Experimental Brain Research

, Volume 173, Issue 2, pp 196–204

Parkinson’s disease: a rethink of rodent models

Authors

  • Heather L. Melrose
    • Department of Neuroscience, Genetics of Parkinsonism and Related DisordersMorris K. Udall Parkinson’s Disease Research Center of Excellence, Birdsall Bldg., Mayo Clinic
  • Sarah J. Lincoln
    • Department of Neuroscience, Genetics of Parkinsonism and Related DisordersMorris K. Udall Parkinson’s Disease Research Center of Excellence, Birdsall Bldg., Mayo Clinic
  • Glenn M. Tyndall
    • Department of Neuroscience, Genetics of Parkinsonism and Related DisordersMorris K. Udall Parkinson’s Disease Research Center of Excellence, Birdsall Bldg., Mayo Clinic
    • Department of Neuroscience, Genetics of Parkinsonism and Related DisordersMorris K. Udall Parkinson’s Disease Research Center of Excellence, Birdsall Bldg., Mayo Clinic
Review

DOI: 10.1007/s00221-006-0461-3

Cite this article as:
Melrose, H.L., Lincoln, S.J., Tyndall, G.M. et al. Exp Brain Res (2006) 173: 196. doi:10.1007/s00221-006-0461-3

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.

Keywords

Parkinson’s diseaseMouseToxinGenetic

Copyright information

© Springer-Verlag 2006