Center for Neuroscience and Cell Biology, University of Coimbra, Portugal.
Curr Pharm Des. 2011;17(31):3390-7. doi: 10.2174/138161211798072508.
During the past decades, we have witnessed significant advances in our understanding of the molecular etiology of Parkinson's disease (PD). The unearthing of the causative genes for hereditary PD accelerated not only the studies of the molecular mechanisms underlying this pathology, but also set mitochondria at the center of PD pathology. In this review we revisit mitochondrial key role and propose a hypothesis for PD, that allows the unification of both sporadic and familial PD forms. In light of this we also discuss new promising disease-modified therapies.
在过去的几十年中，我们见证了对帕金森病 (PD) 分子病因的理解的重大进展。遗传性 PD 致病基因的发现不仅加速了该病理学基础分子机制的研究，而且使线粒体成为 PD 病理学的中心。在这篇综述中，我们重新审视了线粒体的关键作用，并提出了一个 PD 的假设，该假设允许统一散发性和家族性 PD 形式。有鉴于此，我们还讨论了新的有前途的疾病修饰疗法。
