Synaptic vesicle trafficking and Parkinson's disease

被引：72

作者：

Esposito, Giovanni ^{[1
,2
]}

Clara, Fernandes Ana ^{[1
,2
]}

Verstreken, Patrik ^{[1
,2
]}

机构：

[1] VIB, Dept Mol & Dev Genet, Louvain, Belgium

[2] Katholieke Univ Leuven, Ctr Human Genet, Program Mol & Dev Genet, Program Cognit & Mol Neurosci, Louvain, Belgium

来源：

DEVELOPMENTAL NEUROBIOLOGY | 2012年 / 72卷 / 01期

基金：

欧洲研究理事会;

关键词：

synaptic vesicle; exocytosis; endocytosis; a-synuclein; SNARE complex; UBIQUITIN-PROTEIN LIGASE; ALPHA-SYNUCLEIN; RESERVE POOL; ALZHEIMERS-DISEASE; LRRK2; MUTATION; GENE-PRODUCT; CSP-ALPHA; DOPAMINE; BINDING; LOCALIZATION;

D O I：

10.1002/dneu.20916

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Presynaptic terminals maintain neurotransmitter release during repeated rounds of stimulation using local recycling of synaptic vesicles (SV). During each SV cycle, protein complex assembly and disassembly results in accumulation of inactive (unfolded) protein intermediates that may render synaptic terminals vulnerable to activity-dependent degeneration. SV trafficking is affected in many neurodegenerative conditions including Alzheimer' and Parkinson's disease (PD) suggesting that alteration of this process might be an important aspect of disease pathogenesis. This article reviews our current understanding for a role of causative PD genes in the SV cycle and speculates on the potential role of aberrant SV trafficking in the neurodegenerative cascade of PD. (c) 2011 Wiley Periodicals, Inc. Develop Neurobiol 72: 134144, 2012

引用

页码：134 / 144

页数：11

共 132 条

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