the irreversibly inhibited adduct, or a combination of both these factors. Selegiline 37-47 monoamine oxidase B Homo sapiens 52-57 1639115-7 1992 The observed in vitro selectivity of L-deprenyl for MAO-B may be accounted for by differences in the affinities of the two MAO subtypes for reversible interaction with L-deprenyl, differences in the rates of reaction within the noncovalent complexes to form the irreversibly inhibited adduct, or a combination of both these factors. Selegiline 168-178 monoamine oxidase B Homo sapiens 52-57 1600360-1 1992 Selegiline (10 mg per day) selectively inhibits monoamine oxidase type B and thus thwarts the metabolism of dopamine by this enzyme. Selegiline 0-10 monoamine oxidase B Homo sapiens 48-72 1350053-6 1992 The rational for starting treatment with selegiline at this time is discussed in the context of the role that increased MAO-B activity plays in the progression of Parkinson"s disease. Selegiline 41-51 monoamine oxidase B Homo sapiens 120-125 1592575-1 1992 In a double blind randomized crossover trial lasting 6 months selegiline, a selective MAO-B inhibitor, was tested against placebo for activity on verbal memory performances in Alzheimer-type dementia (DAT). Selegiline 62-72 monoamine oxidase B Homo sapiens 86-91 1571860-1 1992 Deprenyl is a synthetic, selective inhibitor of the monoamine oxidase-B enzyme system. Selegiline 0-8 monoamine oxidase B Homo sapiens 52-71 1482291-1 1992 Selegiline (R(-)-N-methyl-N-(1-phenyl-2-propyl)-2-propinylamine), a selective MAO-B inhibitor used as an antiparkinsonian, is excreted in urine as N-desmethyl selegiline (norselegiline), R(-)-methamphetamine (R(-)-MA), R(-)-amphetamine (R(-)-AM) and their conjugated p-hydroxy derivatives. Selegiline 0-10 monoamine oxidase B Homo sapiens 78-83 1513186-3 1992 (-)Deprenyl was the first selective inhibitor of MAO-B described in literature, became the worldwide research tool used for blocking selectively B-type MAO, and is still the only MAO-B inhibitor in clinical use. Selegiline 3-11 monoamine oxidase B Homo sapiens 49-54 1513186-3 1992 (-)Deprenyl was the first selective inhibitor of MAO-B described in literature, became the worldwide research tool used for blocking selectively B-type MAO, and is still the only MAO-B inhibitor in clinical use. Selegiline 3-11 monoamine oxidase B Homo sapiens 179-184 1634730-4 1992 (-)Deprenyl, the first selective inhibitor of MAO-B described in literature, has become the universally used research tool for selectively blocking B-type MAO. Selegiline 3-11 monoamine oxidase B Homo sapiens 46-51 1349639-10 1992 By using the MAOA-specific inhibitor clorgyline and the MAOB-specific inhibitor deprenyl we were able to confirm that the MAOA form of the enzyme is involved in DA metabolism in this preparation. Selegiline 80-88 monoamine oxidase B Homo sapiens 56-60 1584187-7 1992 Another approach is the use of selegiline (deprenyl), MAO-B inhibitor slowing the breakdown of dopamine and thereby extending the duration of levodopa effect. Selegiline 31-41 monoamine oxidase B Homo sapiens 54-59 1350073-1 1992 Studies indicate that selegiline, a monoamine oxidase type B inhibitor, slows progression of Parkinson"s disease (PD) and delays the need for levodopa. Selegiline 22-32 monoamine oxidase B Homo sapiens 36-60 1729144-5 1992 The monoamine oxidase type B inhibitor selegiline is also being used by many physicians to delay the onset of disability. Selegiline 39-49 monoamine oxidase B Homo sapiens 4-28 1388699-3 1992 As anticipated, MAO-B was lowest in PD cases on selegiline (L-deprenyl) therapy (mean 1.10). Selegiline 48-58 monoamine oxidase B Homo sapiens 16-21 1388699-3 1992 As anticipated, MAO-B was lowest in PD cases on selegiline (L-deprenyl) therapy (mean 1.10). Selegiline 60-70 monoamine oxidase B Homo sapiens 16-21 1388699-4 1992 There was a slight deficit of MAO-B among male cases not taking selegiline compared to controls (3.78 vs. 4.15), but the opposite trend was observed for females (6.18 vs. 4.16). Selegiline 64-74 monoamine oxidase B Homo sapiens 30-35 1418862-2 1992 L-deprenyl binds irreversibly and quantitatively to the B-form of monoamine oxidase, MAO, and is an ideal 3H-ligand to measure the MAO-B enzyme protein in tissues by means of in vitro autoradiography. Selegiline 0-10 monoamine oxidase B Homo sapiens 131-136 1418862-6 1992 There was a high correlation between glial cell count and 3H-L-deprenyl binding with a relation indicating enhanced MAO-B protein in glial cells within areas of neurodegeneration. Selegiline 61-71 monoamine oxidase B Homo sapiens 116-121 1609114-16 1992 In subjects with Parkinson"s disease the MAO-B inhibitor L-deprenyl exerts a L-dopa-sparing effect, prolongs L-dopa action and seems to have a favorable influence regarding on-off disabilities. Selegiline 57-67 monoamine oxidase B Homo sapiens 41-46 1773423-8 1991 We suggest that L-deprenyl, through selective inhibition of MAO-B and by increasing the activity of the catecholaminergic systems, positively influences cognitive functions and behaviour founded on memory efficiency. Selegiline 16-26 monoamine oxidase B Homo sapiens 60-65 1658311-0 1991 Deprenyl (selegiline), a selective MAO-B inhibitor with active metabolites; effects on locomotor activity, dopaminergic neurotransmission and firing rate of nigral dopamine neurons. Selegiline 0-8 monoamine oxidase B Homo sapiens 35-40 1776388-1 1991 Eighteen patients with Parkinson"s disease were treated with placebo for 4 weeks and with the MAO-B inhibitor selegiline for 8 weeks without levodopa in a randomized double-blind clinical study. Selegiline 110-120 monoamine oxidase B Homo sapiens 94-99 1658311-1 1991 Utilizing behavioral, biochemical and electrophysiological methods, central effects of the monoamine oxidase-B inhibitor deprenyl (selegiline) were analyzed. Selegiline 121-129 monoamine oxidase B Homo sapiens 91-110 1776993-4 1991 The cells could be protected against the reduced toxins, but not MPP+, by either the MAO A selective inhibitor, clorgyline or the MAO B selective inhibitor, deprenyl. Selegiline 157-165 monoamine oxidase B Homo sapiens 130-135 1794016-2 1991 Selegiline (deprenyl) is a selective inhibitor of cerebral monoamine oxidase type B at the dosage (10 mg/day) used in patients with Parkinson"s disease. Selegiline 0-10 monoamine oxidase B Homo sapiens 59-83 1759390-3 1991 Pretreatment of the organelles with a mixture containing chlorgyline and deprenyl completely inhibited monoamine oxidase (MAO) activity and prevented the effects of all the amines studied on mitochondrial enzymes. Selegiline 73-81 monoamine oxidase B Homo sapiens 122-125 1909485-1 1991 We treated 20 early Parkinson"s disease subjects with the dopamine agonist lisuride in combination with the MAO-B inhibitor selegiline (L-deprenyl). Selegiline 124-134 monoamine oxidase B Homo sapiens 108-113 21229030-3 1991 Research suggests that monoamine oxidase B inhibitors, such as selegiline, should benefit Parkinson"s patients. Selegiline 63-73 monoamine oxidase B Homo sapiens 23-42 1922929-3 1991 An MAO-B inhibitor, deprenyl also decreased the neuronal necrosis, but it inhibited only the changes in 3,4-dihydroxyphenylacetic acid (DOPAC) content after reperfusion. Selegiline 20-28 monoamine oxidase B Homo sapiens 3-8 1794016-2 1991 Selegiline (deprenyl) is a selective inhibitor of cerebral monoamine oxidase type B at the dosage (10 mg/day) used in patients with Parkinson"s disease. Selegiline 12-20 monoamine oxidase B Homo sapiens 59-83 1905757-3 1991 Both molecular forms of MAO, MAO A and MAO B, were found using specific inhibitors clorgyline and deprenyl. Selegiline 98-106 monoamine oxidase B Homo sapiens 39-44 1801538-2 1991 1.4.3.4) are of obvious interest in relation to Parkinson"s disease and its treatment with the irreversible and selective MAO-B inhibitor L-deprenyl and are discussed in this review: 1) To what extent the two forms of MAO are of importance for the deamination of dopamine and to what degree MAO localised inside and outside of dopaminergic nerve terminals contributes 2) The kinetics of the MAO-protein, i.e. the rate of recovery of MAO after irreversible inhibition. Selegiline 138-148 monoamine oxidase B Homo sapiens 122-127 1686954-2 1991 Because in the human brain, dopamine is metabolised mainly by MAO-B, selegiline increases dopamine content in the central nervous system. Selegiline 69-79 monoamine oxidase B Homo sapiens 62-67 1686954-3 1991 Besides the inhibition of MAO-B, selegiline also inhibits the uptake of dopamine and noradrenaline into presynaptic nerve and increases the turnover of dopamine. Selegiline 33-43 monoamine oxidase B Homo sapiens 26-31 1801542-11 1991 The inhibition of MAO-B by DP may have been the means by which progression of Parkinsonism was attenuated, although other mechanisms are also tenable. Selegiline 27-29 monoamine oxidase B Homo sapiens 18-23 1901185-3 1991 Selegiline (also known as deprenyl), is a selective irreversible monoamine oxidase type B inhibitor virtually devoid of the tyramine reaction at the recommended dosage of 10 mg/d. Selegiline 0-10 monoamine oxidase B Homo sapiens 65-89 1901185-3 1991 Selegiline (also known as deprenyl), is a selective irreversible monoamine oxidase type B inhibitor virtually devoid of the tyramine reaction at the recommended dosage of 10 mg/d. Selegiline 26-34 monoamine oxidase B Homo sapiens 65-89 22282124-7 1991 The MAO-B inhibitor, selegiline (5 mg once daily), also lowered the oral tyramine threshold significantly. Selegiline 21-31 monoamine oxidase B Homo sapiens 4-9 1712206-3 1991 L-deprenyl (LD), a selective and irreversible MAO-B inhibitor, has recently been proposed for the treatment of AD. Selegiline 0-10 monoamine oxidase B Homo sapiens 46-51 1712206-3 1991 L-deprenyl (LD), a selective and irreversible MAO-B inhibitor, has recently been proposed for the treatment of AD. Selegiline 12-14 monoamine oxidase B Homo sapiens 46-51 1754059-8 1991 A high correlation coefficient (r approximately 0.9) was obtained between [3H]L-deprenyl binding and monoamine oxidase-B activity, both in the senile dementia of Alzheimer type and in the control brains. Selegiline 78-88 monoamine oxidase B Homo sapiens 101-120 2196964-5 1990 The same depressant effect was observed in animals pretreated with the monoamine oxidase B inhibitor (IMAO-B) deprenyl which is known to reduce milacemide metabolism into glycinamide and glycine. Selegiline 110-118 monoamine oxidase B Homo sapiens 71-90 2121360-1 1990 Selegiline, an inhibitor of monoamine oxidase B, was tested on patients with mild to moderate dementia of the Alzheimer type. Selegiline 0-10 monoamine oxidase B Homo sapiens 28-47 2125242-1 1990 The efficacy and tolerability of the monoamine oxidase B inhibitor selegiline and of the nootropic agent oxiracetam were compared in a single-blind, controlled, parallel study. Selegiline 67-77 monoamine oxidase B Homo sapiens 37-56 34867348-5 2021 In an epithelial cell culture model, RG0216 significantly decreased LPS-induced interleukin (IL)-6 and IL-1beta gene and protein expression and was as effective as equimolar concentrations of deprenyl (an existing irreversible MAO-B inhibitor). Selegiline 192-200 monoamine oxidase B Homo sapiens 227-232 2089094-4 1990 In addition to the description of the neuroprotective mechanism of the MAO-B-inhibitor L-deprenyl a new aspect focuses the role of the endogenous MAO-B substrates "polyamines" which occur both in neurons and glia. Selegiline 87-97 monoamine oxidase B Homo sapiens 71-76 2128498-1 1990 The DATATOP study is a clinical trial in which deprenyl, a selective inhibitor of monoamine