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A tale on animal models of Parkinson's disease§

Authors

  • Erwan Bezard PhD,

    1. Insitute of Neurodegenerative Diseases, Université Victor Ségalen-Bordeaux II, Centre National de la Recherche Scientifique, Bordeaux, France
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  • Serge Przedborski MD, PhD

    Corresponding author
    1. Departments of Neurology, Pathology, and Cell Biology and the Center for Motor Neuron. Biology and Disease, Columbia University, New York, New York, USA
    • Center for Motor Neuron. Biology and Disease, P&S 5-420, Columbia University, 630 West 168th Street, New York, NY 10032, USA
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  • Relevant conflicts of interest/financial disclosures: Erwan Bezard is supported by Agence Nationale de la Recherche grants (ANR-07-JCJC-0090, ANR-08-MNP-018, ANR-07-MNP-Trafinlid) and Serge Przedborski by NIH grants AG021617, NS042269, NS062180, NS064191, and NS38370; U.S. Department of Defense grants (W81XWH-08-1-0522 and W81XWH-08-1-0465); the Parkinson Disease Foundation (New York, NY); the Thomas Hartman Foundation for Parkinson's Research, and the MDA/Wings-over-Wall Street. Serge Przedborski is the Page and William Black Professor of Neurology.

  • Infrastructural support for this study was provided by the Université Victor-Segalen Bordeaux 2 and the Centre National de la Recherche Scientifique.

  • §

    Full financial disclosures and author roles may be found in the online version of this article.

Abstract

Parkinson's disease is a neurodegenerative disorder whose cardinal manifestations are due primarily to a profound deficit in brain dopamine. Since the 1980s, several therapeutic strategies have been discovered to treat the symptoms of this neurological disorder, but as of yet, none halts or retards the neurodegenerative process. In an attempt to shed light on the neurobiology of Parkinson's disease, a number of experimental models have been developed, especially during the last 25 years. They come essentially in 3 flavors: pharmacological (eg, reserpine), toxic (eg, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), and genetic (eg, transgenic synuclein mice). These models can also be recast as etiologic, pathogenic, and symptomatic/pathophysiologic, as each may contribute to our understanding of the cause, the mechanisms, and the treatment of Parkinson's disease. In this review, we will discuss the question of Parkinson's disease models, starting from the period when this journal was born to today. During this journey of 25 years, we will discuss both the significant contributions of the Parkinson's disease models and hurdles that remain to be overcome to one day cure this neurological disease. © 2011 Movement Disorder Society

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