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The effects of aging, injury and disease on microglial function: a case for cellular senescence

Published online by Cambridge University Press:  24 April 2008

Kelly R. Miller
Department of Neuroscience, University of Florida College of Medicine, McKnight Brain Institute, Florida, USA
Wolfgang J. Streit*
Department of Neuroscience, University of Florida College of Medicine, McKnight Brain Institute, Florida, USA
Correspondence should be addressed to Wolfgang J. Streit Ph.D., Department of Neuroscience, PO Box 100244, Gainesville, Florida 32610-0244, USA phone: +1 352 392 3910 fax: +1 352 392 8347 email:


Neuroinflammation resulting from chronic reactive microgliosis is thought to contribute to age-related neurodegeneration, as well as age-related neurodegenerative diseases, specifically Alzheimer's disease (AD). Support of this theory comes from studies reporting a progressive, age-associated increase in microglia with an activated phenotype. Although the underlying cause(s) of this microglial reactivity is idiopathic, an accepted therapeutic strategy for the treatment of AD is inhibition of microglial activation using anti-inflammatory agents. Although the effectiveness of anti-inflammatory treatment for AD remains equivocal, microglial inhibition is being tested as a potential treatment for additional neurodegenerative disorders including amyotrophic lateral sclerosis and Parkinson's disease. Given the important and necessary functions of microglia in normal brain, careful evaluation of microglial function in the aged brain is a necessary first step in targeting more precise treatment strategies for aging-related neurodegenerative diseases. Studies from our laboratory have shown multiple age-related changes in microglial morphology and function that are suggestive of cellular senescence. In this manuscript, we review current knowledge of microglia in the aging brain and present new, unpublished work that further supports the theory that microglia experience an age-related decline in proliferative function as a result of cellular senescence.

Review Article
Copyright © Cambridge University Press 2008

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