线粒体功能障碍与帕金森病

Mitochondrial dysfunction and Parkinson’s disease

帕金森病(Parkinson’s disease,PD)是一种以大脑黑质致密部(SNpc)多巴胺能神经元进行性丧失为主要特征的神经退行性疾病,好发于中老年人,以运动障碍和认知缺陷为主要临床症状。近年来,在关于帕金森病发病机制的探讨中,线粒体功能障碍一直被认为是多巴胺能神经元丢失的重要起始因素,目前认为是线粒体生物发生调控机制、基因突变等几种因素相互作用的结果。本文总结了线粒体生物发生、线粒体动力学、线粒体自噬、线粒体基因突变等线粒体功能障碍在帕金森病中的作用,以期为帕金森病的线粒体靶向治疗提供参考。

Parkinson’s disease(PD)is a neurodegenerative disease characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta(SNpc)of the brain,mainly affecting middle-aged and elderly people,with movement disorders and cognitive deficits as the main clinical symptoms.In recent years,mitochondrial dysfunction has been considered as an important starting point for the loss of dopaminergic neurons in the pathogenesis of Parkinson’s disease.At present,it is considered to be the result of the interaction of several factors such as mitochondrial biogenesis regulation mechanism and gene mutation.This article focuses on the role of mitochondrial dysfunction in Parkinson’s disease,such as mitochondrial biogenesis,mitochondrial dynamics,mitochondrial autophagy,and mitochondrial gene mutations,in order to provide references for mitochon⁃dria-targeting therano stics of PD.