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Parkinson’s Disease
Volume 2011, Article ID 951709, 14 pages
Review Article

Toxin-Induced and Genetic Animal Models of Parkinson's Disease

Department of Neurology, Sapporo Medical University, South1, West17, chuo-ku, Sapporo 060-8556, Japan

Received 13 October 2010; Accepted 31 October 2010

Academic Editor: Yuzuru Imai

Copyright © 2011 Shin Hisahara and Shun Shimohama. 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 common progressive neurodegenerative disorder. The major pathological hallmarks of PD are the selective loss of nigrostriatal dopaminergic neurons and the presence of intraneuronal aggregates termed Lewy bodies (LBs), but the pathophysiological mechanisms are not fully understood. Epidemiologically, environmental neurotoxins such as pesticides are promising candidates for causative factors of PD. Oxidative stress and mitochondrial dysfunction induced by these toxins could contribute to the progression of PD. While most cases of PD are sporadic, specific mutations in genes that cause familial forms of PD have led to provide new insights into its pathogenesis. This paper focuses on animal models of both toxin-induced and genetically determined PD that have provided significant insight for understanding this disease. We also discuss the validity, benefits, and limitations of representative models.