Journal of Capital Medical University ›› 2015, Vol. 36 ›› Issue (6): 861-864.doi: 10.3969/j.issn.1006-7795.2015.06.006

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Mitochondrial dysfunction, α-synuclein and Parkinson's disease

Zhang Ruyi, Zhang Li, Li Lin   

  1. Department of Pharmacology, Xuanwu Hospital, Capital Medical University, Beijing Geriatric Medical Research Center, Beijing Engineering Research Center for Nerve System Drugs, Beijing 100053, China
  • Received:2015-10-10 Online:2015-12-21 Published:2015-12-18
  • Supported by:
    This study was supported by National Natural Science Foundation of China(81341087, 81273498);The Capital Health Research and Development of Special Project(2011-1001-04).

Abstract: Parkinson's disease(PD) is a common neurodegenerative disorder. The disease is characterized by the loss of dopamine neurons in the substantia nigra and the presence of intraneuronal Lewy bodies. Many studies suggest that mitochondrial dysfunction is the central pathogenesis of PD. The abnormal aggregation of α-synuclein is the key factor in the cascade of PD pathological events. Recently, the interaction between α-synuclein and mitochondrial dysfunction has attracted much attention, but the exact mechanism underlying PD pathogenesis is still unclear. In this review, we discuss the key roles of mitochondria and α-synuclein in the pathogenesis of PD and the interaction between them. Understanding the functional consequences of α-synuclein's interactions with mitochondria is likely to provide important insights into disease pathophysiology, and may also reveal therapeutic strategies.

Key words: Parkinson's disease, α-Synuclein, mitochondria

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