神经科学
蛋白质稳态
疾病
物候学
帕金森病
病态的
帕金森病
生物
多巴胺
陶氏病
医学
心理学
神经退行性变
病理
遗传学
生物化学
基因
突变体
作者
Erwan Bézard,Margaux Teil,Marie-Laure Arotçarena,Grégory Porras,Qin Li,Benjamin Dehay
标识
DOI:10.1101/cshperspect.a041612
摘要
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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