oxidase-B (MAO-B), is being given to newly diagnosed Parkinsonian patients in an attempt to halt the progression of their disorder. Selegiline 47-55 monoamine oxidase B Homo sapiens 82-101 2128498-1 1990 The DATATOP study is a clinical trial in which deprenyl, a selective inhibitor of monoamine oxidase-B (MAO-B), is being given to newly diagnosed Parkinsonian patients in an attempt to halt the progression of their disorder. Selegiline 47-55 monoamine oxidase B Homo sapiens 103-108 2128498-4 1990 In addition, we point out that with long-term administration to rodents, deprenyl loses its selectivity as an inhibitor of MAO-B and also inhibits MAO-A. Selegiline 73-81 monoamine oxidase B Homo sapiens 123-128 2300680-3 1990 The investigation was later continued in an open fashion by giving a single 10 mg dose of the MAO-B inhibitor deprenyl to the same subjects. Selegiline 110-118 monoamine oxidase B Homo sapiens 94-99 34784871-11 2021 Of monoamine oxidase B inhibitors, safinamide is the least susceptible for interaction with the tyramine-rich food, whereas selegiline and rasagiline may lose selectivity to monoamine oxidase B when administered in supratherapeutic doses. Selegiline 124-134 monoamine oxidase B Homo sapiens 174-193 2113756-1 1990 Twenty patients with Parkinson"s disease were treated with the MAO-B inhibitor selegiline (l-deprenyl) and placebo without levodopa (L-dopa) in a randomized double-blind clinical cross-over study to analyze relative importances of dopamine (DA) synthesis and metabolism. Selegiline 79-89 monoamine oxidase B Homo sapiens 63-68 2113756-1 1990 Twenty patients with Parkinson"s disease were treated with the MAO-B inhibitor selegiline (l-deprenyl) and placebo without levodopa (L-dopa) in a randomized double-blind clinical cross-over study to analyze relative importances of dopamine (DA) synthesis and metabolism. Selegiline 91-101 monoamine oxidase B Homo sapiens 63-68 2109658-3 1990 Twenty patients with a clinical diagnosis of DAT and with a slight-moderate mental deterioration were treated with 10 mg/day of L-deprenyl, a selective MAO-B inhibitor, according to a double-blind crossover design vs. placebo. Selegiline 128-138 monoamine oxidase B Homo sapiens 152-157 2248084-3 1990 Toloxatone and low doses of deprenyl (a MAO-B inhibitor) caused 20% and 17% inhibition respectively; higher doses of deprenyl, however, strongly inhibited MAO-A. Selegiline 28-36 monoamine oxidase B Homo sapiens 40-45 2122649-0 1990 L-deprenyl, a MAO-B inhibitor, as an adjunct to conventional L-dopa therapy in Parkinson"s disease: experience in 200 patients. Selegiline 0-10 monoamine oxidase B Homo sapiens 14-19 34970960-4 2021 The very first MAO-B used therapeutically was selegiline, followed by rasagiline, its indane derivative which has superior efficacy and selectivity. Selegiline 46-56 monoamine oxidase B Homo sapiens 15-20 34553601-5 2021 From the Protein Data Bank, MAO-B protein structures complexed with selegiline, 6-hydroxy-N-propargyl-1(R)-aminoindan, or a chromen derivative have been selected as templates for shape-based virtual screening (SB-VS) against the Traditional Chinese Medicinal (TCM) natural database. Selegiline 68-78 monoamine oxidase B Homo sapiens 28-33 33818516-9 2021 All the tested compounds were capable to inhibit human monoamine oxidase-B enzyme to a significant extent, however, compound 7 exerted the most prominent inhibitory activity, similar to selegiline and rasagiline. Selegiline 186-196 monoamine oxidase B Homo sapiens 55-74 34352710-3 2021 Compound 20 exhibited the best activity and selectivity towards hMAO-B with IC50 value of 53 nM and selectivity index of 1122 folds over MAO-A, compared to the reference drugs rasagiline (IC50 = 66 nM) and selegiline (IC50 = 40 nM). Selegiline 206-216 monoamine oxidase B Homo sapiens 64-70 35447344-4 2022 An important consideration is that selegiline and rasagiline display specificity for MAO-B over the MAO-A isoform thus reducing the risk of tyramine-induced changes in blood-pressure. Selegiline 35-45 monoamine oxidase B Homo sapiens 85-90 34290084-5 2021 Both inhibition of MAO-B by selegiline or rasagiline and siRNA-mediated knockdown of MAO-B facilitated alpha-syn secretion. Selegiline 28-38 monoamine oxidase B Homo sapiens 19-24 35447344-2 2022 Two propargylamine-containing MAO-B inhibitors, selegiline ((R)-deprenyl) and rasagiline, are currently used in the clinic for this purpose. Selegiline 48-58 monoamine oxidase B Homo sapiens 30-35 35624406-2 2022 Following introduction of the monoamine oxidase type B inhibitor selegiline for the treatment of Parkinson"s disease (PD), discovery of the action mechanism of Alzheimer"s disease-modifying agent memantine, the role of iron in PD, and the loss of electron transport chain complex I in PD, and development of the concept of clinical neuroprotection, Peter Riederer launched one of the most challenging research project neurodevelopmental aspects of neuropsychiatric disorders. Selegiline 65-75 monoamine oxidase B Homo sapiens 30-54 35587267-6 2022 The inhibitory activity of two mimotopes against MAO-B was analyzed using HeLa cells overexpressing MAO-B, as well as using activated human astrocytes; their inhibitory activity was compared to that of a commercial inhibitor of MAO-B, selegiline. Selegiline 235-245 monoamine oxidase B Homo sapiens 49-54 35198978-9 2022 (3H)L-deprenyl quantified a monoamine oxidase-B target density of 304.23 +- 115.93 nM (n = 8 cases; mean +- standard deviation) in healthy control tissue and is similar to the target density in chronic traumatic encephalopathy tissues (365.80 +- 128.55 nM; n = 12 cases; mean +- standard deviation). Selegiline 4-14 monoamine oxidase B Homo sapiens 28-47 2509446-2 1989 Both activities were inhibited 100% by 10(-7) M deprenyl (a specific MAO-B inhibitor) and were not affected by clorgyline (a specific MAO-A inhibitor) or by polyclonal antibodies to MAO-A. Selegiline 48-56 monoamine oxidase B Homo sapiens 69-74 2694735-4 1989 In addition to these two major medications the essential therapeutic additives such as the decarboxylase inhibitor benserazide, the monoamineoxidase B inhibitor deprenyl and the dopamine receptor agonist lisuride should be used for the fine adjustment of the individual patient. Selegiline 161-169 monoamine oxidase B Homo sapiens 132-150 2503040-4 1989 The presence of MAO-B was corroborated by the inhibition of PEA oxidation with nanomolar deprenyl concentrations and by inhibition of TYR oxidation with high clorgyline concentrations, as well as by the simple sigmoid curve obtained in both cases. Selegiline 89-97 monoamine oxidase B Homo sapiens 16-21 2496202-6 1989 In contrast, the expressed MAO B prefers phenylethylamine as a substrate and is sensitive to the inhibitor deprenyl. Selegiline 107-115 monoamine oxidase B Homo sapiens 27-32 2515715-1 1989 Selegiline is a selective, irreversible inhibitor of monoamine oxidase type B (MAO-B). Selegiline 0-10 monoamine oxidase B Homo sapiens 53-77 2515715-1 1989 Selegiline is a selective, irreversible inhibitor of monoamine oxidase type B (MAO-B). Selegiline 0-10 monoamine oxidase B Homo sapiens 79-84 2515726-3 1989 It is the L-form of selegiline that is an active MAO-B inhibitor, the D-(+)-form being 25 times less active. Selegiline 20-30 monoamine oxidase B Homo sapiens 49-54 2501102-1 1989 L-Deprenyl is an inhibitor of monoamine oxidase B and dopamine uptake. Selegiline 0-10 monoamine oxidase B Homo sapiens 30-49 2501102-2 1989 Chronic L-deprenyl (10 mg/kg i.p., twice weekly for 4 weeks) was shown to inhibit monoamine oxidase B activity by 89%, and also to induce an up-regulation of the [3H]mazindol binding site associated with the striatal dopamine uptake carrier. Selegiline 8-18 monoamine oxidase B Homo sapiens 82-101 2469451-3 1989 The investigation was thereafter continued in an open fashion by administering a single 10 mg dose of the MAO-B inhibitor deprenyl to the same subjects. Selegiline 122-130 monoamine oxidase B Homo sapiens 106-111 2469451-7 1989 In contrast, deprenyl, in a dose which almost totally inhibited MAO-B activity in blood platelets, did not appreciably affect the plasma concentrations of DHPG or DOPAC. Selegiline 13-21 monoamine oxidase B Homo sapiens 64-69 2618592-2 1989 DA is a good substrate for MAO-B and selegiline enhances DA-transmission and improves akinesia of Parkinson"s disease (PD) by selective MAO-B blockade. Selegiline 37-47 monoamine oxidase B Homo sapiens 136-141 2618592-6 1989 In addition, synthesis of hydrogen peroxide generated via MAO-B is blocked by selegiline. Selegiline 78-88 monoamine oxidase B Homo sapiens 58-63 2618592-9 1989 As conclusion, selegiline is a safe inhibitor of MAO-B that reduces neurotoxicity possibly triggering PD. Selegiline 15-25 monoamine oxidase B Homo sapiens 49-54 3107514-12 1987 The greater effect of low-dose L-deprenyl therapy suggests that it is the inhibition of MAO-B, and not MAO-A, that may be important in the behavioral effects of L-deprenyl administration to patients with DAT. Selegiline 31-41 monoamine oxidase B Homo sapiens 88-93 2501449-0 1989 Localization of monoamine oxidase B in human brain by autoradiographical use of 11C-labelled L-deprenyl. Selegiline 93-103 monoamine oxidase B Homo sapiens 16-35 2501449-1 1989 11C-labelled L-deprenyl in vitro autoradiography was used to study the regional distribution of MAO-B in human brain. Selegiline 13-23 monoamine oxidase B Homo sapiens 96-101 3126263-5 1988 The presence of the irreversible MAO-B inhibitor l-deprenyl completely abolished the irreversible labelling of the membranes by [3H]Ro 16-6491. Selegiline 49-59 monoamine oxidase B Homo sapiens 33-38 3127050-1 1988 Deprenyl, a selective inhibitor of monoamine oxidase, type B, which is free of the "tyramine effect," may ameliorate symptom fluctuations in advanced Parkinson"s disease (PD). Selegiline 0-8 monoamine oxidase B Homo sapiens 35-60 3110375-3 1987 This influx constant was used as a measure of functional enzyme activity for sequential determinations of MAO-B recovery following a single high dose of unlabeled L-deprenyl. Selegiline 163-173 monoamine oxidase B Homo sapiens 106-111 2677243-4 1989 The efficacy of specific MAO inhibitors such as moclobemide (MAO-A) and deprenyl (MAO-B) are yet to be investigated. Selegiline 72-80 monoamine oxidase B Homo sapiens 82-87 3126263-6 1988 The selective inactivation of MAO-B, e.g., by l-deprenyl prevented the covalent incorporation of [3H]Ro 16-6491 whereas selective inhibition of the MAO-A by clorgyline was without effect. Selegiline 46-56 monoamine oxidase B Homo sapiens 30-35 3346666-5 1988 In vitro MAO-B (l-deprenyl and AGN 1135) rather than MAO-A (clorgyline) selectively inhibited the oxidation of milacemide. Selegiline 16-26 monoamine oxidase B Homo sapiens 9-14 2451963-11 1988 Selective inhibition of MAO-B with selegiline (10 mg kg-1, i.p.) Selegiline 35-45 monoamine oxidase B Homo sapiens 24-29 3145523-1 1988 Blood pressure and heart rate responses to oral tyramine have been measured in healthy volunteers before and after administration of the selective monoamine oxidase B inhibitor selegiline at high dosage (30 mg/day). Selegiline 177-187 monoamine oxidase B Homo sapiens 147-166 3118881-5 1987 The radioactivity in the heart 15 min after administration was reduced in a dose-dependent manner by pretreatment with a specific MAO-B inhibitor, l-deprenyl, but not with a specific MAO-A inhibitor, clorgyline. Selegiline 147-157 monoamine oxidase B Homo sapiens 130-135 3114597-7 1987 An atypical irreversible MAO-B selective inhibitor, selegiline (deprenyl) does not exhibit an