Trojanowski John Q, Lee Virginia M-Y
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, the University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.
Ann N Y Acad Sci. 2003 Jun;991:107-10. doi: 10.1111/j.1749-6632.2003.tb07468.x.
A paradigm shift in understanding Parkinson's disease (PD) and related disorders is emerging from studies showing that alpha-synuclein (AS) gene mutations cause familial PD; AS is abnormally nitrated, phosphorylated, and ubiquitinated; AS forms neuronal and glial inclusions; AS fibrillizes in vitro; and AS transgenic animals develop neurodegeneration with AS amyloid inclusions. Thus, PD and related synucleinopathies are brain amyloidoses that may share similar mechanisms and targets for drug discovery.
对帕金森病（PD）及相关疾病的理解正在经历范式转变，研究表明α-突触核蛋白（AS）基因突变会导致家族性PD；AS会发生异常硝化、磷酸化和泛素化；AS会形成神经元和胶质细胞内含物；AS在体外会形成纤维；并且AS转基因动物会出现神经退行性变并伴有AS淀粉样蛋白内含物。因此，PD及相关突触核蛋白病是脑淀粉样变性疾病，可能具有相似的机制和药物研发靶点。
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