Drp1相关线粒体异常与阿尔茨海默病的研究进展  

Increased Mitochondrial Fission in the Pathogenesis of Alzheimer's Disease

作　　者：王祯莲[1] 宋国强[1] WANG Zhenlian;SONG Guoqiang(School of Pharmaceutical Engineering & Life Sciences, Changzhou University, Changzhou 213164,China)

机构地区：[1]常州大学制药与生命科学学院,江苏常州213164

出　　处：《常州大学学报（自然科学版）》2020年第2期74-79,共6页Journal of Changzhou University：Natural Science Edition

基　　金：国家自然科学基金资助项目(81201657)。

摘　　要：线粒体动力学异常是阿尔茨海默病(AD)发病过程中的早期事件。β-淀粉样蛋白(Aβ)引起线粒体分裂增加,融合减少,导致线粒体功能障碍和神经元损伤。动力学相关蛋白1(Drp1)是调控线粒体过度分裂的关键分子。理解AD发病过程中线粒体过度分裂的机制有利于为研究以Drp1为靶点治疗AD提供理论和实验依据。Abnormal mitochondrial dynamics is an early event in Alzheimer’s disease.Aβ,in associ-ation with mitochondria,causes excessive mitochondrial fission and reduced mitochondrial fusion,leading to mitochondrial dysfunction and neuronal damage in AD-affected neurons.Increased mitochondrial fission is a key factor in mitochondrial dysfunction,probably caused by mutant protein(s)interacting with Drp1,resulting in the initiation of abnormal mitochondrial fission.Understanding the mechanism of excessive mitochondrial fission in the pathogenesis of AD is beneficial for providing a theoretical and experimental basis in the study of Drp1 as a target treatment of AD.

关 键 词：线粒体过度分裂 阿尔茨海默病 AΒ Drp1 

分 类 号：TK8[动力工程及工程热物理—流体机械及工程]