α-核突触蛋白(α-synuclein)是路易小体的重要组分与帕金森病(PD)发病机制密切相关,如何调控其表达一直是阐明其致病机制以及防治的研究热点。在蛋白质量调控系统中,泛素-蛋白酶体系统(UPS)和自噬-溶酶体途径(ALP)都参与了α-核突触蛋白的降解。在老化、外源性毒素和基因突变等情况下,UPS和ALP都可以被诱导。如果上述两条途径,尤其是自噬出现功能障碍就会导致神经变性和细胞死亡。因而,通过调控自噬进而促进易聚集蛋白α-核突触蛋白的清除成为延缓PD疾病进展的一个潜在治疗靶点。 α-synuclein is an important component of Lewy bodies and Parkinson’s disease (PD) is closely related to the pathogenesis, how to regulate its expression has been clarified its pathogenesis and prevention and treatment of research hot spots. In the protein quality control system, both the ubiquitin-proteasome system (UPS) and the autophagy-lysosomal pathway (ALP) are involved in the degradation of a-nuclear synaptophysin. In aging, exogenous toxins and gene mutations, both UPS and ALP can be induced. If these two pathways, especially autophagy dysfunction will lead to neurodegeneration and cell death. Therefore, it is a potential therapeutic target to delay the progress of PD disease through the regulation of autophagy to promote the clearance of the aggregation protein α-nucleoside synaptophysin.