adverse reaction on the ingestion of amine-containing foods. Selegiline 52-62 monoamine oxidase B Homo sapiens 25-30 3114597-7 1987 An atypical irreversible MAO-B selective inhibitor, selegiline (deprenyl) does not exhibit an adverse reaction on the ingestion of amine-containing foods. Selegiline 64-72 monoamine oxidase B Homo sapiens 25-30 3107514-12 1987 The greater effect of low-dose L-deprenyl therapy suggests that it is the inhibition of MAO-B, and not MAO-A, that may be important in the behavioral effects of L-deprenyl administration to patients with DAT. Selegiline 161-171 monoamine oxidase B Homo sapiens 88-93 3030067-2 1987 L-Deprenyl, a selective inhibitor of MAO-B, was introduced by us into clinical use as an adjunct to L-DOPA some years ago. Selegiline 0-10 monoamine oxidase B Homo sapiens 37-42 3099392-6 1987 A comparison of the brain uptake and retention of the 11C-labeled inactive (D-) and active (L-) enantiomers of deprenyl showed rapid clearance of the inactive enantiomer and retention of the active enantiomer within MAO B-rich brain structures, in agreement with the known stereoselectivity of MAO B for L-deprenyl. Selegiline 111-119 monoamine oxidase B Homo sapiens 216-221 3099392-6 1987 A comparison of the brain uptake and retention of the 11C-labeled inactive (D-) and active (L-) enantiomers of deprenyl showed rapid clearance of the inactive enantiomer and retention of the active enantiomer within MAO B-rich brain structures, in agreement with the known stereoselectivity of MAO B for L-deprenyl. Selegiline 111-119 monoamine oxidase B Homo sapiens 294-299 3030067-0 1987 Localization of MAO-A and MAO-B in human brain: a step in understanding the therapeutic action of L-deprenyl. Selegiline 98-108 monoamine oxidase B Homo sapiens 26-31 3030067-4 1987 The mechanism underlying the action of L-deprenyl is thought to be related to its inhibition of MAO-B and thus increased levels of PEA and DA, as measured in the striatal and limbic region of human brain. Selegiline 39-49 monoamine oxidase B Homo sapiens 96-101 3123605-1 1987 L-deprenyl is a potent, well tolerated and safe inhibitor agent of MAO-B. Selegiline 0-10 monoamine oxidase B Homo sapiens 67-72 3123595-0 1987 MAO-B-Inhibitor selegiline (R-(-)-deprenyl). Selegiline 16-26 monoamine oxidase B Homo sapiens 0-5 3123606-1 1987 The selective monoamine oxidase (MAO) B inhibitor L-deprenyl (Eldepryl, Jumex, Movergan, Selegiline) has gained acceptance as a useful form of adjunctive therapy in the treatment of Parkinson"s disease. Selegiline 50-60 monoamine oxidase B Homo sapiens 14-39 3123606-1 1987 The selective monoamine oxidase (MAO) B inhibitor L-deprenyl (Eldepryl, Jumex, Movergan, Selegiline) has gained acceptance as a useful form of adjunctive therapy in the treatment of Parkinson"s disease. Selegiline 89-99 monoamine oxidase B Homo sapiens 14-39 3083305-3 1986 In human brain the reaction was inhibited by selective doses of the MAO-B inhibitor (-)-deprenyl. Selegiline 84-96 monoamine oxidase B Homo sapiens 68-73 3097589-2 1986 Further, utilization of specific inhibitors, deprenyl and clorgyline, also provides evidence that serotonergic neurons contain exclusively MAO-B and catecholaminergic ones contain MAO-A. Selegiline 45-53 monoamine oxidase B Homo sapiens 139-144 2436247-1 1987 Deprenyl, a monoamine oxidase (MAO) inhibitor with selective effects on MAO type-B at low doses, was administered to 13 patients with dementia of the Alzheimer type (DAT), a disorder reported to be associated with increased brain MAO-B activity. Selegiline 0-8 monoamine oxidase B Homo sapiens 230-235 2436247-5 1987 These dose-dependent reductions are consistent with in vitro biochemical and anatomical data from primate brain suggesting that at low doses of deprenyl, MAO-B inhibition might be expected to selectively affect dopamine and serotonin-containing neurons, while at higher doses (which lead to MAO-A as well as MAO-B inhibition), noradrenergic neurons may become relatively more affected by the drug. Selegiline 144-152 monoamine oxidase B Homo sapiens 154-159 2436247-5 1987 These dose-dependent reductions are consistent with in vitro biochemical and anatomical data from primate brain suggesting that at low doses of deprenyl, MAO-B inhibition might be expected to selectively affect dopamine and serotonin-containing neurons, while at higher doses (which lead to MAO-A as well as MAO-B inhibition), noradrenergic neurons may become relatively more affected by the drug. Selegiline 144-152 monoamine oxidase B Homo sapiens 308-313 3108930-3 1987 L-Deprenyl is a monoamine oxidase (MAO) inhibitor which may selectively inhibit MAO-B at low doses, while at high doses it nonselectively inhibits MAO-A as well as MAO-B. Selegiline 0-10 monoamine oxidase B Homo sapiens 80-85 3108930-3 1987 L-Deprenyl is a monoamine oxidase (MAO) inhibitor which may selectively inhibit MAO-B at low doses, while at high doses it nonselectively inhibits MAO-A as well as MAO-B. Selegiline 0-10 monoamine oxidase B Homo sapiens 164-169 3088511-0 1986 [Treatment of extra-puerperal galactorrhea with the MAO-B inhibitor selegiline]. Selegiline 68-78 monoamine oxidase B Homo sapiens 52-57 2420928-6 1986 Brains obtained at autopsy from l-deprenyl-treated Parkinsonian patients showed that, whereas MAO-B was fully inhibited by the therapeutic doses of l-deprenyl, substantial MAO-A activity was still evident. Selegiline 32-42 monoamine oxidase B Homo sapiens 94-99 2420928-6 1986 Brains obtained at autopsy from l-deprenyl-treated Parkinsonian patients showed that, whereas MAO-B was fully inhibited by the therapeutic doses of l-deprenyl, substantial MAO-A activity was still evident. Selegiline 148-158 monoamine oxidase B Homo sapiens 94-99 2420928-8 1986 These data indicate that the therapeutic actions of l-deprenyl may lie in its selective inhibition of MAO-B resulting in increased brain levels of DA formed from L-dihydroxyphenylacetic acid (L-DOPA). Selegiline 52-62 monoamine oxidase B Homo sapiens 102-107 3082793-1 1986 A multicenter trial was conducted at 9 Neurology Departments to evaluate the action of L-Deprenyl, a specific monoamine oxidase-B inhibitor, combined with L-Dopa in the treatment of Parkinson disease. Selegiline 87-97 monoamine oxidase B Homo sapiens 110-129 3008207-6 1986 In contrast, the selective MAO-B inhibitor deprenyl (10-30 mg/day for 3 weeks) led to a 96 +/- 4% inhibition of platelet MAO-B activity but no significant change in plasma melatonin (5.1 +/- SD 4.2 pg/ml). Selegiline 43-51 monoamine oxidase B Homo sapiens 27-32 3008207-6 1986 In contrast, the selective MAO-B inhibitor deprenyl (10-30 mg/day for 3 weeks) led to a 96 +/- 4% inhibition of platelet MAO-B activity but no significant change in plasma melatonin (5.1 +/- SD 4.2 pg/ml). Selegiline 43-51 monoamine oxidase B Homo sapiens 121-126 3011983-7 1986 Monoamine oxidase inhibitors such as deprenyl, pargyline and harmaline have affinities to the MPTP receptors which parallel their affinity for the B type of monoamine oxidase (MAO B). Selegiline 37-45 monoamine oxidase B Homo sapiens 176-181 3097257-3 1986 Deprenyl is a selective MAO-B inhibitor thought to be able to slow down the catabolism of dopamine and therefore to allow a decrease of the therapeutic regimen of L-dopa while in the meantime to obtain a more stable plasma and tissue levels and a constant therapeutic response. Selegiline 0-8 monoamine oxidase B Homo sapiens 24-29 3097257-7 1986 The association with (-)deprenyl was able to reverse this trend and when the inhibition of MAOB was really effective patients showed an improvement of symptoms even when compared to baseline values. Selegiline 24-32 monoamine oxidase B Homo sapiens 91-95 3097261-5 1986 Inhibition of hydrogen peroxide stimulated MAO-B activity in human cortex by (-)deprenyl was found to be of similar potency compared to hydrogen peroxide free estimations. Selegiline 77-88 monoamine oxidase B Homo sapiens 43-48 3929314-1 1985 Deprenyl has previously been reported to be a selective monoamine oxidase (MAO) type B inhibitor, which is associated with little or no enhancement of the pressor effects of tyramine. Selegiline 0-8 monoamine oxidase B Homo sapiens 56-86 3091762-1 1986 MPTP is oxidized to its toxic metabolite MPP+ by MAO B in both primate and rodent brains and this reaction can be inhibited by (-)-deprenyl. Selegiline 127-139 monoamine oxidase B Homo sapiens 49-54 3097263-0 1986 Pharmacology of MAO B inhibitors: mode of action of (-)deprenyl in Parkinson"s disease. Selegiline 55-63 monoamine oxidase B Homo sapiens 16-21 3097263-2 1986 Although not all features of its anti-Parkinson action is known, studies on brains obtained at autopsy from patients on (-)deprenyl show that the selective inhibition of MAO B with a concomitant increase of dopamine, but not of serotonin, in the basal ganglia may be responsible for its mode of action. Selegiline 123-131 monoamine oxidase B Homo sapiens 170-175 3928010-5 1985 At the doses used selegiline and AGN 1135 caused a near total selective inhibition of liver and brain MAO-B, while clorgyline inhibited MAO-A only in the brain. Selegiline 18-28 monoamine oxidase B Homo sapiens 102-107 3921065-3 1985 With L-deprenyl 10-30 mg/day, the expected MAO B inhibition occurred, as indicated by significant increase in urinary PEA excretion and virtual disappearance of platelet MAO activity. Selegiline 5-15 monoamine oxidase B Homo sapiens 43-48 6335034-2 1984 MPTP is oxidized by brain mitochondrial preparations in a process which is blocked by deprenyl and pargyline, implying catalysis by monoamine oxidase B. Selegiline 86-94 monoamine oxidase B Homo sapiens 132-151 6437857-5 1984 In parkinsonian patients under long-term L-DOPA therapy monoamine oxidase inhibitors type B (MAO-B) e.g. (-)deprenyl and direct dopamine receptor agonists (bromocriptine, lisuride, pergolide etc. Selegiline 108-116 monoamine oxidase B Homo sapiens 93-98 6437857-7 1984 However, since (-)deprenyl, due to its metabolism to (-)methamphetamine and (-)amphetamine, seem to have indirect sympathomimetic activity, new selective MAO-B inhibitors devoid of indirect sympathomimetic effects should be tested clinically to assess the functional role of pure MAO-B inhibition in the therapy of PD. Selegiline 18-26 monoamine oxidase B Homo sapiens 154-159 6437857-7 1984 However, since (-)deprenyl, due to its metabolism to (-)methamphetamine and (-)amphetamine, seem to have indirect sympathomimetic activity, new selective MAO-B inhibitors devoid of indirect sympathomimetic effects should be tested clinically to assess the functional role of pure MAO-B inhibition in the therapy of PD. Selegiline 18-26 monoamine oxidase B Homo sapiens 280-285 6430257-1 1984 We investigated the antidepressant efficacy of l-deprenyl (selegiline), a selective monoamine oxidase B inhibitor (MAOI), in a six-week open trial of 17 patients with atypical depression. Selegiline 47-57 monoamine oxidase B Homo sapiens 84-103 6145282-6 1983 Our findings indicate that MAO-B inhibitors like deprenyl act by blocking neuronal and extra-neuronal MAO-B. Selegiline 49-57 monoamine oxidase B Homo sapiens 27-32 6428144-3 1983 Deprenyl, a selective MAO-B inhibitor, has produced good therapeutic effects in combination either with levodopa alone or with levodopa plus decarboxylase inhibitor in the treatment of end-of-dose akinesia and on-off phenomena. Selegiline 0-8 monoamine oxidase B Homo sapiens 22-27 6428147-1 1983 The role of deprenyl, a selective monoamine oxidase B inhibitor, in the treatment of Parkinson"s disease has been evaluated with special reference to the multiple pharmacological