α-突触核蛋白在帕金森病发病机制中的研究进展  

Research progress on the pathogenesis of Parkinson's disease

作　　者：毛婷婷(综述) 陈煜森(审校) MAO Ting-ting;CHEN Yu-sen(Graduate School,Guangdong Medical University,Zhanjiang 524000,Guangdong,CHINA;Department of Neurology,the Affiliated Hospital of Guangdong Medical University,Zhanjiang 524000,Guangdong,CHINA)

机构地区：[1]广东医科大学研究生学院,广东湛江524000 [2]广东医科大学附属医院神经内科,广东湛江524000

出　　处：《海南医学》2020年第11期1460-1463,共4页Hainan Medical Journal

基　　金：国家自然科学基金青年基金(编号:81401061)。

摘　　要：早在20多年前,α-突触核蛋白被发现是路易小体的主要成分,其被认为是帕金森病的致病因子。此后,α-突触核蛋白不仅是帕金森病的一个标志,而且还可以导致神经元功能障碍和死亡。传递假说认为,一个神经元中初始产生的病理性α-突触核蛋白可能被另一个易损害的神经元释放和摄取,从而启动受体神经元中α-突触核蛋白的病理性错误折叠。近年来一些研究证据表明,在人脑中可以发现病理性的α-突触核蛋白传递。本文就病理性α-突触核蛋白在细胞间传递及相关研究进展等方面进行阐述。More than 20 years ago,α-synuclein was found to be the main component of Lewy bodies,which was considered to be the pathogenic factor of Parkinson's disease.Since then,α-synuclein is not only a sign of Parkinson's disease,but also can lead to neuronal dysfunction and death.The transmission hypothesis holds that the pathologicalα-synuclein produced initially in one neuron may be released and ingested by another vulnerable neuron,thus initiating the pathological misfolding ofα-synuclein in the receptor neurons.In recent years,some studies have shown that pathological transmission ofα-synuclein can be found in the human brain.This paper reviews the intercellular transmission and related research progress of pathologicalα-synuclein.

关 键 词：Α-突触核蛋白 帕金森病 路易小体 错误折叠 包涵体 朊病毒 

分 类 号：R742.5[医药卫生—神经病学与精神病学]