Dysregulation of autophagy and mitochondrial function in Parkinson's disease

被引:77
|
作者
Wang, Bao [1 ,2 ]
Abraham, Neeta [2 ]
Gao, Guodong [1 ]
Yang, Qian [1 ]
机构
[1] Fourth Mil Med Univ, Tangdu Hosp, Dept Neurosurg, 569 Xinsi Rd, Xian 710038, Shaanxi Provinc, Peoples R China
[2] Harvard Med Sch, Dept Neurol, Beth Isreal Deaconess Med Ctr, 330 Brookline Ave, Boston, MA 02215 USA
来源
基金
中国国家自然科学基金;
关键词
Parkinson's disease; Autophagy; Macroautophagy; Mitophagy; Chaperone-mediated autophagy; Mitochondria; alpha-synuclein; PINK/Parkin; LRRK2; DJ-1; CHAPERONE-MEDIATED AUTOPHAGY; SURVIVAL FACTOR MEF2D; IPSC-DERIVED NEURONS; COMPLEX-I ACTIVITY; ALPHA-SYNUCLEIN; PINK1/PARKIN PATHWAY; MOLECULAR-MECHANISMS; REGULATES AUTOPHAGY; PROTEIN; LRRK2;
D O I
10.1186/s40035-016-0065-1
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Parkinson's disease (PD) is the second most common neurodegenerative disease. Increasing evidence supports that dysregulation of autophagy and mitochondrial function are closely related with PD pathogenesis. In this review, we briefly summarized autophagy pathway, which consists of macroautophagy, microautophagy and chaperone-mediated autophagy (CMA). Then, we discussed the involvement of mitochondrial dysfunction in PD pathogenesis. We specifically reviewed the recent developments in the relationship among several PD related genes, autophagy and mitochondrial dysfunction, followed by the therapeutic implications of these pathways. In conclusion, we propose that autophagy activity and mitochondrial homeostasis are of high importance in the pathogenesis of PD. Better understanding of these pathways can shed light on the novel therapeutic methods for PD prevention and amelioration.
引用
收藏
页数:9
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