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Animal models of Parkinson's disease: Limits and relevance to neuroprotection studies


  • Erwan Bezard PhD,

    Corresponding author
    1. CNRS, Institut des Maladies Neurodégénératives, UMR 5293, Bordeaux, France
    2. Centre Hospitalier Universitaire, Clinical Neurophysiology Department, Hôpital Pellegrin, Bordeaux, France
    • University de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, Bordeaux, France
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  • Zhenyu Yue PhD,

    1. Departments of Neurology and Neuroscience, Friedman Brain Institute, Mount Sinai School of Medicine, New York, New York, USA
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  • Deniz Kirik MD, PhD,

    1. Brain Repair And Imaging in Neural Systems Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden
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  • Maria Grazia Spillantini PhD

    1. Cambridge Center for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United Kingdom
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  • Funding agencies: The Université Victor-Segalen Bordeaux 2 and the Centre National de la Recherche Scientifique provided the infrastructural support to E.B. E.B. is supported by Agence Nationale de la Recherche grants (ANR-07-JCJC-0090, ANR-08-MNP-018, and ANR-07-MNP-Trafinlid). D.K. is supported by grants from the Swedish Research Council (project grant no. 2009-2318, Senior Researcher Position, Bagadilico Linné program no. 2007-8626, and MultiPark Strategic Research Environment), the European Research Council (TreatPD, no. 242932), and the Michael J Fox Foundation. Z.Y. is supported by National Institutes of Health/NINDS grants (NS060809–01 and NS072359–01) and the Michael J. Fox Foundation for Parkinson's Research. M.G.S. is supported by Parkinson's UK and the Michael J Fox Foundation.

  • Relevant conflicts of interest/financial disclosures: Nothing to report.

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

Correspondence to: Dr. Erwan Bezard, CNRS UMR 5293, IMN, Université Bordeaux Segalen, 146 rue Léo Saignat, 33076 Bordeaux, France;


Over the last two decades, significant strides has been made toward acquiring a better knowledge of both the etiology and pathogenesis of Parkinson's disease (PD). Experimental models are of paramount importance to obtain greater insights into the pathogenesis of the disease. Thus far, neurotoxin-based animal models have been the most popular tools employed to produce selective neuronal death in both in vitro and in vivo systems. These models have been commonly referred to as the pathogenic models. The current trend in modeling PD revolves around what can be called the disease gene-based models or etiologic models. The value of utilizing multiple models with a different mechanism of insult rests on the premise that dopamine-producing neurons die by stereotyped cascades that can be activated by a range of insults, from neurotoxins to downregulation and overexpression of disease-related genes. In this position article, we present the relevance of both pathogenic and etiologic models as well as the concept of clinically relevant designs that, we argue, should be utilized in the preclinical development phase of new neuroprotective therapies before embarking into clinical trials. © 2013 Movement Disorder Society