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Parkinson’s Disease
Volume 2011 (2011), Article ID 716871, 18 pages
Review Article

Mitochondrial Dysfunction in Parkinson's Disease

1Medical Toxicology Centre, Wolfson Unit, Newcastle University, Claremont Place, Newcastle upon Tyne NE2 4AA, UK
2Institute of Human Genetics, Newcastle University, Central Parkway, Newcastle upon Tyne NE1 4EA, UK
3Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne NE4 6BE, UK

Received 1 November 2010; Revised 3 January 2011; Accepted 16 January 2011

Academic Editor: R. H. Swerdlow

Copyright © 2011 P. C. Keane 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.


Parkinson's disease (PD) is a progressive, neurodegenerative condition that has increasingly been linked with mitochondrial dysfunction and inhibition of the electron transport chain. This inhibition leads to the generation of reactive oxygen species and depletion of cellular energy levels, which can consequently cause cellular damage and death mediated by oxidative stress and excitotoxicity. A number of genes that have been shown to have links with inherited forms of PD encode mitochondrial proteins or proteins implicated in mitochondrial dysfunction, supporting the central involvement of mitochondria in PD. This involvement is corroborated by reports that environmental toxins that inhibit the mitochondrial respiratory chain have been shown to be associated with PD. This paper aims to illustrate the considerable body of evidence linking mitochondrial dysfunction with neuronal cell death in the substantia nigra pars compacta (SNpc) of PD patients and to highlight the important need for further research in this area.