Relevant conflict of interest: Nothing to report.
Article first published online: 5 APR 2011
Copyright © 2011 Movement Disorder Society
Volume 26, Issue 7, pages 1198–1205, June 2011
How to Cite
Dehay, B. and Bezard, E. (2011), New animal models of Parkinson's disease. Mov. Disord., 26: 1198–1205. doi: 10.1002/mds.23546
This review was supported by the Université Victor Ségalen-Bordeaux II, the CNRS, European Commission's Marie Curie Reintegration Grant (FP7-PEOPLE-2009-ERG256303, to B.D.), Fondation pour la Recherche Médicale (B.D.) and by Agence Nationale de la Recherche grants (EB). Benjamin Dehay is employed by Université Victor Ségalen-Bordeaux II (France) and has received Marie Curie Reintegration (FP7-PEOPLE-2009-ERG256303, to Benjamin Dehay.) and Fondation pour la Recherche Médicale grants. Erwan Bezard is employed by INSERM (France), owns stocks in Motac Holding Ltd. (Manchester, UK), receives consultancy from Motac neuroscience Ltd. (Manchester, UK), has received grants from the Agence Nationale de la Recherche (France), the Michael J. Fox Foundation for Parkinson Research (USA), the European Commission and is a member of the scientific advisory board of the Michael J. Fox Foundation for Parkinson Research (USA) and of the France Parkinson association.
Full financial disclosures and author roles may be found in the online version of this article.
- Issue published online: 20 JUN 2011
- Article first published online: 5 APR 2011
- Manuscript Accepted: 1 NOV 2010
- Manuscript Revised: 19 OCT 2010
- Manuscript Received: 20 SEP 2010
- animal models;
- Parkinson's disease;
- bacterial artificial chromosome (BAC)
Parkinson's disease is a progressive neurodegenerative disorder mainly characterized by the loss of dopaminergic neurons from the substantia nigra pars compacta and the presence, in the affected brain regions, of protein inclusions named Lewy Bodies. Despite the fact that numerous mutations causing hereditary forms of Parkinson's disease have been identified in the last decade, current transgenic animal models do not adequately reproduce cardinal features of the human disease. Altogether, the animal models derived of human mutations indicate that the nigrostriatal degenerative process results from the combination of several mechanisms that implicate mitochondrial dysfunction, oxidative damage, and protein degradation impairment.
Methods and Results:
We performed a literature search between 2008 and 2010.
The absence of adequate in vivo experimental models of Parkinson's disease has severe repercussions for therapeutic intervention success for this incurable neurodegenerative disorder. The present nonexhaustive review looks at invertebrate and mammalian models of Parkinson's disease generated in the last three years. © 2011 Movement Disorder Society