actions of the monoamine oxidase-inhibitory group of drugs. Selegiline 12-20 monoamine oxidase B Homo sapiens 34-53 6428148-14 1983 The possibility of countering these biochemical lesions of ageing by long-term administration of deprenyl, a selective inhibitor of MAO-B which facilitates dopaminergic and "trace-aminergic" activity in the brain, and is a safe drug in man, is considered in detail. Selegiline 97-105 monoamine oxidase B Homo sapiens 132-137 6145282-6 1983 Our findings indicate that MAO-B inhibitors like deprenyl act by blocking neuronal and extra-neuronal MAO-B. Selegiline 49-57 monoamine oxidase B Homo sapiens 102-107 6314420-0 1983 Clinical efficacy of deprenyl, a specific inhibitor of MAOB. Selegiline 21-29 monoamine oxidase B Homo sapiens 55-59 24875606-8 1983 Clorgyline injection selectively and completely inhibited MAO-A activity, while injection of clorgyline and deprenyl inhibited both MAO-A and MAO-B activities when embryos were assayed after either 2 or 7 days of embryonic development. Selegiline 108-116 monoamine oxidase B Homo sapiens 142-147 6768943-0 1980 L-deprenyl, a selective monoamine oxidase type-B inhibitor in endogenous depression. Selegiline 0-10 monoamine oxidase B Homo sapiens 24-48 6785797-0 1981 Is the failure of (-)deprenyl, a selective monoamine oxidase B inhibitor, to alleviate depression related to freedom from the cheese effect? Selegiline 18-29 monoamine oxidase B Homo sapiens 43-62 6777463-3 1980 The selective monoamine oxidase type B inhibitor deprenyl, which is extensively metabolised to amphetamine and methamphetamine, has this effect as well as possible actions on dopamine release and re-uptake. Selegiline 49-57 monoamine oxidase B Homo sapiens 14-38 20227955-4 1980 At commonly used substrate concentrations, deamination of Bz (sensitive to 10(-7) M deprenyl) was a better indicator of MAO B activity than deamination of PEA. Selegiline 84-92 monoamine oxidase B Homo sapiens 120-125 6802883-0 1982 The relative efficacy of l-deprenyl, a selective monoamine oxidase type B inhibitor, in endogenous and nonendogenous depression. Selegiline 25-35 monoamine oxidase B Homo sapiens 49-73 6791210-6 1981 The MAO-B inhibitor deprenyl appeared to maintain the greatest degree of MAO inhibition selectivity in vivo. Selegiline 20-28 monoamine oxidase B Homo sapiens 4-9 6791210-7 1981 Tyramine pressor sensitivity changes accompanying administration of the MAO inhibitors were highly correlated with decreases in plasma MHPG (r = 0.92), supporting our previous data indicating the rank order of clorgyline greater than pargyline greater than deprenyl for enhancement of tyramine pressor sensitivity and, thus, suggesting that tyramine potentiation is primarily a function of MAO-A rather than MAO-B inhibition. Selegiline 257-265 monoamine oxidase B Homo sapiens 408-413 219389-6 1979 In the present experiments, the administration of the monoamine oxidase type B inhibitor, deprenyl (1 mg per kilogram, IV), did not effect significant changes in cerebral blood flow or cerebral oxygen consumption. Selegiline 90-98 monoamine oxidase B Homo sapiens 54-78 6766730-0 1980 Deprenyl is a selective inhibitor of brain MAO-B in the long-term treatment of Parkinsons"s disease. Selegiline 0-8 monoamine oxidase B Homo sapiens 43-48 6776576-0 1980 The effect of deprenyl, a selective monoamine oxidase B inhibitor, on sleep and mood in man. Selegiline 14-22 monoamine oxidase B Homo sapiens 36-55 6774369-4 1980 The reaction was inhibited by low concentrations of (-)deprenyl, the specific MAO B inhibitor. Selegiline 52-63 monoamine oxidase B Homo sapiens 78-83 96466-0 1978 Deprenyl administration in man: a selective monoamine oxidase B inhibitor without the "cheese effect". Selegiline 0-8 monoamine oxidase B Homo sapiens 44-63 33759401-3 2021 Our aim was to check the clinical impression that some patients who were given selegiline, a selective inhibitor of monoamine oxidase B, experienced an improvement in their daytime somnolence. Selegiline 79-89 monoamine oxidase B Homo sapiens 116-135 745015-5 1978 Of those tried Deprenyl, an MAO-B inhibitor, given with levodopa and carbidopa has shown the most promise. Selegiline 15-23 monoamine oxidase B Homo sapiens 28-33 745019-1 1978 Deprenyl is an inhibitor of monoamine oxidase type B, the enzyme responsible for 2-phenylethylamine oxidation, and is used in conjunction with L-Dopa therapy in Parkinson"s disease. Selegiline 0-8 monoamine oxidase B Homo sapiens 28-52 71602-1 1977 In a double-blind crossover trial, (-)-deprenyl, a fast-acting selective monoamine-oxidase-B inhibitor without a "cheese effect", was given to 41 patients with idiopathic Parkinson"s disease who were receiving maximum tolerated doses of levodopa either alone or combined with carbidopa ("Sinemet"). Selegiline 35-47 monoamine oxidase B Homo sapiens 73-92 139953-2 1977 This decrease was prevented by pretreatment of the vesicles with deprenyl, a specific monoamine oxidase type B inhibitor. Selegiline 65-73 monoamine oxidase B Homo sapiens 86-110 1172524-0 1975 The potentiation of the anti akinetic effect after L-dopa treatment by an inhibitor of MAO-B, Deprenil. Selegiline 94-102 monoamine oxidase B Homo sapiens 87-92 1172524-6 1975 Deprenil is an inhibitor of MAO-B and is characterized by less frequent side effects. Selegiline 0-8 monoamine oxidase B Homo sapiens 28-33 33114548-5 2020 Docking studies revealed that the compounds 8-17 were stabilized in both MAO-B entrance and substrate cavities, thus resembling the binding pose of l-Deprenyl. Selegiline 148-158 monoamine oxidase B Homo sapiens 73-78 32476010-1 2021 Selegiline is a selective, irreversible monoamine oxidase-B inhibitor, used for reducing symptoms in early-stage Parkinson"s disease. Selegiline 0-10 monoamine oxidase B Homo sapiens 40-59 32858935-0 2020 Hydride Abstraction as the Rate-Limiting Step of the Irreversible Inhibition of Monoamine Oxidase B by Rasagiline and Selegiline: A Computational Empirical Valence Bond Study. Selegiline 118-128 monoamine oxidase B Homo sapiens 80-99 31562557-3 2020 The first was the elucidation of the novel pharmacological properties of selegiline as a selective MAO-B inhibitor by Knoll and Magyar and the original idea of Riederer and Youdim, supported by Birkmayer, to explore its effect in parkinsonian patients with on-off phases. Selegiline 73-83 monoamine oxidase B Homo sapiens 99-104 31562557-7 2020 Recently, cell and molecular studies revealed interesting properties of selegiline opening new possibilities for neuroprotective mechanisms and a disease-modifying effect of MAO-B inhibitors. Selegiline 72-82 monoamine oxidase B Homo sapiens 174-179 29309800-0 2018 Partial reversal of the effort-related motivational effects of tetrabenazine with the MAO-B inhibitor deprenyl (selegiline): Implications for treating motivational dysfunctions. Selegiline 102-110 monoamine oxidase B Homo sapiens 86-91 30160213-4 2019 Selegiline and rasagiline are irreversible inhibitors forming a covalent bond within the active site of MAOB. Selegiline 0-10 monoamine oxidase B Homo sapiens 104-108 29498006-9 2018 However, (-) deprenyl, a monoamine oxidase B (MAO B) inhibitor, attenuated MPTP-induced autophagic response and protected cell death. Selegiline 13-21 monoamine oxidase B Homo sapiens 25-44 29498006-9 2018 However, (-) deprenyl, a monoamine oxidase B (MAO B) inhibitor, attenuated MPTP-induced autophagic response and protected cell death. Selegiline 13-21 monoamine oxidase B Homo sapiens 46-51 29847694-11 2018 When ranking the MAO-B inhibitors given in combination with levodopa, selegiline was the most effective and rasagiline was the second best. Selegiline 70-80 monoamine oxidase B Homo sapiens 17-22 29847694-13 2018 Combination therapy with MAO-B inhibitors and levodopa showed that all three MAO-B inhibitors were effective compared to placebo, but selegiline was the most effective drug. Selegiline 134-144 monoamine oxidase B Homo sapiens 25-30 29847694-13 2018 Combination therapy with MAO-B inhibitors and levodopa showed that all three MAO-B inhibitors were effective compared to placebo, but selegiline was the most effective drug. Selegiline 134-144 monoamine oxidase B Homo sapiens 77-82 29671581-9 2018 The evaluation of docking results and pharmacokinetic profile predictions together with the MD simulations enabled us to identify one hit molecule (ligand 1, Otava ID: 3463218) which displayed higher selectivity toward MAO-B than a positive control selegiline which is a commercially used drug for PD therapeutic purposes. Selegiline 249-259 monoamine oxidase B Homo sapiens 219-224 29526790-3 2018 A clinical study in PD patients with motor complications has demonstrated that selegiline, a monoamine oxidase type B inhibitor, is effective in reducing off time without worsening dyskinesia, although another study has shown worsening dyskinesia. Selegiline 79-89 monoamine oxidase B Homo sapiens 93-117 29221756-7 2018 Selective monoamine oxidase B inhibitor, selegiline competed for the same site as [3H]d-deprenyl, but failed to differentiate the samples with regard to their inflammation grade. Selegiline 41-51 monoamine oxidase B Homo sapiens 10-29 32189109-0 2020 Retraction Note to: Meniere"s disease: combined pharmacotherapy with betahistine and the MAO-B inhibitor selegiline-an observational study. Selegiline 105-115 monoamine oxidase B Homo sapiens 89-94 31146671-4 2020 The performed monoamine oxidase B (MAO-B) inhibition study in vitro show that compounds 6g and 6i possess a significant MAO-B inhibition activity close to L-deprenyl. Selegiline 155-165 monoamine oxidase B Homo sapiens 35-40 31146671-4 2020 The performed monoamine oxidase B (MAO-B) inhibition study in vitro show that compounds 6g and 6i possess a significant MAO-B inhibition activity close to L-deprenyl. Selegiline 155-165 monoamine oxidase B Homo sapiens 120-125 31589885-6 2020 In PET studies of NHP brain administration of the MAO-B ligand L-deprenyl inhibited binding of radiolabeled AZD9272 and administration of fenobam inhibited binding of [11C]L-deprenyl-D2. Selegiline 63-73 monoamine oxidase B Homo sapiens 50-55 31264403-3 2019 Still, despite this practical importance, the precise chemical mechanisms underlying the irreversible inhibition of the MAO B isoform with clinical drugs rasagiline (RAS) and selegiline (SEL) remained unknown. Selegiline 175-185 monoamine oxidase B Homo sapiens 120-125 31264403-3 2019 Still, despite this practical importance, the precise chemical mechanisms underlying the irreversible inhibition of the MAO B isoform with clinical drugs rasagiline (RAS) and selegiline (SEL) remained unknown. Selegiline 187-190 monoamine oxidase B Homo sapiens 120-125 30906861-2 2019 Although short-term treatment with irreversible MAO-B inhibitors, such as selegiline, improves cognitive deficits in AD patients, long-term treatments have shown disappointing results. Selegiline 74-84 monoamine oxidase B Homo sapiens 48-53 30857558-9 2019 Of note, [F-18]-MK-6240 and [F-18]-AV-1451 autoradiographic binding signals were only weakly displaced by competing concentrations of selective MAO-B inhibitor deprenyl but not by MAO-A inhibitor clorgyline, suggesting that MAO enzymes do not appear to be a significant binding target of any of these two tracers. Selegiline 160-168 monoamine oxidase B Homo sapiens 144-149 30272370-6 2018 L-deprenyl is known to target monoamine oxidase-B (MAO-B) on the outer membrane of mitochondria, therefore, the activity of MAO-A and -B was measured based on the fluorometric detection of H2O2 produced by the enzyme reaction. Selegiline 0-10 monoamine oxidase