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.
作者
王祯莲
宋国强
WANG Zhenlian;SONG Guoqiang(School of Pharmaceutical Engineering & Life Sciences, Changzhou University, Changzhou 213164,China)
出处
《常州大学学报(自然科学版)》
CAS
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)。