Department of Neurobiology Key Laboratory of Neurodegenerative Diseases (Capital Medical University), Ministry of Education, Xuanwu Hospital of China Capital Medical University, 100053 Beijing, China.
J Chem Neuroanat. 2011 Dec;42(4):242-8. doi: 10.1016/j.jchemneu.2010.12.001. Epub 2010 Dec 16.
Alpha-synuclein (α-syn), a synaptic protein richly expressed in the central nervous system, has been implicated in several neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, multiple system atrophy, and dementia with Lewy bodies, which are collectively known as synucleinopathies. By contrast to the clear evidence for the involvement of α-syn in synucleinopathies, its physiological functions remain elusive, which becomes an impediment for revelation of its pathological mechanism. Since α-syn is richly expressed in presynaptic terminals and associated with synaptic vesicles, a large number of studies have been focused on revealing the potential functions of this protein in neurotransmission and synaptic plasticity. In this review article, we summarized recent advances for the role of α-syn in synaptic vesicle recycling, neurotransmitter synthesis and release, and synaptic plasticity. We discussed the possible relevance between the loss of normal α-syn functions in disease conditions and the onset of some neurodegenerative diseases.
α-突触核蛋白（α-syn）是一种在中枢神经系统中丰富表达的突触蛋白，与几种神经退行性疾病有关，如阿尔茨海默病、帕金森病、多系统萎缩和路易体痴呆，这些疾病统称为突触核蛋白病。与 α-syn 在突触核蛋白病中的作用的明确证据形成对比的是，其生理功能仍然难以捉摸，这成为揭示其病理机制的障碍。由于 α-syn 在突触前末梢中丰富表达，并与突触小泡相关，因此大量研究集中在揭示该蛋白在神经传递和突触可塑性中的潜在功能。在这篇综述文章中，我们总结了 α-syn 在突触小泡再循环、神经递质合成和释放以及突触可塑性中的作用的最新进展。我们讨论了在疾病条件下正常 α-syn 功能丧失与某些神经退行性疾病发病之间的可能相关性。
