线粒体功能障碍与帕金森病研究进展

Advances in mitochondrial dysfunction and parkinson disease

帕金森病(Parkinson disease,PD)是一种常见的中枢神经退行性疾病,其特征性病理表现为黑质纹状体区多巴胺神经元凋亡以及Lewy小体的形成。尸检病理证实的帕金森病患者中,线粒体形态及功能存在异常,且线粒体损伤随着年龄的增长而加剧,尤其在PD患者黑质纹状体区的神经元中更为显著。因此,线粒体形态异常与功能障碍是调控PD发病的重要机制之一。线粒体DNA(mtDNA)突变、缺失,PD相关基因异常表达,环境毒素等都会引起帕金森病,但它们拥有一个共同的特点就是在不同程度上都会造成线粒体功能障碍。本文主要阐述这些因素引起的线粒体功能障碍在PD发病过程中作用的研究进展。

Parkinson disease(PD)is a common neurodegenerative disease in the central nervous system,which is characterized by apoptosis of dopamine neurons in the substantia nigra and the formation of Lewy bodies.In PD patients confirmed by autopsy and pathologic diagnoses,the morphology and function of mitochondria are abnormal,and mitochondrial damages worsen over age,especially in neurons in the substantia nigra of PD patients.Therefore,morphological abnormality and dysfunction of mitochondria are some of the most important factors regulating the pathogenesis of PD.Mutations of mtDNA,abnormal expression of PD-related genes,and environmental toxins may all cause Parkinson disease,though via a common pathway of causing varying degrees of mitochondrial dysfunction.Therefore,this paper mainly summarizes the research progress of mitochondrial dysfunction caused by these factors in the pathogenesis of PD.