title: Molecular pathways of programmed cell death in experimental Parkinson's disease.
abstract: Dysfunction of mitochondrial complex I leads to degeneration of dopaminergic neurons of the substantia nigra pars compacta, as seen in Parkinson's disease, through activation of mitochondria-dependent programmed cell death pathways. In this scenario, complex I blockade increases the soluble pool of cytochrome c in the mitochondrial intermembrane space through oxidative mechanisms, whereas activation of pro-cell death protein Bax triggers neuronal death by permeabilizing the outer mitochondrial membrane and releasing cytochrome c into the cytosol. Targeting either Bax transcriptional or post-translational activation results in a marked attenuation of dopaminergic cell death caused by complex I inhibition.
authors.affiliation: Catalan Institution for Research and Advanced Studies, Barcelona, Spain. mvila@it.vhebron.net
authors.forename: Miquel
authors.initials: M
authors.lastname: Vila
authors.forename: Celine
authors.initials: C
authors.lastname: Perier
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D042967:Electron Transport Complex I / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D008928:Mitochondria / Q000378:metabolism; D020734:Parkinsonian Disorders / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology
chemical_list: D042967:Electron Transport Complex I