自噬缺陷影响阿尔茨海默病的病理改变  

Autophagy defects affect pathological changes of Alzheimer's disease

作　　者：李敏[1] 黄俊宇 魏珍 Li Min;Huang Junyu;Wei Zhen(Hubei Provincial Clinical Research Center for Alzheimer's Disease,Brain Science and Advanced Technology Institute,School of Medicine,Wuhan University of Science and Technology,Wuhan 430065,China)

机构地区：[1]湖北省阿尔茨海默病临床医学研究中心、脑科学先进技术研究院、武汉科技大学医学部,武汉430065

出　　处：《中华老年医学杂志》2025年第1期16-20,共5页Chinese Journal of Geriatrics

基　　金：国家自然科学基金项目(82101248);武汉科技大学研究生创新创业基金项目(JCX2023102)。

摘　　要：阿尔茨海默病(AD)是一种起病隐匿的进行性发展的神经退行性疾病,是老年期痴呆最常见的类型,确切的发病机制仍有待进一步阐明。近年来的研究发现自噬缺陷(autophagy defects)在AD病理进展中发挥关键作用。自噬缺陷通过诱导Aβ蛋白沉积、tau蛋白聚集、神经元丢失、突触损伤、神经炎症以及线粒体功能受损等病理改变可能促进AD的发展。本文旨在深入探讨自噬缺陷的发生机制,分析其如何影响AD的病理改变,并探讨针对自噬缺陷的潜在治疗策略,以期为AD的预防和治疗提供新的见解。Alzheimer's disease(AD),the most prevalent form of dementia among the elderly,is a progressive neurodegenerative disorder characterized by an insidious onset.Although the precise pathogenesis of AD has not been fully elucidated,recent studies have identified autophagy defects as a pivotal factor in the progression of the disease.These autophagy defects lead to the deposition of Aβprotein,aggregation of tau protein,neuronal loss,synaptic damage,neuroinflammation,and mitochondrial dysfunction,all of which may contribute to the development of AD and influence its occurrence and progression.This review aims to examine the mechanisms underlying defective autophagy,highlight its impact on the pathological changes associated with AD,and discuss potential therapeutic strategies to address autophagy deficiencies,thereby providing new insights for the prevention and treatment of AD.

关 键 词：自噬缺陷 阿尔茨海默病 Aβ蛋白沉积 tau蛋白聚集 靶向治疗 

分 类 号：R749.16[医药卫生—神经病学与精神病学]