帕金森病是一种以静止性震颤、肌强直、运动迟缓和姿势异常为主要临床特征的神经退行性疾病，其病理特征表现为中脑黑质多巴胺能神经元的进行性丢失。帕金森病的确切发病机制尚不完全清楚，涉及遗传、环境等多种因素，其中线粒体功能障碍和氧化应激反应在帕金森病发病过程中起着重要作用。本文旨在阐明线粒体功能障碍在帕金森病发病中的作用机制以及神经营养因子对于线粒体的保护作用。

Parkinson’s disease (PD) is a disabling neurodegenerative disorder characterized clinically by static tremor, rigidity, bradykinesia and postural instability, and pathologically by the extensive loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). The precise etiology of PD is mostly unknown and the pathogenesis is related to several factors such as hereditary and environmental factors. Current studies have found that mitochondrial dysfunction and oxidative stress play important roles in the pathogenesis of PD. This paper aims to elucidate the mechanism of mitochondrial dysfunction in the pathogenesis of PD and the protective effect of neurotrophic factors on mitochondria.