Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/5828
Title: Tacrine-6-ferulic acid, a novel multifunctional dimer, inhibits amyloid-β-mediated alzheimer’s disease-associated pathogenesis in vitro and in vivo
Authors: Pi, R
Mao, X
Chao, X
Cheng, Z
Liu, M
Duan, X
Ye, M
Chen, X
Mei, Z
Liu, P
Li, W
Han, Y 
Keywords: Ferulic acid
Oxidative stress
Acetylcholinesterase inhibitors
Cognitive deficits
Fibrils
Tacrine
Derivatives
Toxicity
Mice
Impairment
Issue Date: 23-Feb-2012
Publisher: Public Library of Science
Source: PLoS one, 23 Feb, 2012, v. 7, no. 2, e31921, p. 1-8 How to cite?
Journal: PLoS one 
Abstract: We 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.
URI: http://hdl.handle.net/10397/5828
EISSN: 1932-6203
DOI: 10.1371/journal.pone.0031921
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.
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