B Homo sapiens 30-49 30272370-6 2018 L-deprenyl is known to target monoamine oxidase-B (MAO-B) on the outer membrane of mitochondria, therefore, the activity of MAO-A and -B was measured based on the fluorometric detection of H2O2 produced by the enzyme reaction. Selegiline 0-10 monoamine oxidase B Homo sapiens 51-56 29279995-7 2018 MAO-B inhibitors selegiline and rasagiline protect neurons via increase expression of anti-apoptotic Bcl-2 and pro-survival neurotrophic factors in human neuroblastoma SH-SY5Y and glioblastoma U118MG cell lines. Selegiline 17-27 monoamine oxidase B Homo sapiens 0-5 29279995-8 2018 MAO-A knockdown suppressed the rasagiline-induced gene expression in SH-SY5Y cells, whereas MAO-B silencing enhanced the basal- and selegiline-induced gene expression in U118MG cells. Selegiline 132-142 monoamine oxidase B Homo sapiens 92-97 29417334-0 2018 Pharmacological aspects of the neuroprotective effects of irreversible MAO-B inhibitors, selegiline and rasagiline, in Parkinson"s disease. Selegiline 89-99 monoamine oxidase B Homo sapiens 71-76 29417334-6 2018 Extensive studies with selegiline indicated its complex pharmacological activity profile with MAO-B-independent mechanisms involved. Selegiline 23-33 monoamine oxidase B Homo sapiens 94-99 30341696-6 2018 Selective inhibitors of MAO-B (selegiline, rasagiline and safinamide) have found a therapeutic role in the treatment of Parkinson"s disease and reversible inhibitors of MAO-A offered antidepressant activity without the serious side effects of the earlier nonselective MAO inhibitors. Selegiline 31-41 monoamine oxidase B Homo sapiens 24-29 29532287-0 2018 Meniere"s disease: combined pharmacotherapy with betahistine and the MAO-B inhibitor selegiline-an observational study. Selegiline 85-95 monoamine oxidase B Homo sapiens 69-74 29532287-11 2018 CONCLUSIONS: The achievement of the same clinical effect with a significantly lower (about 1/5) dosage of betahistine can be explained by the inhibition of the MAO-B by selegiline leading to higher serum concentrations of betahistine. Selegiline 169-179 monoamine oxidase B Homo sapiens 160-165 30016860-2 2018 To target peripheral tissues using MAO-B inhibitors that do not permeate the blood-brain barrier (BBB) the MAO-B-selective inhibitor deprenyl was remodeled by replacing the terminal acetylene with a CO2H function, and incorporating a para-OCH2Ar motif (compounds 10a-s). Selegiline 133-141 monoamine oxidase B Homo sapiens 35-40 30016860-2 2018 To target peripheral tissues using MAO-B inhibitors that do not permeate the blood-brain barrier (BBB) the MAO-B-selective inhibitor deprenyl was remodeled by replacing the terminal acetylene with a CO2H function, and incorporating a para-OCH2Ar motif (compounds 10a-s). Selegiline 133-141 monoamine oxidase B Homo sapiens 107-112 30077198-4 2018 The most widely used MAO-B inhibitor to maintain the bioavailability of dopamine in the brain of PD patients is L-deprenyl, despite of its potential side-effects. Selegiline 112-122 monoamine oxidase B Homo sapiens 21-26 29955193-7 2018 Data Synthesis: The search identified 8 studies evaluating the potential interaction between SSRIs and the MAO-B inhibitors selegiline and rasagiline. Selegiline 124-134 monoamine oxidase B Homo sapiens 107-112 29309800-0 2018 Partial reversal of the effort-related motivational effects of tetrabenazine with the MAO-B inhibitor deprenyl (selegiline): Implications for treating motivational dysfunctions. Selegiline 112-122 monoamine oxidase B Homo sapiens 86-91 29309800-7 2018 These effects of 0.75mg/kg tetrabenazine were attenuated by co-administration of the MAO-B inhibitor deprenyl (selegiline). Selegiline 101-109 monoamine oxidase B Homo sapiens 85-90 29309800-7 2018 These effects of 0.75mg/kg tetrabenazine were attenuated by co-administration of the MAO-B inhibitor deprenyl (selegiline). Selegiline 111-121 monoamine oxidase B Homo sapiens 85-90 29229003-12 2017 Both THK5117 and T807 demonstrated off-target binding in the hippocampus and putamen with a ten times lower binding affinity to the MAO-B inhibitor deprenyl compared with 3H-THK5351. Selegiline 148-156 monoamine oxidase B Homo sapiens 132-137 28550482-1 2017 Monoamine oxidase type B (MAO-B) inhibitors, such as selegiline and rasagiline, can be used as monotherapy or adjuvant therapy to levodopa in Parkinson"s disease (PD). Selegiline 53-63 monoamine oxidase B Homo sapiens 0-24 29114238-2 2017 Methods: Using the PGR, we recorded the daily walking profiles of 14 PD patients before and after the addition or increase in dose of an MAO-B inhibitor (selegiline, average dose: 4.0 mg/day) as part of their medicine regimen, and evaluated their gait using the unified Parkinson"s disease rating scale (UPDRS) and scores from a freezing of gait (FOG) questionnaire. Selegiline 154-164 monoamine oxidase B Homo sapiens 137-142 28738644-4 2017 Inhibition of hMAO B is evaluated by adding different concentrations of the inhibitor selegiline hydrochloride to the enzyme and applying a defined amount of the hMAO B substrate phenylethylamine (PEA). Selegiline 86-110 monoamine oxidase B Homo sapiens 14-20 28577058-2 2017 MAO-B inhibitors, rasagiline and selegiline [(-)deprenyl], protect neurons in animal and cellular models of neurodegeneration. Selegiline 45-56 monoamine oxidase B Homo sapiens 0-5 28577058-5 2017 Selegiline significantly increased Mao-B, which was suppressed by Mao-A knockdown with short interfering (si)RNA, whereas rasagiline less markedly increased Mao-B, which was not affected by Mao-A knockdown. Selegiline 0-10 monoamine oxidase B Homo sapiens 35-40 28577058-6 2017 Mao-A mRNA was also markedly increased by rasagiline and selegiline, and Mao-B knockdown significantly enhanced the induction by selegiline, but not by rasagiline. Selegiline 129-139 monoamine oxidase B Homo sapiens 73-78 28577058-8 2017 Selegiline synergistically enhanced the expression of these genes in Mao-B knockdown cells, but Mao-A knockdown suppressed the increase. Selegiline 0-10 monoamine oxidase B Homo sapiens 69-74 28577058-10 2017 These results show that MAO-B might function as a repressor and MAO-A as a mediator in the constitutional expression of pro-survival genes, and that MAO-B and MAO-A might regulate different signal pathways for rasagiline and selegiline to induce neuroprotective genes. Selegiline 225-235 monoamine oxidase B Homo sapiens 149-154 28299453-4 2017 We confirm with this design, that rasagiline and selegiline inhibit monoamine oxidase-B but not monoamine oxidase-A after single dosing. Selegiline 49-59 monoamine oxidase B Homo sapiens 68-87 28550482-1 2017 Monoamine oxidase type B (MAO-B) inhibitors, such as selegiline and rasagiline, can be used as monotherapy or adjuvant therapy to levodopa in Parkinson"s disease (PD). Selegiline 53-63 monoamine oxidase B Homo sapiens 26-31 28359327-0 2017 Monoamine oxidase B inhibitor, selegiline, reduces 18F-THK5351 uptake in the human brain. Selegiline 31-41 monoamine oxidase B Homo sapiens 0-19 28301816-8 2017 The reference drugs selegiline (IC50 = 0.040 muM) and rasagiline (IC50 = 0.066 muM) also displayed a significant inhibition against hMAO-B. Selegiline 20-30 monoamine oxidase B Homo sapiens 132-138 25604428-3 2016 It has been suggested that the irreversible MAO-B inhibitors selegiline and rasagiline exert a neuroprotective effect in Parkinson"s and Alzheimer"s diseases. Selegiline 61-71 monoamine oxidase B Homo sapiens 44-49 27373997-5 2016 It was found to be better than the standard drug, selegiline (hMAO-B with Ki = 0.20 +- 0.020 muM) with a selectivity index of 30.55. Selegiline 50-60 monoamine oxidase B Homo sapiens 62-68 27058977-0 2016 High-throughput screening and radioligand binding studies reveal monoamine oxidase-B as the primary binding target for d-deprenyl. Selegiline 119-129 monoamine oxidase B Homo sapiens 65-84 27058977-7 2016 KEY FINDINGS: Our high-throughput investigation identified monoamine oxidase-B, monoamine oxidase-A and angiotensin converting enzyme as potential targets for d-deprenyl. Selegiline 159-169 monoamine oxidase B Homo sapiens 59-78 27058977-11 2016 It verified 249 candidate proteins and confirmed the role of monoamine oxidase - B in d-deprenyl binding. Selegiline 86-96 monoamine oxidase B Homo sapiens 61-82 26964672-3 2016 Compound 3u (IC50=221 nM) exhibited the best inhibitory activity and isoform selectivity against hMAO-B, superior to selegiline (IC50=321 nM), which is a commercial selective hMAO-B inhibitor used to Parkinson"s disease. Selegiline 117-127 monoamine oxidase B Homo sapiens 175-181 27061066-0 2016 Rotigotine in Combination with the MAO-B Inhibitor Selegiline in Early Parkinson"s Disease: A Post Hoc Analysis. Selegiline 51-61 monoamine oxidase B Homo sapiens 35-40 26590367-6 2016 Deprenyl is a selective and irreversible inhibitor of monoamine oxidase-B, and administration of deprenyl produced a dose-related suppression of TBZ-induced TJMs. Selegiline 0-8 monoamine oxidase B Homo sapiens 54-73 26585057-1 2016 UNLABELLED: The aim of this study was to radiolabel a novel bis-deuterium substituted l-deprenyl analog (fluorodeprenyl-D2) with (18)F and to evaluate its potential to visualize and quantify monoamine oxidase (MAO) B activity in vivo. Selegiline 86-96 monoamine oxidase B Homo sapiens 191-216 26585057-13 2016 Administration of a 1 mg/kg dose of l-deprenyl yielded 70% inhibition of MAO-B in all regions. Selegiline 36-46 monoamine oxidase B Homo sapiens 73-78 28108387-0 2017 Inhibition of monoamine oxidase-B by selegiline reduces cigarette smoke-induced oxidative stress and inflammation in airway epithelial cells. Selegiline 37-47 monoamine oxidase B Homo sapiens 14-33 28108387-4 2017 Pretreatment with MAO-B selective inhibitor selegiline reversed the CSM-induced changes in MAO-B activity, ROS levels and IL-8 release in a dose-dependent manner. Selegiline 44-54 monoamine oxidase B Homo sapiens 18-23 28108387-4 2017 Pretreatment with MAO-B selective inhibitor selegiline reversed the CSM-induced changes in MAO-B activity, ROS levels and IL-8 release in a dose-dependent manner. Selegiline 44-54 monoamine oxidase B Homo sapiens 91-96 28108387-8 2017 Our study demonstrated that in AECs, inhibition of MAO-B using selegiline reversed the CSM-induced oxidative stress and inflammation. Selegiline 63-73 monoamine oxidase B Homo sapiens 51-56 26352677-3 2015 The most potent selective hMAO-B inhibitor D7 has a selectivity ratio of 20.93, with an IC50 value of 2.78 muM, similar or better than selegiline (IC50 = 2.89 muM), a selective hMAO-B inhibitor currently in the market for the treatment of Parkinson"s disease. Selegiline 135-145 monoamine oxidase B Homo sapiens 26-32 24769350-3 2014 In designing the compounds we focused on the structures of rasagiline and selegiline, two well known MAO-B inhibitors and proposed neuroprotective agents. Selegiline 74-84 monoamine oxidase B Homo sapiens 101-106 25677185-9 2015 Moreover, maturation of MP-MUS is highly dependent on MAO-B, and inhibition of MAO-B activity with selegiline protected human glioma cells from apoptosis. Selegiline 99-109 monoamine oxidase B Homo sapiens 79-84 25514361-1 2015 Rasagiline (N-propargyl-1-R-aminoindan) and selegiline (1-deprenyl) are MAO-B inhibitors which are used in the treatment of Parkinson"s disease. Selegiline 44-54 monoamine oxidase B Homo sapiens 72-77 24964753-13 2015 MAO-B inhibitors of the N-propargylamine type (e.g., selegiline) also counteract the DSP4-induced neurotoxicity with another, yet unknown mechanism. Selegiline 53-63 monoamine oxidase B Homo sapiens 0-5 24937131-9 2014 The adenosine A2A