Cited by 179Neuroinflammation and Neurodegeneration MechanismsTryptophan and brain disordersInflammasome and immune disorders

Dysregulated neuronal–microglial cross-talk during aging, stress and inflammation

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Jurgens, Heidi A., Johnson, Rodney W.·2012·Experimental Neurology

Abstract

Communication between neurons and microglia is essential for maintaining homeostasis in the central nervous system (CNS) during both physiological and inflammatory conditions. While microglial activation is necessary and beneficial in response to injury or disease, excessive or prolonged activation can have deleterious effects on brain function and behavior. To prevent inflammation-associated damage, microglia reactivity is actively modulated by neurons in the healthy brain. Age or stress-induced disruption of normal neuronal-microglial communication could lead to an aberrant central immune response when additional stressors are applied. Recent work suggests that both aging and stress shift the CNS microenvironment to a pro-inflammatory state characterized by increased microglial reactivity and a reduction in anti-inflammatory and immunoregulatory factors. This review will discuss how heightened neuroinflammation associated with aging and stress may be compounded by the concomitant loss of neuronally derived factors that control microglial activation, leaving the brain vulnerable to excessive inflammation and neurobehavioral complications upon subsequent immune challenge.

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Crossref · 10.1016/j.expneurol.2010.11.014

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  • The inflammatory profiles altered during stress and during aging revealed striking similarities.

    “Moreover, the inflammatory profiles altered during stress and during aging revealed striking similarities (Jurgens and Johnson, 2012).”

    From Microglia Priming with Aging and Stress (2017) · cites this paper as Jurgens and Johnson, 2012

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Authors
Jurgens, H. A., & Johnson, R. W.
Affiliations
University of Illinois Urbana-Champaign (US)
Corresponding author
Johnson, Rodney W.
Venue
Experimental Neurology
Publisher
Elsevier BV
Published
2012-01
Volume
233
Issue
1
Pages
40-48
ISSN
0014-4886 (ISSN-L)
OpenAlex
W2036956824
Cited by
179
References
148
Citations by year
2026: 8 · 2025: 6 · 2024: 8 · 2023: 8 · 2022: 8 · 2021: 8 · 2020: 10 · 2019: 10 · 2018: 11 · 2017: 14 · 2016: 15 · 2015: 14 · 2014: 13 · 2013: 19 · 2012: 18
FWCI
1.24
Type
journal article
Language
en
Open access
Locations
  • Experimental Neurology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
NIH (AG016710)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Keywords
microglial activation, neuroinflammation, brain aging, psychological stress, neuroimmune homeostasis, anti-inflammatory factors, neurobehavioral impairment
MeSH terms
Aging, Animals, Cell Communication, Humans, Inflammation, Neurons, Stress, Psychological, Cytokines, Microglia

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