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氧化应激与阿尔茨海默病

刘晓杰, 杨威, 祁金顺^*

山西医科大学生理学系，细胞生理学省部共建教育部重点实验室，太原 030001

摘要

阿尔茨海默病(Alzheimer’s disease, AD)已经成为医学科学研究的重点和热点研究领域之一。迄今为止，人们还不能完全解释AD的发病机制。但是AD患者脑中出现的大量高密度的淀粉样β-蛋白(amyloid β-protein, Aβ)以及Aβ具有的神经毒性作用是导致AD的重要原因，这已经成为不争的事实。然而，Aβ发挥神经毒作用的机制十分复杂，涉及钙超载、炎症反应、离子通道功能异常和氧化应激等诸多方面。其中，关于Aβ通过氧化应激参与AD发病机制以及抗氧化药物在AD治疗中的实验研究进展，近年来已有不少的报道。本文主要就此方面的研究状况进行综述，以期为AD的抗氧化治疗提供线索和依据。

关键词： 淀粉样β-蛋白; 氧化应激; 阿尔茨海默病; 抗氧化制剂

分类号：R338

[Oxidative stress and Alzheimer's disease.] [Article in Chinese]

LIU Xiao-Jie, YANG Wei, QI Jin-Shun^*

Department of Physiology, Key Laboratory for Cellular Physiology of Ministry of Education, Shanxi Medical University, Taiyuan 030001, China

Abstract

Alzheimer’s disease (AD) has become one of the most important and most interesting focuses in the field of medical and scientific research. Up to now, the pathogenesis of AD has not been completely clarified. However, the high-density of amyloid β-protein (Aβ) in senile plaques of AD brain and the neurotoxicity of Aβ have been indisputable facts. The mechanisms underlying Aβ neurotoxicity are very complicated, involving calcium overload, inflammation, ion channel dysfunction, oxidative stress and so on. Among all of those, the mechanism of oxidative stress in Aβ neurotoxicity and the experimental progress of antioxidants in AD treatment have been widely reported in recent years. This review mainly discussed current research progresses on the oxidative stress of Aβ, so as to provide readers with some clues to the antioxidant therapy of AD.

Key words: amyloid β-protein; oxidative stress; Alzheimer’s disease; antioxidants

收稿日期：2011-07-04　　录用日期：2011-08-29

通讯作者：祁金顺　　E-mail: jinshunqi@sohu.com

引用本文：

刘晓杰, 杨威, 祁金顺. 氧化应激与阿尔茨海默病[J]. 生理学报 2012; 64 (1): 87-95.

LIU Xiao-Jie, YANG Wei, QI Jin-Shun. [Oxidative stress and Alzheimer's disease.] [Article in Chinese]. Acta Physiol Sin 2012; 64 (1): 87-95 (in Chinese with English abstract).