【摘要】 帕金森病（PD）是一种以运动障碍和认知障碍为主要临床症状的神经系统变性疾病，以大脑黑质致密部（SNpc）多巴胺能神经元进行性丧失和α-突触核蛋白（α-syn）在残存的多巴胺能神经元中形成嗜酸性包涵体——路易小体为主要特征，好发于中老年人。线粒体功能障碍产生的氧化应激会导致多巴胺能神经元丢失，因此线粒体功能障碍被认为是帕金森病主要的发病原因，而线粒体生物发生对于线粒体的功能有着重要影响，线粒体生物发生调控系统的异常与帕金森病的的发生与发展密切相关。本文重点阐述线粒体生物发生控制系统的调控机制，以期为帕金森病提供有前途的治疗靶点。更多还原

【Abstract】 Parkinson disease is a neurodegenerative disorder with motor and cognitive impairments as the main clinical symptoms. The disease is characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta and the formation of Lewy bodies, which are eosinophilic inclusions composed of α-synuclein, in the remaining dopaminergic neurons. The disease predominantly affects middle-aged and elderly individuals. Oxidative stress caused by mitochondrial dysfunction can lead to the loss of dopaminergic neurons, so mitochondrial dysfunction is considered as the main cause of Parkinson disease. Mitochondrial biogenesis has an important effect on the function of mitochondria. Therefore, abnormality of the regulation system of mitochondrial biogenesis is closely related to the occurrence and development of Parkinson disease. This review focuses on the regulatory mechanism of mitochondrial biogenesis control system and aims to provide promising therapeutic targets for Parkinson disease.更多还原