氧化应激与阿尔茨海默病的病理关系及干预措施  

Pathological relationship between oxidative stress and Alzheimer’s disease and intervention strategies

作　　者：王准 孙谕莹 黄汉昌[1,2] WANG Zhun;SUN Yu-Ying;HUANG Han-Chang(Beijing Key Laboratory of Bioactive Substances and Functional Food,Beijing Union University,Beijing 100191,China;Research Institute of Functional Factors and Brain Science,Beijing Union University,Beijing 100023,China)

机构地区：[1]北京联合大学生物活性物质与功能食品北京市重点实验室,北京100191 [2]北京联合大学功能因子与脑科学研究院,北京100023

出　　处：《生命科学》2023年第4期519-528,共10页Chinese Bulletin of Life Sciences

基　　金：北京联合大学科研项目(JZ10202001,XP202008,ZK70202101)。

摘　　要：阿尔茨海默病(Alzheimer’s disease,AD)是一种神经退行性疾病,其病因复杂。活性氧(reactive oxygen species,ROS)是生理代谢的副产物,机体中有多个ROS来源,异常水平的ROS会破坏抗氧化系统并产生氧化应激现象。越来越多的证据表明,氧化应激可能是认知老化和诱发AD的关键因素之一。本文综述了机体中氧化应激的来源,并分析了氧化应激对自噬功能、β-淀粉样蛋白(amyloid-β,Aβ)、Tau蛋白、突触功能障碍以及风险基因ApoEε4的影响,探讨了针对氧化损伤的干预措施,为AD的发病机制研究和潜在治疗策略提供参考。Alzheimer’s disease(AD)is a kind of neurodegenerative disease with complex etiology.Reactive oxygen species(ROS)are the by-products of physiological metabolism.There are multiple sources of ROS in the body.Abnormal levels of ROS will damage the antioxidant system and lead to oxidative stress.Accumulating evidence suggests that oxidative stress may be one of the key factors in cognitive aging and AD development.This article reviews the origin of oxidative stress in vivo,analyzes the effects of oxidative stress on autophagy,amyloid-β(Aβ),Tau protein,synaptic dysfunction,and the risk gene ApoEε4,and further discusses the interventions against oxidative damage,so as to provide reference for the elucidation of the pathogenesis and potential treatment strategies of AD.

关 键 词：阿尔茨海默病 活性氧 氧化应激 Β-淀粉样蛋白 ApoEε4 

分 类 号：R749.1[医药卫生—神经病学与精神病学]