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胆碱能对突触可塑性的调节作为阿尔茨海默病的治疗靶点

Cholinergic regulation of synaptic plasticity as a therapeutic target in Alzheimer's disease.

作者信息

Small David H, Fodero Lisa R

机构信息

Laboratory of Molecular Neurobiology, University of Melbourne, Victoria 3010, Australia.

出版信息

J Alzheimers Dis. 2002 Oct;4(5):349-55. doi: 10.3233/jad-2002-4502.

Abstract

There is increasing evidence for disturbances in nicotinic acetylcholine receptor (nAChR) function in Alzheimer's disease (AD). nAChRs are involved in the regulation of many processes, including synaptic plasticity and memory. Levels of nAChRs are altered in the Alzheimer brain and there is evidence that the amyloid betaprotein (Abeta) can directly bind to nAChRs. Nicotinic agonists may also protect cells from Abeta toxicity. Drugs which interact with the nAChR or which inhibit Abeta binding to nAChRs may be of value for the treatment of AD.

摘要

越来越多的证据表明,阿尔茨海默病(AD)中烟碱型乙酰胆碱受体(nAChR)功能存在紊乱。nAChR参与许多过程的调节,包括突触可塑性和记忆。阿尔茨海默病患者大脑中的nAChR水平发生了改变,并且有证据表明淀粉样β蛋白(Aβ)可直接与nAChR结合。烟碱型激动剂也可能保护细胞免受Aβ毒性。与nAChR相互作用或抑制Aβ与nAChR结合的药物可能对AD治疗有价值。

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