阿尔茨海默病中的β淀粉样肽与氧化应激  

Amyloid-βprotein and oxidative stress in Alzheimer’s disease

作　　者：邵思迈 史洺 余姊阳 原野 游言文[1] 郝莉[1] 张紫娟[1] 张振强[2] SHAO Simai;SHI Ming;YU Ziyang;YUAN Ye;YOU Yanwen;HAO Li;ZHANG Zijuan;ZHANG Zhenqiang(School of Basic Medical Science,Henan University of Chinese Medicine,Zhengzhou 450046,China;College of Traditional Chinese Medicine,Henan University of Chinese Medicine,Zhengzhou 450046)

机构地区：[1]河南中医药大学基础医学院,郑州450046 [2]河南中医药大学中医药科学院,郑州450046

出　　处：《中国比较医学杂志》2021年第10期131-135,共5页Chinese Journal of Comparative Medicine

基　　金：中原千人计划-科技创新领军人才项目(204200510022);河南省科技攻关项目(202102310078,172102310286,212102310828);河南省高校重点科研项目(19A310012)。

摘　　要：氧化应激(oxidative stress)是影响衰老和神经系统疾病的重要因素,在多种神经退行性疾病发生发展过程中起重要作用。老年斑的主要成分是β淀粉样蛋白(amyloid-beta protein,Aβ),它在脑中的异常沉积是阿尔茨海默病(Alzheimer’s disease,AD)发病的关键因素。研究表明,Aβ沉积引发的氧化应激会诱导认知记忆相关脑区的神经元丢失、死亡,最终引起AD病理的发生与发展。本文重点论述AD发生发展中淀粉样肽毒性产生的机制,大分子的氧化过程及淀粉样肽与氧化应激相互影响的过程,旨在阐明AD发生发展过程中淀粉样肽与氧化应激的关系,为促进AD抗氧化剂研究提供有力的理论支持和研究思路。Oxidative stress is an major factor that affects aging and neurological diseases,which plays an crucial role in the development and progression of multiple neurodegenerative diseases.Amyloid-beta protein(Aβ)is a major component of senile plaques,and its aggregation and abnormal deposition are major contributors to the pathogenesis of Alzheimer’s disease(AD).Studies have shown that oxidative stress triggered by Aβdeposition induces neuronal loss,cell death in cognitive memory-related brain regions,and finally causes the occurrence and development of AD pathology.This article focuses on the mechanism of toxic production of amyloid peptide in the occurrence and development of AD,the oxidation process of macromolecules and the process of the interaction between amyloid peptide and oxidative stress to clarify the relationship between amyloid peptide and oxidative stress in the occurrence and development of AD.This review provides strong theoretical support and research directions to promote studies on antioxidants in AD.

关 键 词：阿尔茨海默病 淀粉样肽 氧化应激 

分 类 号：R-33[医药卫生]