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ACCEPTED MANUSCRIPT Mitochondrial dysfunction in Parkinson's disease Konstanze F. Winkhofer* and Christian Haass German Center for Neurodegenerative Diseases (DZNE) Munich and Adolf Butenandt Institute, Biochemistry, Ludwig Maximilians University, 80336 Munich, Germany *To whom correspondence should be addressed: Konstanze F. Winklhofer, Schillerstr. 44, D-80336 Munich, telephone: +49 89 2180 75483, fax: +49 89 2180 75415, E-mail: Konstanze.Winklhofer@med.uni- muenchen.de ACCEPTED MANUSCRIPT Key words: Parkinson's disease, mitochondria, parkin, PINK1, a-synuclein, DJ-1, LRRK2 1
Abstract ACCEPTED MANUSCRIPT Mitochondria are highly dynamic organelles which fulfill a plethora of functions. In addition to their prominent role in energy metabolism, mitochondria are intimately involved in various key cellular processes, such as the regulation of calcium homeostasis, stress response and cell death pathways. Thus, it is not surprising that an impairment of mitochondrial function results in cellular damage and is linked to aging and neurodegeneration. Many lines of evidence suggest that mitochondrial dysfunction plays a central role in the pathogenesis of Parkinson's disease (PD), starting in the early 1980s with the observation that an inhibitor of complex I of the electron transport chain can induce parkinsonism. Remarkably, recent research indicated that several PD-associated genes interface with pathways regulating mitochondrial function, morphology, and dynamics. In fact, sporadic and familial PD seem to converge at the level of mitochondrial integrity. ACCEPTED MANUSCRIPT 2
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