Cited by 919Neuroinflammation and Neurodegeneration MechanismsNeurological Disease Mechanisms and TreatmentsNeuroscience and Neuropharmacology Research

Microglia as neuroprotective, immunocompetent cells of the CNS

Streit, Wolfgang J.·2002·Glia

Abstract

The role of glial cells is to support and sustain proper neuronal function and microglia are no exception to this. This viewpoint article emphasizes the fundamental interdependence of microglia and neurons and takes a look at the possibility of what could happen if microglial cells became dysfunctional as a result of aging, genetics, or epigenetics. Could microglial senescence be a factor in the pathogenesis of Alzheimer's and other neurodegenerative diseases? The cautious answer to that question is 'yes'. Future studies along these lines may provide novel insights into microglial involvement in neurodegenerative disease pathogenesis.

Integrity signals

Registry

Crossref · 10.1002/glia.10154

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54 of 54 references verified0 citation errors · 0 not checkable

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  • IL-6 originates in skeletal muscle.

    “Specifically, IL-6, which originates in skeletal muscle, has been shown with exercise to elicit an anti-inflammatory response that includes elevated expression of a number of factors including IL-10 and IL-1RA, and as well as inhibition of factors like tumor necrosis factor alpha (TNF-alpha).113–115”
  • In the context of exercise, IL-6 may play an anti-inflammatory role.

    “In addition, the cytokine IL-6, while generally considered a pro-inflammatory marker in PD that correlates with functional impairment (decreased walking speed), may in the context of exercise, play an anti-inflammatory role.”
  • Exercise-induced IL-6 elicits an anti-inflammatory response including elevated expression of IL-10 and IL-1RA and inhibition of TNF-alpha.

    “Specifically, IL-6, which originates in skeletal muscle, has been shown with exercise to elicit an anti-inflammatory response that includes elevated expression of a number of factors including IL-10 and IL-1RA, and as well as inhibition of factors like tumor necrosis factor alpha (TNF-alpha).113–115”

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Authors
Streit, W. J.
Affiliations
University of Florida (US)
Corresponding author
Streit, Wolfgang J.
Venue
Glia
Publisher
Wiley
Published
2002-10-04
Volume
40
Issue
2
Pages
133-139
ISSN
  • 0894-1491 (ISSN-L)
  • 1098-1136
OpenAlex
W2068872768
Cited by
919
References
54
Citations by year
2026: 2 · 2025: 6 · 2024: 15 · 2023: 12 · 2022: 23 · 2021: 24 · 2020: 39 · 2019: 22 · 2018: 40 · 2017: 37 · 2016: 33 · 2015: 40 · 2014: 47 · 2013: 50 · 2012: 62
FWCI
4.14
Type
journal article
Language
en
Open access
closed
Locations
  • Glia (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
microglia, neuroprotection, microglial senescence, neurodegenerative diseases, Alzheimer's disease, aging, epigenetics, genetic factors, CNS immune response
MeSH terms
Animals, Central Nervous System, Endocrine System, Endothelium, Vascular, Humans, Interleukins, Neuroglia, Neurons, Signal Transduction, Cytokines, Microglia, Chemokines

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