Cited by 134Neuroinflammation and Neurodegeneration MechanismsNeurogenesis and neuroplasticity mechanismsGenetics, Aging, and Longevity in Model Organisms

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

Miller, Kelly R., Streit, Wolfgang J.·2007·Neuron Glia Biology

DOI 10.1017/s1740925x08000136

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Abstract

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 In this manuscript, we review current knowledge of microglia in the aging brain and present new, unpublished work that further supports the theory that microglia experience an age-related decline in proliferative function as a result of cellular senescence.

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Authors: Miller, K. R., & Streit, W. J.
Affiliations: University of Florida (US)
Corresponding author: Streit, Wolfgang J.
ORCID: Streit, Wolfgang J.
Venue: Neuron Glia Biology
Publisher: Cambridge University Press (CUP)
Published: 2007-08
Volume: 3
Issue: 3
Pages: 245-253
ISSN: 1740-925X (ISSN-L)
1741-0533
DOI: 10.1017/s1740925x08000136
OpenAlex: W2099508568
Cited by: 134
References: 24
Citations by year: 2026: 1 · 2025: 3 · 2024: 2 · 2023: 1 · 2022: 7 · 2021: 13 · 2020: 3 · 2019: 8 · 2018: 8 · 2017: 5 · 2016: 11 · 2015: 5 · 2014: 14 · 2013: 17 · 2012: 9
FWCI: 3.59
Type: journal article
Language: en
Open access: closed
Licence: www.cambridge.org/core/terms (unspecified, 267 d)
Locations: Neuron Glia Biology (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Keywords: microglia, cellular senescence, brain aging, reactive microgliosis, neuroinflammation, Alzheimer's disease, age-related neurodegeneration, microglial proliferation, anti-inflammatory therapy, amyotrophic lateral sclerosis, Parkinson's disease

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

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