| Literature DB >> 19688332 |
Gary E Landreth1, Erin G Reed-Geaghan.
Abstract
Alzheimer's disease (AD) is characterized by the formation of insoluble deposits of beta-amyloid (Abeta) 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 Abeta-stimulated release of neurotoxic products.Entities:
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Year: 2009 PMID: 19688332 PMCID: PMC3032986 DOI: 10.1007/978-3-642-00549-7_8
Source DB: PubMed Journal: Curr Top Microbiol Immunol ISSN: 0070-217X Impact factor: 4.291