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Parkinson’s Disease
Volume 2011, Article ID 767230, 13 pages
Review Article

Mitochondrial Fusion/Fission, Transport and Autophagy in Parkinson's Disease: When Mitochondria Get Nasty

1Center for Neuroscience and Cell Biology (CNC), University of Coimbra, Largo Marquês de Pombal, 3004-517 Coimbra, Portugal
2Faculty of Medicine, University of Coimbra, Largo Marquês de Pombal, 3004-517 Coimbra, Portugal

Received 1 October 2010; Revised 26 November 2010; Accepted 5 January 2011

Academic Editor: Charleen T. Chu

Copyright © 2011 Daniela M. Arduíno et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Understanding the molecular basis of Parkinson's disease (PD) has proven to be a major challenge in the field of neurodegenerative diseases. Although several hypotheses have been proposed to explain the molecular mechanisms underlying the pathogenesis of PD, a growing body of evidence has highlighted the role of mitochondrial dysfunction and the disruption of the mechanisms of mitochondrial dynamics in PD and other parkinsonian disorders. In this paper, we comment on the recent advances in how changes in the mitochondrial function and mitochondrial dynamics (fusion/fission, transport, and clearance) contribute to neurodegeneration, specifically focusing on PD. We also evaluate the current controversies in those issues and discuss the role of fusion/fission dynamics in the mitochondrial lifecycle and maintenance. We propose that cellular demise and neurodegeneration in PD are due to the interplay between mitochondrial dysfunction, mitochondrial trafficking disruption, and impaired autophagic clearance.