Deconvoluting the complexity of autophagy and Parkinson’s disease for potential therapeutic purpose
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Jingjing Li1,*, Sijia Li2,*, Lan Zhang1,*, Liang Ouyang1 and Bo Liu1
1 State Key Laboratory of Biotherapy and Cancer Center, Collaborative Innovation Center of Biotherapy, West China Hospital, Sichuan University, Chengdu, China
2 State Key Laboratory of Stomatology, West China Hospital of Stomatology, Sichuan University, Chengdu, China
* These authors have contributed equally to this work
Bo Liu, email:
Liang Ouyang, email:
Keywords: Parkinson’s disease (PD), autophagy, α-synuclein, LRRK2, PD therapy
Received: July 31, 2015 Accepted: September 12, 2015 Published: September 22, 2015
Parkinson’s disease (PD) is a neurodegenerative disorder characterized by the preferential death of dopaminergic neurons. In the past two decades, great progress has been made toward understanding the pathogenesis of PD; however, its precise pathogenesis still remains unclear. Recently, accumulating evidence has suggested that macroautophagy (herein referred to as autophagy) is tightly linked to PD. Dysregulation of autophagic pathways has been observed in the brains of PD patients and in animal models of PD. More importantly, a number of PD-associated proteins, such as α-synuclein, LRRK2, Parkin and PINK1 have been further revealed to be involved in autophagy. Thus, it is now acknowledged that constitutive autophagy is essential for neuronal survival and that dysregulation of autophagy leads to PD. In this review, we focus on summarizing the relationships amongst PD-associated proteins, autophagy and PD. Moreover, we also demonstrate some autophagy-modulating compounds and autophagic microRNAs in PD models, which may provide better promising strategies for potential PD therapy.
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