Microglia, scavenger receptors, and the pathogenesis of Alzheimer's disease
Microglia, scavenger receptors, and the pathogenesis of Alzheimer's disease
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DOI：
10.1016/s0197-4580(98)00036-0
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发表时间：
1998-01-01
影响因子：
4.2
通讯作者：
Silverstein, SC
中科院分区：
文献类型：
--
作者：
El Khoury, J;Hickman, SE;Silverstein, SC
老年斑是阿尔茨海默病的病理标志。老年斑由β-淀粉样蛋白纤维组成，与激活的小胶质细胞、星形胶质细胞和营养不良神经元相关。我们最近发现A类清道夫受体是介导小胶质细胞与β淀粉样蛋白纤维相互作用的主要受体。小胶质细胞与β淀粉样蛋白纤维的黏附导致这些细胞固定在纤维上，并诱导它们产生活性氧物种。我们认为，小胶质细胞清道夫受体与纤维样β淀粉样蛋白的相互作用可能刺激小胶质细胞分泌载脂蛋白E和补体蛋白，这可能进一步促进神经毒性和神经元变性。因此，小胶质细胞清道夫受体可能成为阿尔茨海默病治疗干预的新靶点。(C)1998年爱思唯尔科学公司。
The senile plaque is the pathological hallmark of Alzheimer's disease. Senile plaques are composed of beta amyloid fibrils, associated with activated microglia, astrocytes, and dystrophic neurons. We have recently identified class A scavenger receptors as the main receptors mediating the interaction of microglia with beta amyloid fibrils. Adhesion of microglia to beta amyloid fibrils leads to immobilization of these cells on the fibrils, and induces them to produce reactive oxygen species. We propose that interactions of microglial scavenger receptors with fibrillar beta amyloid may stimulate the microglia to secrete apolipoprotein E and complement proteins, which may further contribute to neurotoxicity and neuronal degeneration. Therefore, microglial scavenger receptors may be novel targets for therapeutic interventions in Alzheimer's disease. (C) 1998 Elsevier Science Inc.