共核细胞病
α-突触核蛋白
神经科学
机制(生物学)
帕金森病
生物
疾病
动物模型
医学
病理
认识论
内分泌学
哲学
作者
Benjamin Dehay,Miquel Vila,Erwan Bézard,Patrik Brundin,Jeffrey H. Kordower
摘要
ABSTRACT Aggregation of alpha‐synuclein is implicated in several neurodegenerative diseases collectively termed synucleinopathies. Emerging evidence strongly implicates cell‐to‐cell transmission of misfolded alpha‐synuclein as a common pathogenetic mechanism in synucleinopathies. The impact of alpha‐synuclein pathology on neuronal dysfunction and behavioral impairments is being explored in animal models. This review provides an update on how research in animal models supports the concept that misfolded alpha‐synuclein spreads from cell to cell and describes how findings in animal models might relate to the disease process in humans. Finally, we discuss the current underlying molecular and cellular mechanisms and future therapeutic strategies targeting alpha‐synuclein propagation. © 2015 International Parkinson and Movement Disorder Society
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