Department of Pharmacology, MC 0636, Basic Sciences Building, Rm 3014, 9500 Gilman Dr., La Jolla, University of California, San Diego, CA 92093, USA.
EMBO Mol Med. 2009 May;1(2):81-4. doi: 10.1002/emmm.200900020.
For many years research in Parkinson's disease (PD) has linked mitochondrial dysfunction with the characteristic loss of dopaminergic neurons of the substantia nigra, accumulation of cytoplasmic inclusions termed Lewy bodies, and motor dysfunction (Henchcliffe & Beal, 2008). The most compelling connection is that Parkinsonism can be observed in both humans and animals following exposure to inhibitors of complex I of the electron transport chain (Betarbet et al, 2002).
多年来,帕金森病(PD)的研究将线粒体功能障碍与黑质中多巴胺能神经元的特征性丧失、称为路易体的细胞质包涵体的积累以及运动功能障碍联系起来(Henchcliffe 和 Beal,2008)。最引人注目的联系是,在接触电子传递链复合物 I 抑制剂后,人类和动物都可以观察到帕金森病(Betarbet 等人,2002)。