Gandhi Sonia, Wood Nicholas W
Department of Molecular Neuroscience, Institute of Neurology, Queen Square, London, UK.
Hum Mol Genet. 2005 Oct 15;14 Spec No. 2:2749-2755.
Parkinson's disease (PD) is a common and incurable neurodegenerative disease, affecting 1% of the population over the age of 65. Despite a well-described clinical and pathological phenotype, the molecular mechanisms which lead to neurodegeneration remain elusive. However, there is a wealth of evidence from both toxin based models and genetic based models, which suggest a major etiologic role for mitochondrial dysfunction, protein aggregation, the ubiquitin-proteasome system and kinase signalling pathways in the pathogenesis of PD. Ultimately, an understanding of the molecular events which precipitate neurodegeneration in idiopathic PD will enable the development of targeted and effective therapeutic strategies. We review the latest evidence for the proposed molecular processes and discuss their relevance to the pathogenesis of sporadic PD.
帕金森病（PD）是一种常见的、无法治愈的神经退行性疾病，影响着1%的65岁以上人群。尽管其临床和病理表型已有详尽描述，但导致神经退行性变的分子机制仍不清楚。然而，基于毒素模型和基于基因模型的大量证据表明，线粒体功能障碍、蛋白质聚集、泛素-蛋白酶体系统和激酶信号通路在帕金森病发病机制中起主要病因作用。最终，了解特发性帕金森病中引发神经退行性变的分子事件将有助于开发有针对性的有效治疗策略。我们综述了所提出的分子过程的最新证据，并讨论了它们与散发性帕金森病发病机制的相关性。
