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Valproic acid inhibits Abeta production, neuritic plaque formation, and behavioral deficits in Alzheimer's disease mouse models.

Qing, Hong and He, Guiqiong and Ly, Philip T T and Fox, Christopher J and Staufenbiel, Matthias and Cai, Fang and Zhang, Zhuohua and Wei, Shengcai and Sun, Xiulian and Chen, Chia-Hsiung and Zhou, Weihui and Wang, Ke and Song, Weihong (2008) Valproic acid inhibits Abeta production, neuritic plaque formation, and behavioral deficits in Alzheimer's disease mouse models. The Journal of Experimental Medicine, 205 (12). pp. 2781-2789. ISSN 1540-9538

Abstract

Neuritic plaques in the brains are one of the pathological hallmarks of Alzheimer's disease (AD). Amyloid beta-protein (Abeta), the central component of neuritic plaques, is derived from beta-amyloid precursor protein (APP) after beta- and gamma-secretase cleavage. The molecular mechanism underlying the pathogenesis of AD is not yet well defined, and there has been no effective treatment for AD. Valproic acid (VPA) is one of the most widely used anticonvulsant and mood-stabilizing agents for treating epilepsy and bipolar disorder. We found that VPA decreased Abeta production by inhibiting GSK-3beta-mediated gamma-secretase cleavage of APP both in vitro and in vivo. VPA treatment significantly reduced neuritic plaque formation and improved memory deficits in transgenic AD model mice. We also found that early application of VPA was important for alleviating memory deficits of AD model mice. Our study suggests that VPA may be beneficial in the prevention and treatment of AD.

Item Type: Article
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Additional Information: author can archive post-print (ie final draft post-refereeing), On author's personal web site and institutional repository
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Date Deposited: 14 Dec 2009 13:48
Last Modified: 31 Jan 2013 00:55
URI: https://oak.novartis.com/id/eprint/1363

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