《生命科学》 2023, 35(4): 519-528

氧化应激与阿尔茨海默病的病理关系及干预措施

王　准^1,2 , 孙谕莹^1,2 , 黄汉昌^1,2,*

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

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ApoE ε4 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。

通讯作者：黄汉昌 , Email:hanchang@buu.edu.cn

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

WANG Zhun^1,2 , SUN Yu-Ying^1,2 , HUANG Han-Chang^1,2,*

¹Beijing Key Laboratory of Bioactive Substances and Functional Food, Beijing Union University, Beijing 100191, China ²Research Institute of Functional Factors and Brain Science, Beijing Union University, Beijing 100023, China

Abstract:

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 ApoE ε4, 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.

Communication Author：HUANG Han-Chang , Email:hanchang@buu.edu.cn