Dysregulated neuronal–microglial cross-talk during aging, stress and inflammation
Open accessAbstract
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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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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Interleukin (IL)-10 inhibits IL-6 production in microglia by preventing activation of NF-κB
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Self-citationNeuronal regulation of immune responses in the central nervous system
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Cognitive and neuroinflammatory consequences of mild repeated stress are exacerbated in aged mice
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Self-citationAge and Neuroinflammation: A Lifetime of Psychoneuroimmune Consequences
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Self-citationLocalization of Interleukin 1 Type I Receptor mRNA in Rat Brain
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Vagotomy attenuates the behavioural but not the pyrogenic effects of interleukin-1 in rats
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Stereological estimation of total microglia number in mouse hippocampus
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Self-citationCD200R1 Agonist Attenuates Mechanisms of Chronic Disease in a Murine Model of Multiple Sclerosis
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Aging sensitizes mice to behavioral deficits induced by central HIV-1 gp120
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Neuroinflammation: The Devil Is in the Details
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Neurogenesis and Neuroinflammation in Dialogue: Mapping Gaps, Modulating Microglia, Rewiring Aging
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- Authors
- Jurgens, H. A., & Johnson, R. W.
- Affiliations
- University of Illinois Urbana-Champaign (US)
- Corresponding author
- Johnson, Rodney W.
- ORCID
- Johnson, Rodney W.
- Venue
- Experimental Neurology
- Publisher
- Elsevier BV
- Published
- 2012-01
- Volume
- 233
- Issue
- 1
- Pages
- 40-48
- ISSN
- 0014-4886 (ISSN-L)
- PMC
- PMC3071456
- 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
- green
- www.ncbi.nlm.nih.gov
- 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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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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