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Microglia in neurodegenerative disease

Microglia in neurodegenerative disease
Microglia in neurodegenerative disease
Microglia, the resident macrophages of the CNS, are exquisitely sensitive to brain injury and disease, altering their morphology and phenotype to adopt a so-called activated state in response to pathophysiological brain insults. Morphologically activated microglia, like other tissue macrophages, exist as many different phenotypes, depending on the nature of the tissue injury. Microglial responsiveness to injury suggests that these cells have the potential to act as diagnostic markers of disease onset or progression, and could contribute to the outcome of neurodegenerative diseases. The persistence of activated microglia long after acute injury and in chronic disease suggests that these cells have an innate immune memory of tissue injury and degeneration. Microglial phenotype is also modified by systemic infection or inflammation. Evidence from some preclinical models shows that systemic manipulations can ameliorate disease progression, although data from other models indicates that systemic inflammation exacerbates disease progression. Systemic inflammation is associated with a decline in function in patients with chronic neurodegenerative disease, both acutely and in the long term. The fact that diseases with a chronic systemic inflammatory component are risk factors for Alzheimer disease implies that crosstalk occurs between systemic inflammation and microglia in the CNS.
193-201
Perry, V. Hugh
8f29d36a-8e1f-4082-8700-09483bbaeae4
Nicoll, James A.R.
88c0685f-000e-4eb7-8f72-f36b4985e8ed
Holmes, Clive
ada5abf3-8459-4cf7-be40-3f4e9391cc96
Perry, V. Hugh
8f29d36a-8e1f-4082-8700-09483bbaeae4
Nicoll, James A.R.
88c0685f-000e-4eb7-8f72-f36b4985e8ed
Holmes, Clive
ada5abf3-8459-4cf7-be40-3f4e9391cc96

Perry, V. Hugh, Nicoll, James A.R. and Holmes, Clive (2010) Microglia in neurodegenerative disease. Nature Reviews Neurology, 6 (4), 193-201. (doi:10.1038/nrneurol.2010.17).

Record type: Article

Abstract

Microglia, the resident macrophages of the CNS, are exquisitely sensitive to brain injury and disease, altering their morphology and phenotype to adopt a so-called activated state in response to pathophysiological brain insults. Morphologically activated microglia, like other tissue macrophages, exist as many different phenotypes, depending on the nature of the tissue injury. Microglial responsiveness to injury suggests that these cells have the potential to act as diagnostic markers of disease onset or progression, and could contribute to the outcome of neurodegenerative diseases. The persistence of activated microglia long after acute injury and in chronic disease suggests that these cells have an innate immune memory of tissue injury and degeneration. Microglial phenotype is also modified by systemic infection or inflammation. Evidence from some preclinical models shows that systemic manipulations can ameliorate disease progression, although data from other models indicates that systemic inflammation exacerbates disease progression. Systemic inflammation is associated with a decline in function in patients with chronic neurodegenerative disease, both acutely and in the long term. The fact that diseases with a chronic systemic inflammatory component are risk factors for Alzheimer disease implies that crosstalk occurs between systemic inflammation and microglia in the CNS.

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Published date: April 2010

Identifiers

Local EPrints ID: 152263
URI: http://eprints.soton.ac.uk/id/eprint/152263
PURE UUID: 01d4594d-028f-4667-91f7-2b31e9a1b9f6
ORCID for James A.R. Nicoll: ORCID iD orcid.org/0000-0002-9444-7246
ORCID for Clive Holmes: ORCID iD orcid.org/0000-0003-1999-6912

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Date deposited: 14 May 2010 09:24
Last modified: 14 Mar 2024 02:46

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