PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
25044076-0	2014	Lamotrigine attenuates deficits in synaptic plasticity and accumulation of amyloid plaques in APP/PS1 transgenic mice.	Lamotrigine	0-11	presenilin 1	Mus musculus	98-101	
25854934-2	2015	Chronic LTG treatment rescues the suppressed long-term potentiation, loss of spines and cognitive deficits in AbetaPP/PS1 mice, known to overexpress a chimeric mouse/human mutant amyloid-beta protein precursor (AbetaPP) and a mutant human presenilin 1 (PS1).	Lamotrigine	8-11	presenilin 1	Mus musculus	118-121	
25044076-4	2014	We showed that the chronic treatment with lamotrigine (LTG), a broad-spectrum AED, suppressed abnormal spike activity, prevented the loss of spines, synaptophysin immunoreactivity, and neurons, and thus attenuated the deficits in synaptic plasticity and learning and memory in APP and presenilin 1 (PS1) mice, which express human mutant APP and PS1.	Lamotrigine	42-53	presenilin 1	Mus musculus	285-297	
25044076-4	2014	We showed that the chronic treatment with lamotrigine (LTG), a broad-spectrum AED, suppressed abnormal spike activity, prevented the loss of spines, synaptophysin immunoreactivity, and neurons, and thus attenuated the deficits in synaptic plasticity and learning and memory in APP and presenilin 1 (PS1) mice, which express human mutant APP and PS1.	Lamotrigine	42-53	presenilin 1	Mus musculus	299-302	
25044076-4	2014	We showed that the chronic treatment with lamotrigine (LTG), a broad-spectrum AED, suppressed abnormal spike activity, prevented the loss of spines, synaptophysin immunoreactivity, and neurons, and thus attenuated the deficits in synaptic plasticity and learning and memory in APP and presenilin 1 (PS1) mice, which express human mutant APP and PS1.	Lamotrigine	55-58	presenilin 1	Mus musculus	285-297	
25044076-4	2014	We showed that the chronic treatment with lamotrigine (LTG), a broad-spectrum AED, suppressed abnormal spike activity, prevented the loss of spines, synaptophysin immunoreactivity, and neurons, and thus attenuated the deficits in synaptic plasticity and learning and memory in APP and presenilin 1 (PS1) mice, which express human mutant APP and PS1.	Lamotrigine	55-58	presenilin 1	Mus musculus	299-302	
25044076-5	2014	In contrast with LEV, which failed to reduce the generation of amyloid beta, the chronic LTG treatment reduced the cleavage of APP by beta-secretase and thus the numbers and the size of amyloid plaques in the brains of APP and PS1 mice.	Lamotrigine	89-92	presenilin 1	Mus musculus	227-230	
25044076-6	2014	Moreover, the levels of brain-derived neurotrophic growth factor (BDNF) and nerve growth factor (NGF) were enhanced in the brains of APP and PS1 mice by the chronic LTG treatment.	Lamotrigine	165-168	presenilin 1	Mus musculus	141-144