在阿尔茨海默病中，RAGE是β淀粉样蛋白诱导的细胞功能紊乱的关键细胞靶点。
RAGE is a key cellular target for Abeta-induced perturbation in Alzheimer's disease.
作者信息
Yan Shirley ShiDu, Chen Doris, Yan Shiqian, Guo Lan, Du Heng, Chen John Xi
机构信息
Department of Surgery, Physicians and Surgeons College of Columbia University, New York, NY 10032, USA.
出版信息
Front Biosci (Schol Ed). 2012 Jan 1;4(1):240-50. doi: 10.2741/s265.
Abstract
RAGE, a receptor for advanced glycation endproducts, is an immunoglobulin-like cell surface receptor that is often described as a pattern recognition receptor due to the structural heterogeneity of its ligand. RAGE is an important cellular cofactor for amyloid beta-peptide (Abeta)-mediated cellular perturbation relevant to the pathogenesis of Alzheimer's disease (AD). The interaction of RAGE with Abeta in neurons, microglia, and vascular cells accelerates and amplifies deleterious effects on neuronal and synaptic function. RAGE-dependent signaling contributes to Abeta-mediated amyloid pathology and cognitive dysfunction observed in the AD mouse model. Blockade of RAGE significantly attenuates neuronal and synaptic injury. In this review, we summarize the role of RAGE in the pathogenesis of AD, specifically in Abeta-induced cellular perturbation.
摘要
晚期糖基化终产物受体（RAGE）是一种免疫球蛋白样细胞表面受体，由于其配体的结构异质性，它常被描述为一种模式识别受体。RAGE是淀粉样β肽（Aβ）介导的与阿尔茨海默病（AD）发病机制相关的细胞扰动的重要细胞辅因子。RAGE与神经元、小胶质细胞和血管细胞中的Aβ相互作用，加速并放大了对神经元和突触功能的有害影响。在AD小鼠模型中观察到，RAGE依赖性信号传导促成了Aβ介导的淀粉样病理和认知功能障碍。阻断RAGE可显著减轻神经元和突触损伤。在本综述中，我们总结了RAGE在AD发病机制中的作用，特别是在Aβ诱导的细胞扰动中的作用。
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