Surmeier D James, Obeso José A, Halliday Glenda M
Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611,
CINAC, HM Puerta del Sur, Hospitales de Madrid, Mostoles and CEU-San Pablo University, 28938 Madrid, Spain.
J Neurosci. 2017 Oct 11;37(41):9799-9807. doi: 10.1523/JNEUROSCI.1787-16.2017.
The notion that prion-like spreading of misfolded α-synuclein (α-SYN) causes Parkinson's disease (PD) has received a great deal of attention. Although attractive in its simplicity, the hypothesis is difficult to reconcile with postmortem analysis of human brains and connectome-mapping studies. An alternative hypothesis is that PD pathology is governed by regional or cell-autonomous factors. Although these factors provide an explanation for the pattern of neuronal loss in PD, they do not readily explain the apparently staged distribution of Lewy pathology in many PD brains, the feature of the disease that initially motivated the spreading hypothesis by Braak and colleagues. While each hypothesis alone has its shortcomings, a synthesis of the two can explain much of what we know about the etiopathology of PD. Prying into the Prion Hypothesis for Parkinson's Disease, by Patrik Brundin and Ronald Melki.
错误折叠的α-突触核蛋白（α-SYN）的朊病毒样传播导致帕金森病（PD）这一观点已受到广泛关注。尽管该假说简单诱人，但难以与人类大脑的尸检分析及连接组图谱研究相协调。另一种假说是，PD病理学受区域或细胞自主因素支配。虽然这些因素为PD中神经元丢失的模式提供了解释，但它们并不能轻易解释许多PD大脑中路易体病理明显的阶段性分布，而这一疾病特征最初促使Braak及其同事提出了传播假说。虽然每个假说都有其缺点，但将两者结合起来可以解释我们目前对PD病因病理学的许多认识。《探究帕金森病的朊病毒假说》，作者Patrik Brundin和Ronald Melki 。
