阿尔茨海默病的病因与发病机制研究进展  

Research progress on the etiology and pathogenesis of Alzheimer’s disease

作　　者：郭佳越 汤燚 杨银[2] 张云智 GUO Jiayue;TANG Yi;YANG Yin;ZHANG Yunzhi(School of Public Health,Dali University,Yunnan Province,Dali 671000,China;Department of Outpatient,Dali Second People’s Hospital,Yunnan Province,Dali 671000,China)

机构地区：[1]大理大学公共卫生学院,云南大理671000 [2]大理州第二人民医院门诊部,云南大理671000

出　　处：《中国医药导报》2024年第1期39-42,共4页China Medical Herald

基　　金：国家自然科学基金资助项目(81874274);云南省大理州科技计划项目(D2021NA05)。

摘　　要：阿尔茨海默病(AD)是以认知功能进行性损害为特征的神经系统退行性疾病,然而目前AD的发病机制仍不明确。AD的发生与多种因素相关,其中β淀粉样蛋白沉积和Tau蛋白的异常磷酸化引起的神经原纤维缠结是AD的两种特征性病理改变。随着分子生物学的进展,基因突变、线粒体损伤、细胞内异常氧化应激及神经递质的异常代谢也被认为是AD发生的共同机制。本文综述了AD的病因和发病机制的最新研究进展,以期为AD的防治药物研发和潜在靶点选择提供新的方向。Alzheimer’s disease(AD)is a neurodegenerative disease characterized by progressive cognitive impairment.However,the pathogenesis of AD remains unclear.The occurrence of AD is related to a variety of factors,among whichβ-amyloid deposition and neurofibrillary tangles caused by abnormal phosphorylation of Tau protein are two characteristic pathological changes of AD.With the advancement of molecular biology,genetic mutations,mitochondrial damage,abnormal intracellular oxidative stress and abnormal metabolism of neurotransmitters are also considered as common mechanisms of AD.This article reviews the latest research progress on the etiology and pathogenesis of AD,with a view to providing new directions for the development of preventive and therapeutic drugs and the selection of potential targets for AD.

关 键 词：阿尔茨海默病 发病机制 基因 淀粉样蛋白 线粒体 氧化应激 

分 类 号：R742[医药卫生—神经病学与精神病学]