Evidence map›Paper›PMID 30009999›Full record

ReviewBrain, behavior, and immunity2018

Stress and aging act through common mechanisms to elicit neuroinflammatory priming.

Laura K Fonken, Matthew G Frank, Andrew D Gaudet, Steven F Maier

Abstract readReview
In one paragraph

Review in Brain, behavior, and immunity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Laura K FonkenUniversity of Texas at Austin, Division of Pharmacology and Toxicology, Austin, TX 78712, USA. Electronic address: laura.fonken@austin.utexas.edu.
Matthew G FrankUniversity of Colorado Boulder, Department of Psychology and Neuroscience, Boulder, CO 80309, USA.
Andrew D GaudetUniversity of Colorado Boulder, Department of Psychology and Neuroscience, Boulder, CO 80309, USA.
Steven F MaierUniversity of Colorado Boulder, Department of Psychology and Neuroscience, Boulder, CO 80309, USA.

Funding

Stress-induced neuroinflammatory priming: Glucocorticoids, inflammasomes, alarminsR01MH108523 · NIMH · UNIVERSITY OF COLORADO · PI MAIER, STEVEN F · 2016 to 2020
$2.1M
The role of the NLRP3 inflammasome in aging-associated cognitive impairmentsF32AG048672 · NIA · UNIVERSITY OF COLORADO · PI FONKEN, LAURA K · 2014 to 2016
$164k
NIA NIH HHS F32 AG048672NIMH NIH HHS R01 MH108523
6 · The paper itself

Abstract

Over the course of an animal's lifespan, there is a protracted breakdown in basic homeostatic functions. Stressors (both psychological and physiological) can accelerate this process and compromise multiple homeostatic mechanisms. For example, both stress and aging can modulate neuroinflammatory function and cause a primed phenotype resulting in a heightened neuroinflammatory profile upon immune activation. Microglia, the brain's resident myeloid cell, produce "silent" immune machinery in response to stress and aging that does not cause immediate immune activation; rather, these changes prime the cell for a subsequent immune insult. Primed microglia exhibit a hyperinflammatory response upon immune activation that can exacerbate pathology. In this review, we will explore parallels between stress- and aging-induced neuroinflammatory priming. First, we will provide a background on the basic principles of neuroimmunology. Next, we will discuss evidence that neuroinflammatory responses become primed in the context of both stress and aging. We will also describe cell-specific contributions to neuroinflammatory priming with a focus on microglia. Finally, common mechanisms underlying priming in the context of stress and aging will be discussed: these mechanisms include glucocorticoid signaling; accumulation of danger signals; dis-inhibition of microglia; and breakdown of circadian rhythms. Overall, there are multifarious parallels between stress- and aging-elicited neuroinflammatory priming, suggesting that stress may promote a form of premature aging. Further unravelling mechanisms underlying priming could lead to improved treatments for buffering against stress- and aging-elicited behavioral pathologies.

Indexed as

AgingAnimalsBrainCircadian RhythmGlucocorticoidsHippocampusHumansInflammationMicrogliaNeuroimmunomodulationStress, PsychologicalGlucocorticoids

Identifiers

PMID30009999
PMCPMC6129421

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.