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TFEB：帕金森病中的致病作用和治疗靶点。

TFEB: Pathogenic role and therapeutic target in Parkinson disease.

机构信息

Department of Experimental Medical Sciences; Wallenberg Neuroscience Center; Lund University; Lund, Skane Sweden.

出版信息

Autophagy. 2013 Aug;9(8):1244-6. doi: 10.4161/auto.25044. Epub 2013 May 22.

DOI:10.4161/auto.25044
PMID:23715007
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3748195/
Abstract

Parkinson disease (PD) is characterized by the progressive loss of nigral dopamine neurons and the presence of accumulations containing the disease-causing protein SNCA/α-synuclein. Here we review our recent findings describing how SNCA impairs the function of the master regulator of the autophagy-lysosomal pathway (ALP), the transcription factor EB (TFEB), and that genetic or pharmacological stimulation of its activity promotes protection of dopamine neurons. These findings suggest that strategies aimed at enhancing autophagy-mediated degradation of SNCA may hold great promise for disease intervention in PD.

摘要

帕金森病（PD）的特征是黑质多巴胺神经元的进行性丧失和含有致病蛋白 SNCA/α-突触核蛋白的堆积物的存在。在这里，我们回顾了我们最近的发现，描述了 SNCA 如何损害自噬溶酶体途径 (ALP) 的主调控因子转录因子 EB (TFEB) 的功能，以及其活性的遗传或药理学刺激如何促进多巴胺神经元的保护。这些发现表明，旨在增强 SNCA 介导的自噬降解的策略可能为 PD 疾病干预提供巨大的希望。