antagonist MSX-3, the antidepressant and catecholamine uptake inhibitor bupropion, and the MAO-B inhibitor deprenyl, all reversed the impairments induced by tetrabenazine. Selegiline 125-133 monoamine oxidase B Homo sapiens 109-114 26189013-4 2015 The most potent compound (2E)-1-(4-methoxyphenyl)-3-[4-(trifluoromethyl)phenyl] prop-2-en-1-one showed the best activity and higher selectivity towards hMAO-B with Ki and SI values of 0.22+-0.01muM and 0.05 comparable to that standard drug, Selegiline Ki and SI values were found as 0.33+-0.03muM and 0.04, respectively. Selegiline 241-251 monoamine oxidase B Homo sapiens 152-158 26337020-2 2015 Among them, compound 10b including alpha,beta-unsaturated ketone group showed the most potent and selective MAO-B inhibitory activity (IC50 human MAO-B 16 nM, >6000-fold selective vs MAO-A) and compound 10b exhibited good reversibility compared with selegiline, a well-known irreversible MAO-B inhibitor. Selegiline 253-263 monoamine oxidase B Homo sapiens 108-113 25863936-1 2015 Rasagiline and selegiline, inhibitors of type B monoamine oxidase (MAO-B), protect neurons from cell death in cellular and animal models. Selegiline 15-25 monoamine oxidase B Homo sapiens 67-72 25572450-2 2015 A potential pharmaceutical treatment for smoking cessation is selegiline, a selective and irreversible monoamine oxidase B inhibitor. Selegiline 62-72 monoamine oxidase B Homo sapiens 103-122 26164425-2 2015 Selegiline was the first MAO-B to be used therapeutically, while rasagiline is a second-generation drug with higher potency and selectivity. Selegiline 0-10 monoamine oxidase B Homo sapiens 25-30 25592412-1 2015 INTRODUCTION: Selegiline (l-deprenyl) is a selective monoamine oxidase type B inhibitor that has been shown to have neurotrophic and anti-apoptotic properties and to protect neurons in different experimental models of cerebral ischaemia. Selegiline 14-24 monoamine oxidase B Homo sapiens 53-77 25592412-1 2015 INTRODUCTION: Selegiline (l-deprenyl) is a selective monoamine oxidase type B inhibitor that has been shown to have neurotrophic and anti-apoptotic properties and to protect neurons in different experimental models of cerebral ischaemia. Selegiline 26-36 monoamine oxidase B Homo sapiens 53-77 25532905-2 2015 Compounds 2, 3, 5 and 6 presented a better activity and selectivity profile against the hMAO-B isoform (IC50 values between 2 and 6nM) than selegiline. Selegiline 140-150 monoamine oxidase B Homo sapiens 88-94 25249059-0 2015 Evidence that formulations of the selective MAO-B inhibitor, selegiline, which bypass first-pass metabolism, also inhibit MAO-A in the human brain. Selegiline 61-71 monoamine oxidase B Homo sapiens 44-49 25249059-1 2015 Selegiline (L-deprenyl) is a selective, irreversible inhibitor of monoamine oxidase B (MAO-B) at the conventional dose (10 mg/day oral) that is used in the treatment of Parkinson"s disease. Selegiline 0-10 monoamine oxidase B Homo sapiens 66-85 25249059-1 2015 Selegiline (L-deprenyl) is a selective, irreversible inhibitor of monoamine oxidase B (MAO-B) at the conventional dose (10 mg/day oral) that is used in the treatment of Parkinson"s disease. Selegiline 0-10 monoamine oxidase B Homo sapiens 87-92 25249059-1 2015 Selegiline (L-deprenyl) is a selective, irreversible inhibitor of monoamine oxidase B (MAO-B) at the conventional dose (10 mg/day oral) that is used in the treatment of Parkinson"s disease. Selegiline 12-22 monoamine oxidase B Homo sapiens 66-85 25249059-1 2015 Selegiline (L-deprenyl) is a selective, irreversible inhibitor of monoamine oxidase B (MAO-B) at the conventional dose (10 mg/day oral) that is used in the treatment of Parkinson"s disease. Selegiline 12-22 monoamine oxidase B Homo sapiens 87-92 24012376-11 2013 An efficient radiolabeling of 9 was successfully established and in the monkey brain 9 binds to MAO-B rich regions and its binding is blocked by the selective MAO-B compound l-deprenyl. Selegiline 174-184 monoamine oxidase B Homo sapiens 96-101 24012376-11 2013 An efficient radiolabeling of 9 was successfully established and in the monkey brain 9 binds to MAO-B rich regions and its binding is blocked by the selective MAO-B compound l-deprenyl. Selegiline 174-184 monoamine oxidase B Homo sapiens 159-164 24005822-3 2013 Selegiline is a selective and irreversible MAO-B inhibitor and, although clinical trials already shown the beneficial effect of selegiline on cognition of AD patients, its mechanism of action remains to be elucidated. Selegiline 0-10 monoamine oxidase B Homo sapiens 43-48 23410524-4 2013 l-Deprenyl and rasagiline, both selective MAO-B inhibitors, are used in the management of Parkinson"s disease, but these drugs may be useful in the treatment of other neurodegenerative disorders given that they demonstrate neuroprotective/neurorescue properties in a wide variety of models in vitro and in vivo. Selegiline 0-10 monoamine oxidase B Homo sapiens 42-47 23611731-3 2013 In this study, however, we found that selective MAO-A inhibitors, moclobemide and Ro41-1049, and a selective MAO-B inhibitor, selegiline, promoted adiponectin production during adipocyte differentiation in hBM-MSCs, which suggested the anti-diabetic potential of these drugs. Selegiline 126-136 monoamine oxidase B Homo sapiens 109-114 23474901-5 2013 This in vitro MAO-B inhibitory activity is comparable with that of the selegiline, the reference compound (IC50 against MAO-B = 20 nM). Selegiline 71-81 monoamine oxidase B Homo sapiens 14-19 23420173-4 2013 Selegiline, a selective MAO-B inhibitor, known to have beneficial effects in the brain regions which are rich by dopamine receptors, however, studies based on brain targeting of selegiline are limited. Selegiline 0-10 monoamine oxidase B Homo sapiens 24-29 23420173-5 2013 Since some recent studies showed the possible Abeta-fibril destabilizing effects of MAO inhibitors, present study was designed to (1) prepare the selective MAO-B inhibitor selegiline-loaded Poly (lactic-co-glycolic acid)-poly (ethylene glycol) (PLGA-b-PEG) nanoparticles (2) to investigate the in vitro Abeta-fibril destabilizing effect of the loaded particles. Selegiline 172-182 monoamine oxidase B Homo sapiens 156-161 23328949-4 2013 Among the compounds examined, compound 16 was found to be more selective than selegiline, a known MAO-B inhibitor, in respect to the K i values experimentally found. Selegiline 78-88 monoamine oxidase B Homo sapiens 98-103 23506388-4 2013 The selective monoamine oxidase B inhibitor, selegiline , is widely used in the treatment of Parkinson"s disease. Selegiline 45-55 monoamine oxidase B Homo sapiens 14-33 23474901-5 2013 This in vitro MAO-B inhibitory activity is comparable with that of the selegiline, the reference compound (IC50 against MAO-B = 20 nM). Selegiline 71-81 monoamine oxidase B Homo sapiens 120-125 22954444-1 2012 The objective was to investigate the anodal iontophoresis of the MAO-B inhibitors rasagiline (RAS) and selegiline (SEL) across porcine and human skin in vitro. Selegiline 115-118 monoamine oxidase B Homo sapiens 65-70 22968599-2 2013 MAO-B inhibitors, rasagiline and selegiline [(-)deprenyl], protect neuronal cells by direct intervention in mitochondrial death signaling and induction of pro-survival Bcl-2 and neurotrophic factors. Selegiline 33-43 monoamine oxidase B Homo sapiens 0-5 22968599-2 2013 MAO-B inhibitors, rasagiline and selegiline [(-)deprenyl], protect neuronal cells by direct intervention in mitochondrial death signaling and induction of pro-survival Bcl-2 and neurotrophic factors. Selegiline 45-56 monoamine oxidase B Homo sapiens 0-5 23281824-4 2013 Two analogues of 17f, namely 18b and 19a, inhibit MAO-B with IC(50) of 68 and 48 nM, respectively, being 5-7-fold more potent than the prototypical MAO-B inhibitor deprenyl (IC(50) = 334 nM). Selegiline 164-172 monoamine oxidase B Homo sapiens 148-153 23620664-8 2013 Monoamine oxidase-B inhibitors (eg, selegiline) inhibit alpha-synuclein nitration, implicated in Lewy body formation, and inhibit 1-methyl 4-phenylpyridinium and 3-morpholinosydnonimine-induced apoptosis in cultured human dopaminergic neurons and mesencephalic fetal stem cells. Selegiline 36-46 monoamine oxidase B Homo sapiens 0-19 24204150-1 2013 We report a case in which selegiline, an irreversible monoamine oxidase B (MAO-B) inhibitor, greatly improved depressive symptoms in an adult with stage 5 treatment-resistant major depressive disorder. Selegiline 26-36 monoamine oxidase B Homo sapiens 54-73 24204150-1 2013 We report a case in which selegiline, an irreversible monoamine oxidase B (MAO-B) inhibitor, greatly improved depressive symptoms in an adult with stage 5 treatment-resistant major depressive disorder. Selegiline 26-36 monoamine oxidase B Homo sapiens 75-80 22065207-1 2012 Rasagiline and (-)deprenyl (selegiline), irreversible type B monoamine oxidase (MAO-B) inhibitors, protect neuronal cells through gene induction of pro-survival Bcl-2 and neurotrophic factors in the cellular models of neurodegenerative disorders. Selegiline 18-26 monoamine oxidase B Homo sapiens 80-85 22691758-3 2012 In this review, we focus on recent studies with monoamine oxidase type B inhibitors (selegiline and rasagiline), coenzyme Q10, creatine, and exercise in early Parkinson"s disease. Selegiline 85-95 monoamine oxidase B Homo sapiens 48-72 22592509-1 2012 Selegiline at the doses used in Parkinson disease is a selective irreversible monoamine oxidase type B inhibitor, which potentiates dopaminergic function in the brain, and is used as monotherapy in early Parkinson disease or in combination with levodopa in more advanced disease. Selegiline 0-10 monoamine oxidase B Homo sapiens 78-102 22086140-1 2012 Selegiline (R-deprenyl), a monoamine oxidase-B (MAO-B) inhibitor, has complex pharmacological effect that contributes to treatment of neurodegenerative diseases such as Parkinson"s and presumably Alzheimer"s disease and might work as an inhibitor of tumor growth. Selegiline 0-10 monoamine oxidase B Homo sapiens 27-46 22086140-1 2012 Selegiline (R-deprenyl), a monoamine oxidase-B (MAO-B) inhibitor, has complex pharmacological effect that contributes to treatment of neurodegenerative diseases such as Parkinson"s and presumably Alzheimer"s disease and might work as an inhibitor of tumor growth. Selegiline 0-10 monoamine oxidase B Homo sapiens 48-53 22065207-1 2012 Rasagiline and (-)deprenyl (selegiline), irreversible type B monoamine oxidase (MAO-B) inhibitors, protect neuronal cells through gene induction of pro-survival Bcl-2 and neurotrophic factors in the cellular models of neurodegenerative disorders. Selegiline 28-38 monoamine oxidase B Homo sapiens 80-85 22133327-4 2011 Two MAO-B inhibitors, selegiline and rasagiline, are currently licensed in Europe and North America for the symptomatic improvement of early Parkinson"s disease and to reduce off-time in patients with more advanced Parkinson"s disease and motor fluctuations related to levodopa. Selegiline 22-32 monoamine oxidase B Homo sapiens 4-9 23231395-2 2012 MAO-B oxidizes MPTP into MPP+, and an MAO-B inhibitor, deprenyl, prevents the MPTP oxidation and also MPP+neutotoxicity. Selegiline 55-63 monoamine oxidase B Homo sapiens 38-43 23231395-4 2012 On the other hand, deprenyl and rasagiline, selective MAO-B inhibitors, have been proved to protect neuronal cells in cellular and animal models of neurodegeneration. Selegiline 19-27 monoamine oxidase B Homo sapiens 54-59 21858609-0 2011 Effects of selegiline, a monoamine oxidase B inhibitor, on differentiation of P19 embryonal carcinoma stem cells, into neuron-like cells. Selegiline 11-21 monoamine