Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/5828
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dc.contributorDepartment of Applied Biology and Chemical Technology-
dc.creatorPi, R-
dc.creatorMao, X-
dc.creatorChao, X-
dc.creatorCheng, Z-
dc.creatorLiu, M-
dc.creatorDuan, X-
dc.creatorYe, M-
dc.creatorChen, X-
dc.creatorMei, Z-
dc.creatorLiu, P-
dc.creatorLi, W-
dc.creatorHan, Y-
dc.date.accessioned2014-12-11T08:27:17Z-
dc.date.available2014-12-11T08:27:17Z-
dc.identifier.urihttp://hdl.handle.net/10397/5828-
dc.language.isoenen_US
dc.publisherPublic Library of Scienceen_US
dc.rights© 2012 Pi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.subjectFerulic aciden_US
dc.subjectOxidative stressen_US
dc.subjectAcetylcholinesterase inhibitorsen_US
dc.subjectCognitive deficitsen_US
dc.subjectFibrilsen_US
dc.subjectTacrineen_US
dc.subjectDerivativesen_US
dc.subjectToxicityen_US
dc.subjectMiceen_US
dc.subjectImpairmenten_US
dc.titleTacrine-6-ferulic acid, a novel multifunctional dimer, inhibits amyloid-β-mediated alzheimer’s disease-associated pathogenesis in vitro and in vivoen_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.spage1-
dc.identifier.epage8-
dc.identifier.volume7-
dc.identifier.issue2-
dc.identifier.doi10.1371/journal.pone.0031921-
dcterms.abstractWe have previously synthesized a series of hybrid compounds by linking ferulic acid to tacrine as multifunctional agents based on the hypotheses that Alzheimer's disease (AD) generates cholinergic deficiency and oxidative stress. Interestingly, we found that they may have potential pharmacological activities for treating AD. Here we report for the first time that tacrine-6-ferulic acid (T6FA), one of these compounds, can prevent amyloid-β peptide (Aβ)-induced AD-associated pathological changes in vitro and in vivo. Our results showed that T6FA significantly inhibited auto- and acetylcholinesterase (AChE)-induced aggregation of Aβ₁₋₄₀ in vitro and blocked the cell death induced by Aβ₁₋₄₀ in PC12 cells. In an AD mouse model by the intracerebroventricular injection of Aβ₁₋₄₀, T6FA significantly improved the cognitive ability along with increasing choline acetyltransferase and superoxide dismutase activity, decreasing AChE activity and malondialdehyde level. Based on our findings, we conclude that T6FA may be a promising multifunctional drug candidate for AD.-
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationPLoS one, 23 Feb, 2012, v. 7, no. 2, e31921, p. 1-8-
dcterms.isPartOfPLoS one-
dcterms.issued2012-02-23-
dc.identifier.isiWOS:000302916100040-
dc.identifier.scopus2-s2.0-84863144997-
dc.identifier.pmid22384101-
dc.identifier.eissn1932-6203-
dc.description.oaVersion of Recorden_US
dc.identifier.FolderNumberOA_IR/PIRAen_US
dc.description.pubStatusPublisheden_US
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