Microglia and neuroinflammation: a pathological perspective
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BioMed Central
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Microglia and neuroinflammation: a pathological perspective Wolfgang J Streit*1, Robert E Mrak2 and W Sue T Griffin3 Address: 1Department of Neuroscience, University of Florida College of Medicine, P.O. Box 100244, Gainesville, Florida 32610, USA, 2Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA and 3Department of Geriatrics, University of Arkansas for Medical Sciences and GRECC/CAVHS, Little Rock, Arkansas 72205, USA Email: Wolfgang J Streit* - [email protected]; Robert E Mrak - [email protected]; W Sue T Griffin - [email protected] * Corresponding author
Published: 30 July 2004 Journal of Neuroinflammation 2004, 1:14
doi:10.1186/1742-2094-1-14
Received: 08 July 2004 Accepted: 30 July 2004
This article is available from: http://www.jneuroinflammation.com/content/1/1/14 © 2004 Streit et al; licensee BioMed Central Ltd. 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.
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.
Background A role for immune responses, involving antigen presentation and immune-response-generating cytokines, in neurodegenerative diseases such as Alzheimer's disease was recognized for a decade before the term neuroinflammation came into widespread use [1,2]. A PubMed search using "neuroinflammation" as the only key word yields some 300 papers, none before 1995 [3]. While some chronic/remitting neurological diseases, such as multiple sclerosis, have long been recognized as inflammatory, the term neuroinflammation has come to denote chronic, CNS-specific, inflammation-like glial responses that do not reproduce the classic characteristics of inflammation in the periphery but that may engender neurodegenerative events; including plaque formation, dystrophic neurite growth, and excessive tau phosphorylation. In this way, neuroinflammation has been implicated in chronic unremitting neurodegenerative diseases such as Alzheimer's disease – diseases that historically have not been thought of as inflammatory diseases. This new understanding has come from rapid advances in the field of microglial and astrocytic neurobiology over the past fifteen to twenty years. These advances have led to the recognition that glia,
particularly microglia, respond to tissue insult with a complex array of inflammatory cytokines and actions, and that these actions transce
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