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Oxidative Medicine and Cellular Longevity
Volume 2012, Article ID 624925, 25 pages
Review Article

Oxidative Stress in Genetic Mouse Models of Parkinson’s Disease

Department of Pharmaceutical Chemistry, Drug Analysis and Drug Information, Center for Neurosciences, Faculty of Medicine and Pharmacy, Vrije Universiteit Brussel, Laarbeeklaan 103, 1090 Brussels, Belgium

Received 24 February 2012; Revised 12 April 2012; Accepted 12 April 2012

Academic Editor: Krzysztof Ksiazek

Copyright © 2012 Mustafa Varçin 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.


There is extensive evidence in Parkinson’s disease of a link between oxidative stress and some of the monogenically inherited Parkinson’s disease-associated genes. This paper focuses on the importance of this link and potential impact on neuronal function. Basic mechanisms of oxidative stress, the cellular antioxidant machinery, and the main sources of cellular oxidative stress are reviewed. Moreover, attention is given to the complex interaction between oxidative stress and other prominent pathogenic pathways in Parkinson’s disease, such as mitochondrial dysfunction and neuroinflammation. Furthermore, an overview of the existing genetic mouse models of Parkinson’s disease is given and the evidence of oxidative stress in these models highlighted. Taken into consideration the importance of ageing and environmental factors as a risk for developing Parkinson’s disease, gene-environment interactions in genetically engineered mouse models of Parkinson’s disease are also discussed, highlighting the role of oxidative damage in the interplay between genetic makeup, environmental stress, and ageing in Parkinson’s disease.