期刊
NEUROBIOLOGY OF DISEASE
卷 37, 期 3, 页码 503-509出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2009.10.006
关键词
Microglia; Inflammation; Alzheimer's disease; Toll-like receptors; Beta amyloid; Alternative activation; Macrophage; Monocyte
资金
- NIA [AG16740, AG030482]
- Alzheimer Association
- Blanchette Hooker Rockefeller Foundation
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM007250] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG016740, R21AG029926, R01AG030482] Funding Source: NIH RePORTER
Microglia are the brain's tissue macrophage and representative of the innate immune system. These cells normally provide tissue maintenance and immune surveillance of the brain. In the Alzheimer's disease brain, amyloid deposition provokes the phenotypic activation of microglia and their elaboration of proinflammatory molecules. Recent work has implicated Toll-like receptors in microglial recognition and response to amyloid fibrils. It is now evident that these cells exhibit more complex and heterogeneous phenotypes than previously appreciated that reflect both the plasticity of cells in this lineage and their ability to transition between activation states. The phenotypic diversity is associated with inactivation of the inflammatory response and tissue repair. We discuss recent evidence that the brain can be infiltrated by circulating monocytes in the diseased brain and that these cells may comprise a unique subpopulation of myeloid cells that may be functionally distinct from the endogenous microglia. (C) 2009 Elsevier Inc. All rights reserved.
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