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dc.contributor.authorFernandes, Joylee
dc.contributor.authorMudgal, Jayesh
dc.contributor.authorRao, Chamallamudi Mallikarjuna
dc.contributor.authorArora, Devinder
dc.contributor.authorMallik, Sanchari Basu
dc.contributor.authorPai, KSR
dc.contributor.authorNampoothiri, Madhavan
dc.date.accessioned2019-05-29T12:40:40Z
dc.date.available2019-05-29T12:40:40Z
dc.date.issued2018
dc.identifier.issn1537-6516
dc.identifier.doi10.1080/15376516.2017.1411412
dc.identifier.urihttp://hdl.handle.net/10072/381670
dc.description.abstractNeuroinflammation plays an important role in the pathophysiology of Alzheimer’s disease. Neurokinin substance P is a key mediator which modulates neuroinflammation through neurokinin receptor. Involvement of substance P in Alzheimer’s disease is still plausible and various controversies exist in this hypothesis. Preventing the deleterious effects of substance P using N-acetyl-L-tryptophan, a substance P antagonist could be a promising therapeutic strategy. This study was aimed to evaluate the effect of N-acetyl-L-tryptophan on aluminum induced spatial memory alterations in rats. Memory impairment was induced using aluminum chloride (AlCl3) at a dose of 10 mg/kg for 42 d. After induction of dementia, rats were exposed to 30 and 50 mg/kg of N-acetyl-L-tryptophan for 28 d. Spatial memory alterations were measured using Morris water maze. Acetylcholinesterase activity and antioxidant enzyme glutathione level were assessed in hippocampus, frontal cortex and striatum. The higher dose of N-acetyl-L-tryptophan (50 mg/kg) significantly improved the aluminum induced memory alterations. N-acetyl-L-tryptophan exposure resulted in significant increase in acetylcholinesterase activity and glutathione level in hippocampus. The neuroprotective effect of N-acetyl-L-tryptophan could be due to its ability to block substance P mediated neuroinflammation, reduction in oxidative stress and anti-apoptotic properties. To conclude, N-acetyl-L-tryptophan may be considered as a novel neuroprotective therapy in Alzheimer’s disease.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherTaylor & Francis
dc.publisher.placeUnited States
dc.relation.ispartofpagefrom328
dc.relation.ispartofpageto334
dc.relation.ispartofissue5
dc.relation.ispartofjournalToxicology Mechanisms and Methods
dc.relation.ispartofvolume28
dc.subject.fieldofresearchPharmacology and pharmaceutical sciences
dc.subject.fieldofresearchPharmacology and pharmaceutical sciences not elsewhere classified
dc.subject.fieldofresearchcode3214
dc.subject.fieldofresearchcode321499
dc.subject.keywordsN-acetyl-L-tryptophan
dc.subject.keywordsAluminum, dementia
dc.subject.keywordsOxidative stress
dc.titleN-acetyl-L-tryptophan, a substance-P receptor antagonist attenuates aluminum-induced spatial memory deficit in rats
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.hasfulltextNo Full Text
gro.griffith.authorArora, Devinder S.


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