α-Synuclein aggregation and neurodegenerative diseases

被引：57

作者：

Ma, Qiu-Lan ^{[1
,2
]}

Chan, Piu ^{[2
]}

Yoshii, Mitsunobu ^{[1
]}

Ueda, Kenji ^{[1
,2
]}

机构：

[1] Tokyo Inst Psychiat, Dept Neural Plastic, Tokyo 1568585, Japan

[2] Capital Univ Med Sci, Xuanwu Hosp, Beijing Inst Geriatr, Sino Japan Joint Lab Neurodegenerat Dis, Beijing 100053, Peoples R China

来源：

JOURNAL OF ALZHEIMERS DISEASE | 2003年 / 5卷 / 02期

关键词：

D O I：

10.3233/JAD-2003-5208

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

alpha-Synuclein is a neuronal protein originally identified in Alzheimer's disease (AD) amyloid plaques in 1993 and named non-A beta component precursor (NACP) [92]. Later, the discovery of two missense mutations (G88C and G209A), which resulted in Ala30Pro (A30P) and Ala53Thr (A53T) substitutions, of the a-synuclein gene in certain autosomal-dominant early onset familial Parkinson's disease (PD) has greatly promoted the understanding of the role of alpha-synuclein in the pathogenesis of neurodegenerative diseases, such as PD, dementia with Lewy bodies (DLB) and multiple system atrophy (MSA) [5,6,51, 75]. At present, it is widely accepted that alpha-synuclein may play a central role in several neurodegenerative disorders because of the presence of insoluble alpha-synuclein as the major fibrillar component of inclusion bodies. From the cloning of the human alpha-synuclein cDNA in 1993 to the present, alpha-synuclein has been carefully documented in many aspects. In this article, we review the progress of studies on a-synuclein and its role in alpha-synuclein-related neurodegenerative diseases.

引用

页码：139 / 148

页数：10

共 109 条

[1] Mice lacking α-synuclein display functional deficits in the nigrostriatal dopamine system [J].