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Erschienen in: Journal of Neural Transmission 3/2018

22.04.2017 | Neurology and Preclinical Neurological Studies - Review Article

α-Synuclein nonhuman primate models of Parkinson’s disease

verfasst von: David J. Marmion, Jeffrey H. Kordower

Erschienen in: Journal of Neural Transmission | Ausgabe 3/2018

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Abstract

Proper understanding of the mechanism(s) by which α-synuclein misfolds and propagates may hold the key to unraveling the complex pathophysiology of Parkinson’s disease. A more complete understanding of the disease itself, as well as establishing animal models that fully recapitulate pathological and functional disease progression, are needed to develop treatments that will delay, halt or reverse the disease course. Traditional neurotoxin-based animal models fail to mimic crucial aspects of Parkinson’s and thus are not relevant for the study of neuroprotection and disease-modifying therapies. Therefore, a new era of animal models centered on α-synuclein has emerged with the utility of nonhuman primates in these studies beginning to become important. Indeed, disease modeling in nonhuman primates offers a more similar anatomical and genetic background to humans, and the ability to assess complex behavioral impairments that are difficult to test in rodents. Furthermore, results obtained from monkey studies translate better to applications in humans. In this review, we highlight the importance of α-synuclein in Parkinson’s disease and discuss the development of α-synuclein based nonhuman primate models.
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Metadaten
Titel
α-Synuclein nonhuman primate models of Parkinson’s disease
verfasst von
David J. Marmion
Jeffrey H. Kordower
Publikationsdatum
22.04.2017
Verlag
Springer Vienna
Erschienen in
Journal of Neural Transmission / Ausgabe 3/2018
Print ISSN: 0300-9564
Elektronische ISSN: 1435-1463
DOI
https://doi.org/10.1007/s00702-017-1720-0

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