oxidase B Homo sapiens 25-44 21923198-0 2011 Synthesis of three novel fluorine-18 labeled analogues of L-deprenyl for positron emission tomography (PET) studies of monoamine oxidase B (MAO-B). Selegiline 58-68 monoamine oxidase B Homo sapiens 119-138 21923198-0 2011 Synthesis of three novel fluorine-18 labeled analogues of L-deprenyl for positron emission tomography (PET) studies of monoamine oxidase B (MAO-B). Selegiline 58-68 monoamine oxidase B Homo sapiens 140-145 21923198-1 2011 The aim in this project was to synthesize and to study fluorine-18 labeled analogues of l-deprenyl which bind selectively to the enzyme monoamine oxidase B (MAO-B). Selegiline 88-98 monoamine oxidase B Homo sapiens 136-155 21923198-1 2011 The aim in this project was to synthesize and to study fluorine-18 labeled analogues of l-deprenyl which bind selectively to the enzyme monoamine oxidase B (MAO-B). Selegiline 88-98 monoamine oxidase B Homo sapiens 157-162 21939547-4 2011 DISCUSSION: In multiple studies, MAO-B inhibitors, such as selegiline and rasagiline, have shown to provide mild symptomatic effects, delay the need for levodopa, and to reduce the incidence of motor fluctuations. Selegiline 59-69 monoamine oxidase B Homo sapiens 33-38 21858609-1 2011 Selegiline, the irreversible inhibitor of monoamine oxidase B (MAO-B), is currently used to treat Parkinson"s disease. Selegiline 0-10 monoamine oxidase B Homo sapiens 63-68 21858609-2 2011 However, the mechanism of action of selegiline is complex and cannot be explained solely by its MAO-B inhibitory action. Selegiline 36-46 monoamine oxidase B Homo sapiens 96-101 21858609-10 2011 The peak response was in a dose of selegiline significantly lower than required for MAO-B inhibition. Selegiline 35-45 monoamine oxidase B Homo sapiens 84-89 21858609-1 2011 Selegiline, the irreversible inhibitor of monoamine oxidase B (MAO-B), is currently used to treat Parkinson"s disease. Selegiline 0-10 monoamine oxidase B Homo sapiens 42-61 21423589-4 2011 This review focuses on rasagiline and selegiline, two medications that belong to a class of antiparkinsonian drugs called monoamine oxidase B (MAO-B) inhibitors. Selegiline 38-48 monoamine oxidase B Homo sapiens 122-141 21626552-2 2011 A few dopamine agonists and a monoamine oxidase B inhibitor (selegiline) were used as adjuncts in advanced Parkinson"s disease. Selegiline 61-71 monoamine oxidase B Homo sapiens 30-49 25205926-5 2011 Other pharmacological measures like catechol-O-methyltrasferase (COMT) inhibitors like entacopone, telcapone and monoamine oxidase B (MAO-B) inhibitors like selegiline and rasagiline are also useful, while L-dopa remains the gold standard in the treatment of PD. Selegiline 157-167 monoamine oxidase B Homo sapiens 134-139 22110357-4 2011 For the treatment of akinesia and motor fluctuations selective irreversible MAO-B inhibitors selegiline and rasagiline are recommended. Selegiline 93-103 monoamine oxidase B Homo sapiens 76-81 21423589-4 2011 This review focuses on rasagiline and selegiline, two medications that belong to a class of antiparkinsonian drugs called monoamine oxidase B (MAO-B) inhibitors. Selegiline 38-48 monoamine oxidase B Homo sapiens 143-148 21224199-2 2011 The first monoamine oxidase (MAO-B) inhibitor for PD, selegiline (Eldepryl), was approved by the Food and Drug Administration (FDA) in 1996, and rasagiline (Azilect) received FDA approval in 2006. Selegiline 54-64 monoamine oxidase B Homo sapiens 29-34 21224199-2 2011 The first monoamine oxidase (MAO-B) inhibitor for PD, selegiline (Eldepryl), was approved by the Food and Drug Administration (FDA) in 1996, and rasagiline (Azilect) received FDA approval in 2006. Selegiline 66-74 monoamine oxidase B Homo sapiens 29-34 21224199-8 2011 It also says, "the selectivity of selegiline for MAO B may not be absolute, even at the recommended daily dose." Selegiline 34-44 monoamine oxidase B Homo sapiens 49-54 21971003-1 2011 Selegiline, the R-optical enantiomer of deprenyl (phenyl-isopropyl-methyl-propargylamine), was almost exclusively used MAO-B inhibitor during the past decades to treat Parkinson"s disease. Selegiline 0-10 monoamine oxidase B Homo sapiens 119-124 20725780-2 2010 The R-enantiomer of deprenyl (selegiline) is a selective and irreversible inhibitor of the B-isoform of monoamine oxidase (MAO-B) enzyme. Selegiline 20-28 monoamine oxidase B Homo sapiens 123-128 21075154-2 2011 As astrocyte activity and, consequently, the activity of the MAO-B enzyme, is up-regulated in neuroinflammatory processes, radiolabelled analogues of deprenyl may serve as an imaging biomarker in neuroinflammation and neurodegeneration, including Alzheimer"s disease. Selegiline 150-158 monoamine oxidase B Homo sapiens 61-66 21075154-3 2011 In the present study [(11)C]-L-deprenyl, the PET radioligand version of L-deprenyl or selegiline , a selective irreversible MAO-B inhibitor was used in whole hemisphere autoradiographic experiments in human brain sections in order to test the radioligand"s binding to the MAO-B enzyme in human brain tissue, with an eye on exploring the radioligand"s applicability as a molecular imaging biomarker in human PET studies, with special regard to diagnostic detection of reactive astrogliosis. Selegiline 29-39 monoamine oxidase B Homo sapiens 124-129 21075154-3 2011 In the present study [(11)C]-L-deprenyl, the PET radioligand version of L-deprenyl or selegiline , a selective irreversible MAO-B inhibitor was used in whole hemisphere autoradiographic experiments in human brain sections in order to test the radioligand"s binding to the MAO-B enzyme in human brain tissue, with an eye on exploring the radioligand"s applicability as a molecular imaging biomarker in human PET studies, with special regard to diagnostic detection of reactive astrogliosis. Selegiline 29-39 monoamine oxidase B Homo sapiens 272-277 21075154-3 2011 In the present study [(11)C]-L-deprenyl, the PET radioligand version of L-deprenyl or selegiline , a selective irreversible MAO-B inhibitor was used in whole hemisphere autoradiographic experiments in human brain sections in order to test the radioligand"s binding to the MAO-B enzyme in human brain tissue, with an eye on exploring the radioligand"s applicability as a molecular imaging biomarker in human PET studies, with special regard to diagnostic detection of reactive astrogliosis. Selegiline 86-96 monoamine oxidase B Homo sapiens 124-129 21075154-11 2011 Compounds with high affinity for the PBR system did not block the radioligand binding either, providing evidence for the specificity of [(11)C]-L-deprenyl for the MAO-B enzyme. Selegiline 142-154 monoamine oxidase B Homo sapiens 163-168 20725780-2 2010 The R-enantiomer of deprenyl (selegiline) is a selective and irreversible inhibitor of the B-isoform of monoamine oxidase (MAO-B) enzyme. Selegiline 30-40 monoamine oxidase B Homo sapiens 123-128 19687003-3 2009 Moclobemide is a reversible inhibitor of monoamine oxidase (MAO)-A, selegiline is an irreversible selective inhibitor of MAO-B, and paroxetine is a selective serotonin reuptake inhibitor. Selegiline 68-78 monoamine oxidase B Homo sapiens 121-126 20839183-4 2010 The versatility of this new nitrogen protecting group is illustrated with a new synthesis of Selegiline, a monoamine oxidase-B inhibitor marketed for the treatment of Parkinson"s disease. Selegiline 93-103 monoamine oxidase B Homo sapiens 107-126 20022592-10 2010 Knockdown expression of GAPDH or treatment with MAO B inhibitors selegiline (deprenyl) and rasagiline (Azilect) can block this cascade. Selegiline 65-75 monoamine oxidase B Homo sapiens 48-53 20022592-10 2010 Knockdown expression of GAPDH or treatment with MAO B inhibitors selegiline (deprenyl) and rasagiline (Azilect) can block this cascade. Selegiline 77-85 monoamine oxidase B Homo sapiens 48-53 19939587-1 2010 AIM: The primary aim of this study was to determine the safety and efficacy of the monoamine oxidase-B (MAO-B) inhibitor selegiline hydrochloride (SEL, l-Deprenyl; Eldepryl) as an aid for smoking cessation in cigarette smokers. Selegiline 164-172 monoamine oxidase B Homo sapiens 83-102 19939587-1 2010 AIM: The primary aim of this study was to determine the safety and efficacy of the monoamine oxidase-B (MAO-B) inhibitor selegiline hydrochloride (SEL, l-Deprenyl; Eldepryl) as an aid for smoking cessation in cigarette smokers. Selegiline 164-172 monoamine oxidase B Homo sapiens 104-109 20150659-6 2009 However, Knoll demonstrated in his later work that (-)-deprenyl has enhancing qualities already in femto-picomolar concentrations, which leave MAO-B activity unchanged, and the activity of the catecholaminergic neurons in the brain stem and this previously unknown "enhancer effect" is responsible for the peculiar therapeutic benefits caused by (-)-deprenyl. Selegiline 51-63 monoamine oxidase B Homo sapiens 143-148 20659799-4 2010 Compounds 4 (IC(50)=11.05 nM), 5 (IC(50)=3.23 nM) and 6 (IC(50)=7.12 nM) show higher activity than selegiline (IC(50)=19.60 nM) and higher MAO-B selectivity, with more than 9050-fold, 30,960-fold and 14,045-fold inhibition levels, with respect to the MAO-A isoform. Selegiline 99-109 monoamine oxidase B Homo sapiens 139-144 20644207-3 2010 This study examined reported changes in smoking beliefs during an 8-week smoking cessation trial, which evaluated the safety and efficacy of the monoamine oxidase B inhibitor selegiline hydrochloride versus placebo. Selegiline 175-199 monoamine oxidase B Homo sapiens 145-164 19939587-1 2010 AIM: The primary aim of this study was to determine the safety and efficacy of the monoamine oxidase-B (MAO-B) inhibitor selegiline hydrochloride (SEL, l-Deprenyl; Eldepryl) as an aid for smoking cessation in cigarette smokers. Selegiline 121-145 monoamine oxidase B Homo sapiens 83-102 19939587-1 2010 AIM: The primary aim of this study was to determine the safety and efficacy of the monoamine oxidase-B (MAO-B) inhibitor selegiline hydrochloride (SEL, l-Deprenyl; Eldepryl) as an aid for smoking cessation in cigarette smokers. Selegiline 121-145 monoamine oxidase B Homo sapiens 104-109 20195940-3 2010 The MAO B inhibitors selegiline and rasagiline are in use for PD pharmacotherapy; for rasagiline, studies have demonstrated a possible disease-modifying effect. Selegiline 21-31 monoamine oxidase B Homo sapiens 4-9 19697948-5 2009 Increased nitration of Tyr-39 on endogenous alpha-synuclein via elevations in MAO-B levels could be abrogated by the addition of deprenyl, a specific MAO-B inhibitor. Selegiline 129-137 monoamine oxidase B Homo sapiens 78-83 19697948-5 2009 Increased nitration of Tyr-39 on endogenous alpha-synuclein via elevations in MAO-B levels could be abrogated by the addition of deprenyl, a specific MAO-B inhibitor. Selegiline 129-137 monoamine oxidase B Homo sapiens 150-155 19646280-1 2009 BACKGROUND: The selective MAO-B inhibitor selegiline has been evaluated in clinical trials as a potential medication for the treatment of cocaine dependence. Selegiline 42-52 monoamine oxidase B Homo sapiens 26-31 19526291-6 2009 In contrast, the MAO B inhibitors rasagiline and selegiline (0.25 nM) and the rasagiline metabolite, 1-R-aminoindan (1 muM) decreases the ethanol-induced MAO B, prevents nuclear translocation of GAPDH and reduces cell death. Selegiline 49-59 monoamine oxidase B Homo sapiens 17-22 19526291-6 2009 In contrast, the MAO B inhibitors rasagiline and selegiline (0.25 nM) and the rasagiline metabolite, 1-R-aminoindan (1 muM) decreases the ethanol-induced MAO B, prevents nuclear translocation of GAPDH and reduces cell death. Selegiline 49-59 monoamine oxidase B Homo sapiens 154-159 