线粒体功能障碍与帕金森病  

Mitochondrial Dysfunction and Parkinson’s Disease

作　　者：刘洋[1] 雷晶[1] 马建华[1] 

机构地区：[1]新疆医科大学第一附属医院,新疆 乌鲁木齐

出　　处：《临床医学进展》2023年第10期15759-15767,共9页Advances in Clinical Medicine

摘　　要：帕金森病(PD)是一种常见的与年龄相关的神经系统变性疾病,以大脑黑质多巴胺能神经元的进行性丢失为主要病理特征。神经元需要很高的能量来维持其基本的生理活动,因此线粒体稳态对神经元的存活至关重要。研究表明,PD患者黑质多巴胺能神经元的变性和凋亡与多种因素密切相关,线粒体功能障碍可能在其中起关键作用。近年来,越来越多的研究开始关注线粒体与PD的相关性,本文主要阐述可导致线粒体功能障碍并介导PD发生发展的相关机制。Parkinson’s disease (PD) is a common age-related neurodegenerative disorder characterized by progressive loss of dopaminergic neurons in the substantia nigra. Neurons require high energy to maintain their basic physiological activities, so mitochondrial homeostasis is crucial for neuronal survival. Studies have shown that degeneration and apoptosis of nigrostriatal dopaminergic neu-rons in PD patients are closely related to a variety of factors, in which mitochondrial dysfunction may play a key role. In recent years, more and more studies have begun to focus on the relevance of mitochondria to PD, and this article focuses on the relevant mechanisms that can lead to mitochon-drial dysfunction and mediate the development of PD.

关 键 词：帕金森病 线粒体功能障碍 基因 Α-突触核蛋白 

分 类 号：R74[医药卫生—神经病学与精神病学]