Schulz Jörg B
Department of Neurodegeneration & Restorative Research, Center for Neurological Medicine, University Medical Center Göttingen, Germany.
Parkinsonism Relat Disord. 2007;13 Suppl 3:S306-8. doi: 10.1016/S1353-8020(08)70021-X.
The discovery of mutations in hereditary forms of Parkinson's disease has implicated aggregation of a-synuclein, dysfunction of protein turnover and mitochondrial dysfunction as important mediators in the pathogenesis of Parkinson's disease. Subsequent studies have shown that these factors also represent hallmarks of idiopathic Parkinson's disease. Cell death mechanisms include excitotoxicity, calcium overload, apoptosis and autophagia. Here, I will briefly review the molecular mechanisms of neurodegeneration in Parkinson's disease and point out potential treatment options.
帕金森病遗传形式中突变的发现表明，α-突触核蛋白的聚集、蛋白质周转功能障碍和线粒体功能障碍是帕金森病发病机制中的重要介质。随后的研究表明，这些因素也是特发性帕金森病的特征。细胞死亡机制包括兴奋性毒性、钙超载、凋亡和自噬。在此，我将简要回顾帕金森病神经退行性变的分子机制，并指出潜在的治疗选择。
