Cited by 524Neuroinflammation and Neurodegeneration MechanismsNeurogenesis and neuroplasticity mechanismsNeurological Disease Mechanisms and Treatments

Microglia during development and aging

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Harry, G. Jean·2013·Pharmacology & Therapeutics

Abstract

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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Authors
Harry, G. J.
Affiliations
National Institutes of Health (US)
Corresponding author
Harry, G. Jean
Venue
Pharmacology & Therapeutics
Publisher
Elsevier BV
Published
2013-09
Volume
139
Issue
3
Pages
313-326
ISSN
0163-7258 (ISSN-L)
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
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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