神经细胞凋亡机制的研究进展:α-突触核蛋白与线粒体

Recent advances in mechanism of neuronal apoptosis: alpha-synuclein and mitochondria

目的:在帕金森病的病理结构中常常存在反常聚集的α-突触核蛋白和线粒体功能失常,就神经退行性病变中α-突触核蛋白和线粒体功能失常的关系做一综述。资料来源:应用计算机检索Pubmed2000-01/2005-09的相关文章,检索词为“α-synuclein,mitochondriaandParkinson’sdisease”并限定语种为“English”。资料选择:对资料进行初审,查找全文的文献。纳入标准为:①与α-突触核蛋白的作用有关。②与线粒体和神经细胞凋亡有关。排除标准为较陈旧和重复研究的文章。资料提炼:共收集到349篇文章,其中30篇文献符合纳入标准。资料综合:在30篇文献中,15篇与α-突触核蛋白的作用有关;12篇与线粒体和神经细胞凋亡有关;3篇与α-突触核蛋白和线粒体的关系有关。以往的研究证明α-突触核蛋白是一种在神经退行性病变中起关键作用的毒性蛋白。但是近期研究表明,α-突触核蛋白可能具有双重作用。α-突触核蛋白与线粒体之间的相互作用可能是此种作用的关键。结论:α-突触核蛋白与线粒体之间存在复杂的相互作用。未来集中于α-突触核蛋白与线粒体之间的关系的研究可能对帕金森病的病因学研究提供一种新的探索。

OBJECTIVE： Both the abnormal aggregations of alpha-synuclein （α- synuclein） and mitochondrial dysfunction are involved in the pathogenesis of Parkinson disease. This paper was to review the relationship between α-synuclein and mitochondria in the etiology of Parkinson disease. DATA SOURCES： An online search of Pubmed database was undertaken to identify the English articles about α-synuclein published from January 2000 to September 2005 by using the keywords of α-synuclein, mitochondria and Parkinson disease＂. STUDY SELECTION： The articles were primarily screened and then the full-texts were searched. Inclusive criteria： ①relevant to the role of α- synuclein; ②the research mainly about mitochondria and neuronal apoptosis. Articles were excluded because of repetition and obsolescence. DATA EXTRACTION： Totally 349 articles were found and 30 of them were selected according to the inclusive criteria as described above. DATA SYNTHESIS： Of the 30 articles, 15 were related to the role of α- synuclein; 12 were associated with mitochondria and neuronal apoptosis; 3 were involved in the relationship between α-synuclein and mitochondria. Early studies had shown that α-synuclein was a toxic protein which played a key role in the process of neurodegeneration. However, some recent studies have also confirmed that α-synuclein may play a dual role and the interaction between mitochondria and α-synuclein is the key point for this effect. CONCLUSION： There is a complex interplay between α-synuclein and mitochondria. Further studies focused on the relationship between α-synuclein and mitocbendria may provide a new insight into the etiology of Parkinson disease.