α-核突触蛋白和自噬在帕金森病中的作用  

The Role of α-synuclein and Autophagy in Parkinson's disease

作　　者：刘康永[1] 石际俊[2] 倪夏珺[1] 沈黎玮[1] 刘春风[2] 

机构地区：[1]复旦大学附属上海市第五人民医院神经科,200240 [2]苏州大学附属第二医院神经内科,215004

出　　处：《中国临床神经科学》2010年第1期103-107,共5页Chinese Journal of Clinical Neurosciences

摘　　要：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。The major component of Lewy bodies in Parkinson＇s disease （PD） is α-synuclein, which is considered as a substrate of the ubiquitine-proteasome system（UPS）, although autophagy-losomasome pathway （ALP） seemed to be equally involved. Under such circumstance as mutations, ageing, by intracellular or extracellular toxin, both UPS and ALP are induced, if toxic stimuli are prolonged, these pathways will be overwhelmed and cell death will occur. According to the domestic and overseas reports, including our own research, a protective role of autophagy in PD was indicated and considered as a therapeutic target to slow down the progression of the disease.

关 键 词：帕金森病 α-核突触蛋白 自噬 

分 类 号：R741[医药卫生—神经病学与精神病学]