Effect of aging on the microglial response to peripheral nerve injury
Abstract
Microglial morphology and immunophenotype have been studied extensively in aging-related neurodegenerative diseases, but to a lesser extent in the normally aged CNS, and little is known about how aging affects the ability of microglia to respond to neuronal injury. The goal of the current study was to determine if aging affects the ability of microglia to divide during the early response to facial nerve axotomy. In addition, we investigated the incidence of microglial cell death during later post-axotomy time points to determine if aging had an effect on microglial turnover. We employed DNA labeling with 3H-thymidine, TUNEL and lectin histochemistry after facial nerve axotomy in young (3 months), middle-aged (15 months), and old (30 months) Fisher344-Brown Norway hybrid rats. Proliferation of microglia in old rats remained significantly higher than in young rats 4 days after injury, suggesting that regulation of microglial proliferation changes with aging. There was no aging-related difference in microglial TUNEL staining at 7, 14 or 21 days post-axotomy. Lectin histochemistry in the unoperated facial nucleus revealed aging-related morphological changes in resting microglia, including hypertrophy of the cytoplasm with dense perinuclear staining. Aging-related differences in activated microglia on the lesioned side were more subtle, although many activated microglia of aged animals continued to exhibit dense perinuclear lectin reactivity. We propose that aging-related changes in morphology in conjunction with a less regulated proliferative response in the aged facial nucleus may be a reflection of microglial senescence.
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Microglia can become senescent, which affects their ability to mediate immune responses in the CNS in response to injury or infection.
“Microglia also can become senescent, which affects their ability to mediate immune responses in the CNS in response to injury or infection [23].”
From DNA repair deficiency and senescence in concussed professional athletes involved in contact sports (2019) · cites this paper as [23]
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- Authors
- Conde, J. R., & Streit, W. J.
- Affiliations
- University of Florida (US)
- Corresponding author
- Streit, Wolfgang J.
- ORCID
- Streit, Wolfgang J.
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2006-10
- Volume
- 27
- Issue
- 10
- Pages
- 1451-1461
- ISSN
- 0197-4580 (ISSN-L)
- OpenAlex
- W1991963544
- Cited by
- 86
- References
- 57
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 2 · 2023: 3 · 2022: 6 · 2021: 5 · 2020: 4 · 2019: 2 · 2018: 2 · 2017: 4 · 2016: 6 · 2015: 8 · 2014: 7 · 2013: 4 · 2012: 9
- FWCI
- 1.41
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Evelyn F. McKnight Brain Research Foundation
- University of Florida
- National Institutes of Health
- National Institute on Aging (R01AG023665, AG 023665)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- microglia, aging, peripheral nerve injury, facial nerve axotomy, microglial proliferation, microglial cell death, microglial senescence, microglial morphology, microglial activation, facial nucleus
- MeSH terms
- Aging, Animals, Facial Nerve Diseases, Male, Peripheral Nervous System Diseases, Rats, Inbred F344, Apoptosis, Microglia, Rats
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