ReviewNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2017
Microglia Priming with Aging and Stress.
Review in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 245 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
245 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Voluntary versus forced exercise modulates anxiety‑like behaviors and hippocampal inflammation gene expression following traumatic stress in rats.IBRO neuroscience reports · 2026Article
- Oxytocin as regulator of stress and inflammation in aging.Neuroscience and biobehavioral reviews · 2026Review
- Article
- The Gut-Immune-Brain Axis in Aging: Integrating Immunosenescence, Inflammaging, and Neuroinflammation for Precision Medicine.Medical sciences (Basel, Switzerland) · 2026Review
- Immunization with Mycobacterium vaccae attenuates age-associated transcriptional remodeling and microglial reactivity in the rat hippocampus.Journal of neuroimmunology · 2026Article
- STAT6 Targets the Autophagy Pathway to Regulate Microglial Senescence in Cognitive Impairment Caused by Cerebral Small-Vessel Disease.Neuromolecular medicine · 2026Article
- Review
- Article
- Decoding microglial aging through multi-model approaches.Neural regeneration research · 2026Article
- NSAID Use Attenuates the Protective Effect of Physical Activity on Chronic Low Back Pain: A Cross-Sectional Analysis of NHANES 2009-2010.Biomedicines · 2026Article
- A Review of the Effect of Peripheral Amyloid β on the Central Nervous System.Current issues in molecular biology · 2026Review
- Neurovascular and synaptic milieu of brain-resident cells in cognitive dysfunction of myalgic encephalomyelitis/chronic fatigue syndrome.Journal of translational medicine · 2026Review
- The Arp2/3 complex controls the development of homeostatic microglia.EMBO reports · 2026Article
- Store-operated calcium entry drives alcohol-exacerbated neuroinflammation in retinal degeneration.Cell death discovery · 2026Article
- Aurka-Bhlhe41 axis prevents premature aging-like microglial dysfunction and promotes remyelination.Nature communications · 2026Article
- Targeting the Biology of Aging in Cerebrovascular Disease: Inflammation, Metabolism, Senescence, and Regeneration.International journal of molecular sciences · 2026Review
- Neurogenesis and Neuroinflammation in Dialogue: Mapping Gaps, Modulating Microglia, Rewiring Aging.Cells · 2026Review
- Prenatal immune activation and adult Poly(I:C) re-challenge promote neuroimmune priming and AD-related behavioural, cellular and molecular alterations in wild-type mice.Frontiers in immunology · 2026Article
- Environmental determinants of neurotoxicity: role of heavy metals in neurological disorders.Frontiers in neurology · 2026Review
185 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
The population of aged individuals is increasing worldwide and this has significant health and socio-economic implications. Clinical and experimental studies on aging have discovered myriad changes in the brain, including reduced neurogenesis, increased synaptic aberrations, higher metabolic stress, and augmented inflammation. In rodent models of aging, these alterations are associated with cognitive decline, neurobehavioral deficits, and increased reactivity to immune challenges. In rodents, caloric restriction and young blood-induced revitalization reverses the behavioral effects of aging. The increased inflammation in the aged brain is attributed, in part, to the resident population of microglia. For example, microglia of the aged brain are marked by dystrophic morphology, elevated expression of inflammatory markers, and diminished expression of neuroprotective factors. Importantly, the heightened inflammatory profile of microglia in aging is associated with a 'sensitized' or 'primed' phenotype. Mounting evidence points to a causal link between the primed profile of the aged brain and vulnerability to secondary insults, including infections and psychological stress. Conversely, psychological stress may also induce aging-like sensitization of microglia and increase reactivity to secondary challenges. This review delves into the characteristics of neuroinflammatory signaling and microglial sensitization in aging, its implications in psychological stress, and interventions that reverse aging-associated deficits.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.