Microglia during development and aging
Open accessAbstract
Microglia are critical nervous system-specific cells influencing brain development, maintenance of the neural environment, response to injury, and repair. They contribute to neuronal proliferation and differentiation, pruning of dying neurons, synaptic remodeling and clearance of debris and aberrant proteins. Colonization of the brain occurs during gestation with an expansion following birth with localization stimulated by programmed neuronal death, synaptic pruning, and axonal degeneration. Changes in microglia phenotype relate to cellular processes including specific neurotransmitter, pattern recognition, or immune-related receptor activation. Upon activation, microglia cells have the capacity to release a number of substances, e.g., cytokines, chemokines, nitric oxide, and reactive oxygen species, which could be detrimental or beneficial to the surrounding cells. With aging, microglia shift their morphology and may display diminished capacity for normal functions related to migration, clearance, and the ability to shift from a pro-inflammatory to an anti-inflammatory state to regulate injury and repair. This shift in microglia potentially contributes to increased susceptibility and neurodegeneration as a function of age. In the current review, information is provided on the colonization of the brain by microglia, the expression of various pattern recognition receptors to regulate migration and phagocytosis, and the shift in related functions that occur in normal aging.
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Myeloid cells are instrumental in maintaining CNS homeostasis; however, aging significantly alters their properties.
“For example, myeloid cells are instrumental in maintaining CNS homeostasis; however, aging significantly alters their properties (88).”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [88]
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The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease
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Key Aging-Associated Alterations in Primary Microglia Response to Beta-Amyloid Stimulation
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The connection between microbiome and schizophrenia
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- Authors
- Harry, G. J.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Harry, G. Jean
- ORCID
- Harry, G. Jean
- Venue
- Pharmacology & Therapeutics
- Publisher
- Elsevier BV
- Published
- 2013-09
- Volume
- 139
- Issue
- 3
- Pages
- 313-326
- ISSN
- 0163-7258 (ISSN-L)
- PMC
- PMC3737416
- OpenAlex
- W2163179762
- Cited by
- 524
- References
- 48
- Citations by year
- 2026: 28 · 2025: 46 · 2024: 50 · 2023: 65 · 2022: 50 · 2021: 42 · 2020: 32 · 2019: 43 · 2018: 35 · 2017: 25 · 2016: 38 · 2015: 30 · 2014: 32 · 2013: 8
- FWCI
- 3.47
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Pharmacology & Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Health and Human Services
- National Institutes of Health
- National Institute of Environmental Health Sciences (ZIAES101623, Z01ES021164, ES021164, ZIAES021164, F31ES021164, Z01ES101623)
- 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, brain development, brain aging, synaptic pruning, neuronal cell death, pattern recognition receptors, microglial activation, neuroinflammation, neurodegeneration, phagocytosis, microglial migration, neuroprotection
- MeSH terms
- Aging, Animals, Brain, Cell Differentiation, Cell Movement, Humans, Nerve Degeneration, Neurons, Phagocytosis, Microglia, Cell Proliferation
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