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Journal of Biomedicine and Biotechnology
Volume 2012 (2012), Article ID 845618, 10 pages
Review Article

Classic and New Animal Models of Parkinson's Disease

1Department of Pathology and Cell Biology, Columbia University, New York, NY 10032, USA
2Center for Motor Neuron Biology and Disease, Columbia University, New York, NY 10032, USA
3Department of Neurology, Columbia University, New York, NY 10032, USA

Received 9 January 2012; Accepted 23 January 2012

Academic Editor: Monica Fedele

Copyright © 2012 Javier Blesa 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.


Neurological disorders can be modeled in animals so as to recreate specific pathogenic events and behavioral outcomes. Parkinson’s Disease (PD) is the second most common neurodegenerative disease of an aging population, and although there have been several significant findings about the PD disease process, much of this process still remains a mystery. Breakthroughs in the last two decades using animal models have offered insights into the understanding of the PD disease process, its etiology, pathology, and molecular mechanisms. Furthermore, while cellular models have helped to identify specific events, animal models, both toxic and genetic, have replicated almost all of the hallmarks of PD and are useful for testing new neuroprotective or neurorestorative strategies. Moreover, significant advances in the modeling of additional PD features have come to light in both classic and newer models. In this review, we try to provide an updated summary of the main characteristics of these models as well as the strengths and weaknesses of what we believe to be the most popular PD animal models. These models include those produced by 6-hydroxydopamine (6-OHDA), 1-methyl-1,2,3,6-tetrahydropiridine (MPTP), rotenone, and paraquat, as well as several genetic models like those related to alpha-synuclein, PINK1, Parkin and LRRK2 alterations.