17881661-8 2007 This reaction was almost completely inhibited in human hepatic microsomes and mitochondria by the monoamine oxidase (MAO)-B-specific inhibitor selegiline. Selegiline 143-153 monoamine oxidase B Homo sapiens 98-123 19753135-4 2009 The lack of amphetamine metabolites provides an advantage over the first generation MAO-B inhibitor selegiline. Selegiline 100-110 monoamine oxidase B Homo sapiens 84-89 19527191-3 2009 Oral selegiline, at low doses, is a selective monoamine oxidase B (MAO-B) inhibitor, but at higher doses it loses its selectivity and can potentially interact with tyramine. Selegiline 5-15 monoamine oxidase B Homo sapiens 46-65 19527191-3 2009 Oral selegiline, at low doses, is a selective monoamine oxidase B (MAO-B) inhibitor, but at higher doses it loses its selectivity and can potentially interact with tyramine. Selegiline 5-15 monoamine oxidase B Homo sapiens 67-72 19527191-5 2009 The selegiline transdermal system was developed to deliver sustained selegiline blood concentrations sufficient to selectively inhibit MAO-A and MAO-B in the brain, producing antidepressant effects, without substantially inhibiting MAO-A in the gastrointestinal tract, thereby reducing the risk of hypertensive crisis. Selegiline 4-14 monoamine oxidase B Homo sapiens 145-150 19527191-5 2009 The selegiline transdermal system was developed to deliver sustained selegiline blood concentrations sufficient to selectively inhibit MAO-A and MAO-B in the brain, producing antidepressant effects, without substantially inhibiting MAO-A in the gastrointestinal tract, thereby reducing the risk of hypertensive crisis. Selegiline 69-79 monoamine oxidase B Homo sapiens 145-150 19946577-3 2008 We previously reported that ethanol exposure lowered cell proliferation and increased cell apoptosis in all cell types, but affects brain cell lines the most, while ethanol and the anti-depressant drug deprenyl, an monoamine oxidase B (MAO B) inhibitor, exposure in unison increases cell viability. Selegiline 202-210 monoamine oxidase B Homo sapiens 215-234 19946577-3 2008 We previously reported that ethanol exposure lowered cell proliferation and increased cell apoptosis in all cell types, but affects brain cell lines the most, while ethanol and the anti-depressant drug deprenyl, an monoamine oxidase B (MAO B) inhibitor, exposure in unison increases cell viability. Selegiline 202-210 monoamine oxidase B Homo sapiens 236-241 19946577-11 2008 The inhibition of the TIEG2-MAO B pathway may be one of the mechanisms for the neuroprotective effect of deprenyl. Selegiline 105-113 monoamine oxidase B Homo sapiens 28-33 18420288-1 2008 Selegiline, an irreversible inhibitor of monoamine oxidase B used in the treatment of Parkinson"s disease, has been demonstrated to have a potential cognition-improving effect in patients with Alzheimer"s disease (AD) undergoing treatment with an acetylcholinesterase inhibitor donepezil. Selegiline 0-10 monoamine oxidase B Homo sapiens 41-60 18237459-1 2008 Long-term administration of the monoamine oxidase (MAO)-B inhibitor selegiline may reduce neuronal death based on preclinical findings and reduce progression of chronic neurodegeneration due to outcomes of long-term clinical trials in patients with Parkinson"s disease. Selegiline 68-78 monoamine oxidase B Homo sapiens 32-57 18937611-1 2008 BACKGROUND: The role of monoamine oxidase type B inhibitors in the treatment of Parkinson"s disease has expanded with the new monoamine oxidase B inhibitor rasagiline and a new formulation, selegiline oral disintegrating tablets. Selegiline 190-200 monoamine oxidase B Homo sapiens 24-48 18937611-9 2008 The recently released monoamine oxidase B inhibitor rasagiline and a new formulation, selegiline oral disintegrating tablets, have potential advantages over conventional oral selegiline. Selegiline 175-185 monoamine oxidase B Homo sapiens 22-41 18937619-1 2008 The selective monoamine oxidase type B inhibitor selegiline is commonly administered as medical treatment to patients suffering from Parkinson"s disease. Selegiline 49-59 monoamine oxidase B Homo sapiens 14-38 18668620-8 2008 MAO-B inhibitors (selegiline and rasagiline) can decrease FOG frequency or severity, but its clinical significance is still unknown. Selegiline 18-28 monoamine oxidase B Homo sapiens 0-5 17931095-1 2007 Selegiline, a selective monoamine oxidase-B inhibitor, has been used for decades in the treatment of Parkinson"s disease. Selegiline 0-10 monoamine oxidase B Homo sapiens 24-43 18041937-3 2007 The two available MAO-B inhibitors approved for use in the United States, rasagiline and selegiline, each provide symptomatic relief as monotherapy and as adjunctive therapy, and have shown potential disease-modifying effects in experimental models and clinical studies. Selegiline 89-99 monoamine oxidase B Homo sapiens 18-23 18042509-1 2007 OBJECTIVE: To assess the long-term safety (primary aim) and efficacy (secondary aim) of the MAO-B inhibitor Selegiline Transdermal System (STS) for the treatment of HIV-associated cognitive impairment. Selegiline 108-118 monoamine oxidase B Homo sapiens 92-97 17909308-1 2007 BACKGROUND: Selegiline orally disintegrating tablet (ODT; Zelapar) is a selective monoamine oxidase B inhibitor developed as an adjunct to levodopa (LD) for Parkinson disease. Selegiline 12-22 monoamine oxidase B Homo sapiens 82-101 17652642-2 2007 Selegiline is an MAO-B inhibitor with antioxidant and neurotrophic properties. Selegiline 0-10 monoamine oxidase B Homo sapiens 17-22 17909308-1 2007 BACKGROUND: Selegiline orally disintegrating tablet (ODT; Zelapar) is a selective monoamine oxidase B inhibitor developed as an adjunct to levodopa (LD) for Parkinson disease. Selegiline 58-65 monoamine oxidase B Homo sapiens 82-101 17347320-2 2007 It was postulated that certain carbamate esters would inhibit AChE and BChE with the concomitant release in the brain of the OH-derivatives of rasagiline or selegiline that can serve as inhibitors of MAO-B and as antioxidants. Selegiline 157-167 monoamine oxidase B Homo sapiens 200-205 17545750-3 2007 Data have been reported regarding the selective MAO-B inhibitors, rasagiline and selegiline, for the symptomatic treatment of Parkinson disease (PD). Selegiline 81-91 monoamine oxidase B Homo sapiens 48-53 17168653-1 2006 The therapeutic use of enzyme inhibitors in treatment of neurodegenerative diseases has its origin in the anti Parkinson action of the selective monoamine oxidase (MAO) B inhibitor, l-deprenyl (selegiline ), a failed anti depressant in 1975. Selegiline 182-192 monoamine oxidase B Homo sapiens 145-170 17630819-5 2007 Agents that block MAO-B, such as rasagiline and selegiline, are used as both initial and adjunctive therapy in patients with Parkinson"s disease. Selegiline 48-58 monoamine oxidase B Homo sapiens 18-23 18261369-1 2007 PURPOSE: The selective monoamine oxidase-B (MAO-B) inhibitor, l-deprenyl, is still used for treating Parkinson"s patients, however, a disadvantage of its use lies in the formation of l-amphetamine and l-methamphetamine. Selegiline 62-72 monoamine oxidase B Homo sapiens 23-42 18261369-1 2007 PURPOSE: The selective monoamine oxidase-B (MAO-B) inhibitor, l-deprenyl, is still used for treating Parkinson"s patients, however, a disadvantage of its use lies in the formation of l-amphetamine and l-methamphetamine. Selegiline 62-72 monoamine oxidase B Homo sapiens 44-49 17346749-3 2007 L-deprenyl binds to MAO-B and autoradiography with 3H-L-deprenyl has been used to map astrocytosis in vitro. Selegiline 0-10 monoamine oxidase B Homo sapiens 20-25 17284087-1 2007 The monamine oxidase (MAO) inhibitor selegiline is selective for MAO-B at the low oral dosages used in the treatment of Parkinson"s disease. Selegiline 37-47 monoamine oxidase B Homo sapiens 65-70 17348765-5 2007 The second-generation MAOI selegiline is selective for MAO(B) at oral doses of up to 10 mg/day. Selegiline 27-37 monoamine oxidase B Homo sapiens 55-61 17348765-6 2007 At higher doses, selegiline loses selectivity and inhibits both MAO(A) and MAO(B). Selegiline 17-27 monoamine oxidase B Homo sapiens 75-81 16730924-2 2006 Selegiline is an irreversible selective inhibitor of monoamine oxidase type B (MAO-B) which may affect cocaine addiction through several potential mechanisms. Selegiline 0-10 monoamine oxidase B Homo sapiens 53-77 16730924-2 2006 Selegiline is an irreversible selective inhibitor of monoamine oxidase type B (MAO-B) which may affect cocaine addiction through several potential mechanisms. Selegiline 0-10 monoamine oxidase B Homo sapiens 79-84 17168653-1 2006 The therapeutic use of enzyme inhibitors in treatment of neurodegenerative diseases has its origin in the anti Parkinson action of the selective monoamine oxidase (MAO) B inhibitor, l-deprenyl (selegiline ), a failed anti depressant in 1975. Selegiline 194-204 monoamine oxidase B Homo sapiens 145-170 16717254-5 2006 Selegiline is a monamine oxidase type B (MAO-B) inhibitor that incorporates a propargyl ring within its molecular structure. Selegiline 0-10 monoamine oxidase B Homo sapiens 16-39 16717254-5 2006 Selegiline is a monamine oxidase type B (MAO-B) inhibitor that incorporates a propargyl ring within its molecular structure. Selegiline 0-10 monoamine oxidase B Homo sapiens 41-46 16641841-4 2006 Selegiline, a selective monoamine oxidase B inhibitor, has been approved for the adjunctive treatment of Parkinson"s disease at low doses. Selegiline 0-10 monoamine oxidase B Homo sapiens 24-43 16289465-1 2006 The present study shows that deprenyl, a known inhibitor of monoamine oxidase B (MAO B), may generate changes in mitochondrial function. Selegiline 29-37 monoamine oxidase B Homo sapiens 60-79 16289465-1 2006 The present study shows that deprenyl, a known inhibitor of monoamine oxidase B (MAO B), may generate changes in mitochondrial function. Selegiline 29-37 monoamine oxidase B Homo sapiens 81-86 17100591-1 2006 Selegiline inhibits the activity of monoamine oxidase B, enhances the release of dopamine, blocks the uptake of dopamine, acts as a calmodulin antagonist, and enhances the level of cyclic AMP, which in turn protects dopaminergic neurons. Selegiline 0-10 monoamine oxidase B Homo sapiens 36-55 16927880-1 2006 (-)-Deprenyl, the irreversible inhibitor of monoamine oxidase B, has been used for decades in the therapy of Parkinson"s disease. Selegiline 0-12 monoamine oxidase B Homo sapiens 44-63 16927880-4 2006 Recently, (-)-deprenyl has been demonstrated to exert antiapoptotic, neuroprotective effects on a number of in vitro and in vivo models in a dose significantly lower than required for monoamine oxidase B inhibition. Selegiline 10-22 monoamine oxidase B Homo sapiens 184-203 16723097-6 2006 The IC(50) value of clorgyline to MAO-A was 2.99 nmol/L, and that of deprenyl to MAO-B was 7.04 nmol/L, matching those obtained from traditional spectrometric assays. Selegiline 69-77 monoamine oxidase B Homo sapiens 81-86 16343694-4 2006 Actually, the beneficial effect of selegiline, a MAO-B inhibitor, in AD has been noted in several clinical studies. Selegiline 35-45 monoamine oxidase B Homo sapiens 49-54 16485914-18 2006 Buccal administration of the monoamine oxidase-B inhibitor selegiline (deprenyl) provides better absorption and less formation of metabolites compared with standard tablets. Selegiline 59-69 monoamine oxidase B Homo sapiens 29-48 16485914-18 2006 Buccal administration of the monoamine oxidase-B inhibitor selegiline (deprenyl) provides better absorption and less formation of metabolites compared with standard tablets. Selegiline 71-79 monoamine oxidase B Homo sapiens 29-48