Review

Nature Reviews Neurology 6, 193-201 (April 2010) | doi:10.1038/nrneurol.2010.17

Microglia in neurodegenerative disease

See also: Correspondence by Bianchin et al.

V. Hugh Perry, James A. R. Nicoll & Clive Holmes  About the authors

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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.

Author affiliations

V. H. Perry, J. A. R. Nicoll & C. Holmes
School of Biological Sciences, University of Southampton, Building 62, Boldrewood Campus, Southampton SO16 7PX, UK (V. H. Perry).  Division of Clinical Neurosciences, School of Medicine, University of Southampton, Mailpoint 813, Level E, South Pathology Block, Southampton General Hospital, Southampton SO16 6YD, UK (J. A. R. Nicoll, C. Holmes).

Correspondence to: V. H. Perry v.h.perry@soton.ac.uk

Published online 16 March 2010