Microglia and neuroinflammation: a pathological perspective

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Abstract

Microglia make up the innate immune system of the central nervous system and are key cellular mediators of neuroinflammatory processes. Their role in central nervous system diseases, including infections, is discussed in terms of a participation in both acute and chronic neuroinflammatory responses. Specific reference is made also to their involvement in Alzheimer's disease where microglial cell activation is thought to be critically important in the neurodegenerative process.

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Most cited references 23

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Inflammation and Alzheimer's disease.

H Akiyama, S. Barger, S Barnum … (2000)

Inflammation clearly occurs in pathologically vulnerable regions of the Alzheimer's disease (AD) brain, and it does so with the full complexity of local peripheral inflammatory responses. In the periphery, degenerating tissue and the deposition of highly insoluble abnormal materials are classical stimulants of inflammation. Likewise, in the AD brain damaged neurons and neurites and highly insoluble amyloid beta peptide deposits and neurofibrillary tangles provide obvious stimuli for inflammation. Because these stimuli are discrete, microlocalized, and present from early preclinical to terminal stages of AD, local upregulation of complement, cytokines, acute phase reactants, and other inflammatory mediators is also discrete, microlocalized, and chronic. Cumulated over many years, direct and bystander damage from AD inflammatory mechanisms is likely to significantly exacerbate the very pathogenic processes that gave rise to it. Thus, animal models and clinical studies, although still in their infancy, strongly suggest that AD inflammation significantly contributes to AD pathogenesis. By better understanding AD inflammatory and immunoregulatory processes, it should be possible to develop anti-inflammatory approaches that may not cure AD but will likely help slow the progression or delay the onset of this devastating disorder.

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Innate immunity.

R Medzhitov, C A Janeway (2000)

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Microglial response to amyloid plaques in APPsw transgenic mice.

S A Frautschy, F. Yang, M Irrizarry … (1998)

Microglial activation is central to the inflammatory response in Alzheimer's Disease (AD). A recently described mouse line, Tg(HuAPP695.K670N/M671L)2576, expressing human amyloid precursor protein with a familial AD gene mutation, age-related amyloid deposits, and memory deficits, was found to develop a significant microglial response using Griffonia simplicifolia lectin or phosphotyrosine probe to identify microglia Both Griffonia simplicifolia lectin and phosphotyrosine staining showed increased numbers of intensely labeled, often enlarged microglia clustered in and around plaques, consistent with microglial activation related to beta-amyloid formation. Using quantitative image analysis of coronal phosphotyrosine-immunostained sections, transgene-positive 10- to 16-month-old, hemizygous, hybrid Tg2576 (APPsw) animals showed significantly increased microglial density and size in plaque-forming areas of hippocampus and frontal, entorhinal, and occipital cortex. Quantitative analysis of microglia as a function of distance from the center of plaques (double labeled for A beta peptide and microglia) revealed highly significant, two- to fivefold elevations in microglial number and area within plaques compared with neighboring regions. Tg2576 beta-amyloid-plaque-forming mice should be a useful system for assessing the consequences of the microglial-mediated inflammatory response to beta-amyloid and developing anti-inflammatory therapeutic strategies for Alzheimer's disease. These results provide the first quantitative link between beta-amyloid plaque formation and microglial activation in an animal model with neuritic plaques and memory deficits.

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Author and article information

Journal

Journal ID (nlm-ta): J Neuroinflammation

Title: Journal of Neuroinflammation

Publisher: BioMed Central (London )

ISSN (Electronic): 1742-2094

Publication date Collection: 2004

Publication date (Electronic): 30 July 2004

Volume: 1

Page: 14

Affiliations

[1 ]Department of Neuroscience, University of Florida College of Medicine, P.O. Box 100244, Gainesville, Florida 32610, USA

[2 ]Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA

[3 ]Department of Geriatrics, University of Arkansas for Medical Sciences and GRECC/CAVHS, Little Rock, Arkansas 72205, USA

Article

Publisher ID: 1742-2094-1-14

DOI: 10.1186/1742-2094-1-14

PMC ID: 509427

PubMed ID: 15285801

SO-VID: f7e9b5a4-19f9-45fd-9428-89c3b6c79946

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Microglia and neuroinflammation: a pathological perspective

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The Dynamic Brain

Most cited references 23

Inflammation and Alzheimer's disease.

Innate immunity.

Microglial response to amyloid plaques in APPsw transgenic mice.

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