In a flurry of PINK, mitochondrial bioenergetics takes a leading role in Parkinson's disease.
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).
Murphy
Anne N
AN
Department of Pharmacology, MC 0636, Basic Sciences Building, Rm 3014, 9500 Gilman Dr., La Jolla, University of California, San Diego, CA 92093, USA. anmurphy@ucsd.edu
D000818:Animals; D004195:Disease Models, Animal; D004331:Drosophila melanogaster; D004734:Energy Metabolism; D051379:Mice; D008928:Mitochondria / Q000201:enzymology* / Q000378:metabolism; D010300:Parkinson Disease / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D011494:Protein Kinases / Q000378:metabolism*; D000099202:PTEN-Induced Putative Kinase
D011494:Protein Kinases; D000099202:PTEN-Induced Putative Kinase