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阿尔茨海默病中的炎症反应。

Inflammatory response in Alzheimer's disease.

作者信息

Akiyama H

机构信息

Division of Neuropathology, Tokyo Institute of Psychiatry, Japan.

出版信息

Tohoku J Exp Med. 1994 Nov;174(3):295-303. doi: 10.1620/tjem.174.295.

DOI:10.1620/tjem.174.295
PMID:7539162
Abstract

Microglia belong to the mononuclear phagocyte system. They represent the brain resident tissue macrophages and function as the scavenger cells in brain. In Alzheimer's disease (AD), microglia become activated. Reactive microglia aggregate around senile plaque beta-amyloid and neurofibrillary tangles. Heavy accumulation of these pathological debris in postmortem, however, indicates the failure or, at best, partial success of the removal. It is supposed that continued activation of microglia in these lesions elicits a persistent inflammatory response. In fact, activation fragments of the complement system have been detected in association with beta-amyloid deposits and extracellular ghost tangles. Thrombin, a central serine protease of the coagulation pathway, is also deposited in these pathological debris. Both complements and thrombin could augment the biochemical, synthetic and phagocytic capacities of microglia. Microglia, in turn, might play a major role for the activation of complement and coagulation systems in brain. The available evidence strongly suggests a significant similarity between the chronic inflammation and the tissue response in AD lesions, supporting a notion that the inflammatory process is a part of Alzheimer pathology.

摘要

小胶质细胞属于单核吞噬细胞系统。它们是脑内驻留的组织巨噬细胞,在脑中起清道夫细胞的作用。在阿尔茨海默病(AD)中,小胶质细胞被激活。反应性小胶质细胞聚集在老年斑β-淀粉样蛋白和神经原纤维缠结周围。然而,在尸检中这些病理碎片的大量积累表明清除失败,或者充其量只是部分成功。据推测,这些病变中小胶质细胞的持续激活会引发持续的炎症反应。事实上,已检测到补体系统的激活片段与β-淀粉样蛋白沉积物和细胞外空泡缠结有关。凝血酶是凝血途径的中心丝氨酸蛋白酶,也沉积在这些病理碎片中。补体和凝血酶都可以增强小胶质细胞的生化、合成和吞噬能力。反过来,小胶质细胞可能在脑内补体和凝血系统的激活中起主要作用。现有证据有力地表明,AD病变中的慢性炎症与组织反应之间存在显著相似性,支持了炎症过程是阿尔茨海默病病理学一部分的观点。

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