阿尔茨海默病与炎性调控

Alzheimer's Disease and Inflammatory Regulation

阿尔茨海默病(AD)是毁灭性的神经退行性损伤疾病,其特点是细胞外聚积β淀粉样蛋白(Aβ)形成淀粉样斑块和细胞内异常高度磷酸化tau蛋白导致神经纤维缠结(neurobrillary tangles).基于上述特点提出的β淀粉样蛋白假说和tau的高度磷酸化假说,仍不能完全解释其发病机理和神经元的退行性损伤.目前,炎症小体在阿尔茨海默病的病理过程中引起的炎症和组织损伤引起高度关注.因此研究AD患者中炎症小体如何激活、组装、并诱发细胞炎性介质的高表达,可能对深入研究AD病理机制和治疗靶点的突破提供一种新的解释,本文主要针对这一研究领域的进展加以简要的概述介绍.

Alzheimer＇s disease （AD） is a devastating neurodegenerative disease characterized by extra- cellular deposition of amyloid-β （Aβ）plaques and intra-cellular accumulation of hyper-phosphorylated tau protein resulting in NFTs （neurofibrillary tangles）. The Aβ and tau hypotheses postulated by its hallmark are not sufficient in explaining all the features of AD. Currently, inflammation and tissue injury caused by inflammasome have attracted extensive attention in the field of pathogenesis AD. This review will give a brief introduction regarding how inflammasome is to be activated and assembled as well as its relation to the highly expressed inflammatory molecules, which will offer to a new break-through in pathological mechanism and therapeutic targets of AD.