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Cited by 444

The DOI matches its Crossref record; 90 of the 90 references it cites were found in a registry or an index.

Inflammation, microglia, and alzheimer's disease

Open access
Cameron, Brent, Landreth, Gary E.·2010·Neurobiology of Disease

Abstract

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.

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Metadata

Authors
Cameron, B., & Landreth, G. E.
Venue
Neurobiology of Disease
Publisher
Elsevier BV
Published
2010-03
Volume
37
Issue
3
Pages
503-509
ISSN
0969-9961 (ISSN-L)
OpenAlex
W2036735444
Cited by
444
References
90
FWCI
15.69
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Inflammation, microglia, and alzheimer's disease. https://app.cochat.ai/papers/10.1016/j.nbd.2009.10.006
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Cameron, B., & Landreth, G. E. (2010). Inflammation, microglia, and alzheimer's disease. Neurobiology of Disease. https://doi.org/10.1016/j.nbd.2009.10.006

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.