帕金森病线粒体功能障碍机制的研究进展

Research Progress of Mitochondrial Dysfunction in Parkinson′s Disease

帕金森病(PD)是一种常见的神经系统变性疾病,临床表现为多种运动症状(包括运动迟缓、僵硬、静止性震颤、姿势不稳)和非运动症状(自主神经功能障碍、睡眠异常、抑郁和痴呆等),其典型病理特征为黑质多巴胺能神经元变性缺失和路易小体的形成。但PD具体发病机制尚不明确,涉及遗传、环境等多种因素,其中线粒体功能障碍在PD发病过程中起重要作用。因此,了解导致线粒体功能障碍的因素,可能有助于寻找潜在的治疗靶点,以预防或改变PD发展过程。

Parkinson′s disease(PD)is a common neurodegenerative disease with clinical manifestations of a variety of motor symptoms(including bradykinesia,stiffness,resting tremor,postural instability)and non-motor symptoms(autonomic dysfunction,sleep disorders,depression and dementia,etc.),and its typical pathological features are the degeneration of substantia nigra dopaminergic neurons and the formation of Lewy bodies.However,the specific pathogenesis of PD is still unclear,involving multiple genetic and environmental factors,among which mitochondrial dysfunction plays an important role in the pathogenesis of PD.Therefore,understanding the factors that lead to mitochondrial dysfunction may help to discover potential therapeutic targets to prevent or change the development process of PD.