摘要
阿尔茨海默病(AD)的发病机制至今仍未完全阐明。线粒体在神经元功能中起着关键作用,有研究表明线粒体动力学失衡介导的海马神经元损伤是AD的重要病理机制。及时恢复线粒体动力学稳态能够减轻甚至逆转神经元损伤。本文就线粒体分裂、融合及转运调控的基本机制及其与AD发病的关系作一综述,并着重讨论线粒体动力学平衡中的关键调节位点如线粒体分裂蛋白1、线粒体融合蛋白1/2、视神经萎缩蛋白1及Miro/Milton所起的重要作用及其对AD发病的影响。
The pathogenesis of Alzheimer's disease(AD)has not been fully elucidated.Mitochondria play critical roles in neuronal function;and damage of hippocampal neurons by dysfunction of mitochondrial dynamics is the major pathological mechanism of AD.Improvement of mitochondrial dynamics imbalance in time should alleviate or reverse damage of hippocampal neurons.After a brief overview of basic mechanisms involved in regulation of mitochondrial fission,fusion,and transportion,and how mitochondrial dynamics affects AD,this review article focuses on discussing the role of key sites such as Drp1,Mfn1/2,Opa1 and Miro/Milton in regulating mitochondria dynamics and their effects on AD.
作者
高晨皓
孙争宇
张杰文
Gao Chenhao;Sun Zhengyu;Zhang Jiewen(Department of Neurology,People's Hospital of Zhengzhou University,Zhengzhou 450003,China)
出处
《中华神经医学杂志》
CAS
CSCD
北大核心
2019年第4期337-343,共7页
Chinese Journal of Neuromedicine
基金
国家自然科学基金(81671068).
