Toll-Like Receptors in Alzheimer's Disease

被引：149

作者：

Landreth, Gary E. ^{[1
]}

Reed-Geaghan, Erin G. ^{[1
]}

机构：

[1] Case Western Reserve Univ, Dept Neurosci, Alzheimer Res Lab, Cleveland, OH 44106 USA

来源：

TOLL-LIKE RECEPTORS: ROLES IN INFECTION AND NEUROPATHOLOGY | 2009年 / 336卷

关键词：

NF-KAPPA-B; CENTRAL-NERVOUS-SYSTEM; DOMAIN-CONTAINING ADAPTER; INNATE IMMUNE RECEPTOR; AMYLOID-BETA; MICROGLIAL PHAGOCYTOSIS; ALTERNATIVE ACTIVATION; MOLECULAR-PATTERN; MOUSE MODEL; CELL UPTAKE;

D O I：

10.1007/978-3-642-00549-7_8

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Alzheimer's disease (AD) is characterized by the formation of insoluble deposits of beta-amyloid (A beta) within the parenchyma of the brain. These deposits are associated with a robust microglia-mediated inflammatory response. Recent work has demonstrated that Toll-like receptors (TLRs) participate in this inflammatory response. This chapter reviews the mechanisms whereby TLRs contribute to the induction of a microglial inflammatory response to promote AD pathogenesis. Specifically, the involvement of CD14 and the TLRs in microglial activation is delineated. The TLR-mediated microglial response has beneficial roles in stimulating phagocytosis as well as detrimental roles in the AP-stimulated release of neurotoxic products.

引用

页码：137 / 153

页数：17

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