Summary
Ideally, animal models of Parkinson’s should reproduce the clinical manifestation of the disease, a loss of some but not all dopaminergic neurons, a loss of some non dopaminergic neurons and alphasynuclein positive inclusions resembling Lewy bodies. There are at least three ways to develop animal models of PD. The first two are based on the etiology of the disease and consist in 1) reproducing in animals the mutations seen in inherited forms of PD; 2) intoxicating animals with putative environmental toxins causing PD. The last method currently used, which is not exclusive of the first two, is to try to reproduce the molecular or biochemical changes seen post-mortem in the brain of patients with PD. In this review we discuss the advantages and the drawbacks in term of neuroprotection of the currently used models.
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Hirsch, E.C. (2006). How to judge animal models of Parkinson’s disease in terms of neuroprotection. In: Riederer, P., Reichmann, H., Youdim, M.B.H., Gerlach, M. (eds) Parkinson’s Disease and Related Disorders. Journal of Neural Transmission. Supplementa, vol 70. Springer, Vienna . https://doi.org/10.1007/978-3-211-45295-0_39
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DOI: https://doi.org/10.1007/978-3-211-45295-0_39
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