Toll-Like Receptors in Alzheimer's Disease

被引：147
|
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
收藏
页码：137 / 153
页数：17
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