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Parkinson’s disease: a rethink of rodent models

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Abstract

Parkinson’s disease (PD) is a multifactorial disease with a complex etiology that results from genetic risk factors, environmental exposures and most likely a combination of both. Rodent models of parkinsonism aim to reproduce key pathogenic features of the syndrome including movement disorder induced by the progressive loss of dopaminergic neurons in the substantia nigra, accompanied by the formation of α-synuclein containing Lewy body inclusions. Despite the creation of many excellent models, both chemically induced and genetically engineered, there is none that accurately demonstrates these features. Recent pathological staging studies in man have also emphasized the significant non-CNS component of PD that has yet to be tackled. Herein, we summarize rodent models of PD and what they offer to the field, and suggest future challenges and opportunities.

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Acknowledgements

This work was supported by Michael J Fox Fellowship to Dr. Heather Melrose and by research grants from the National Parkinson’s Foundation and the National Institute for Neurological Disease and Stroke (P01 NS40256).

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Correspondence to Matthew J. Farrer.

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Melrose, H.L., Lincoln, S.J., Tyndall, G.M. et al. Parkinson’s disease: a rethink of rodent models. Exp Brain Res 173, 196–204 (2006). https://doi.org/10.1007/s00221-006-0461-3

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  • DOI: https://doi.org/10.1007/s00221-006-0461-3

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