Modeling Parkinson’s Disease in Primates

Bezard E(1)(2)(3), Teil M(4), Arotcarena ML(4), Porras G(2), Li Q(3), Dehay B(3).

Author information:
(1)Université de Bordeaux, Centre National de la Recherche Scientifique (CNRS),
IMN, UMR 5293, F-33000 Bordeaux, France .
(2)Motac Neuroscience, F-33270 Floirac, France.
(3)Motac Beijing Services, PRC-100050 Beijing, China.
(4)Université de Bordeaux, Centre National de la Recherche Scientifique (CNRS),
IMN, UMR 5293, F-33000 Bordeaux, France.

Decades of research have identified the pathological and pathophysiological
hallmarks of Parkinson’s disease (PD): profound deficit in brain dopamine and
other monoamines, pathological α-synuclein aggregation, synaptic and neuronal
network dysfunction, aberrant proteostasis, altered energy homeostasis,
inflammation, and neuronal cell death. The purpose of this contribution is to
present the phenocopy aspect, pathogenic, and etiologic nonhuman primate (NHP)
models of PD to readers with limited prior knowledge of PD so that they are
ready to start working on PD. How NHPs, the closest species to man on which we
can model diseases, contribute to the knowledge progress and how these models
represent an invaluable translational step in therapeutic development are
highlighted.

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Auteurs Bordeaux Neurocampus