Evidence map›Paper›PMID 25549562›Full record

ReviewNeuropharmacology2015

Immune dysregulation and cognitive vulnerability in the aging brain: Interactions of microglia, IL-1β, BDNF and synaptic plasticity.

Susan L Patterson

Open access · greenAbstract readReview
In one paragraph

Review in Neuropharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers.

0numbers the graph read from it
0cells of the map it votes in
160citing papers in PubMed
11.1field-weighted citation impact, top 1% of its field
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

160 citing papers in PubMed, 276 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Comparative Study of Young and MaturePlants (Basel, Switzerland) · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Obesity and Depression: A Pathophysiotoxic Relationship.International journal of molecular sciences · 2025
    Review
  11. Retinoid-X-Receptor as a Mediator of Poststroke Recovery by Reversing Age-Associated Phenotypes of Microglia/Hematogenous Macrophages.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  12. Review
  13. Article
  14. Article
  15. Microorganisms · 2025
    Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. Review

100 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Susan L PattersonTemple University, Biology Life Science Building, 1900 N. 12th Street, Philadelphia, PA, 19122, USA. Electronic address: Susan.patterson@temple.edu.
Temple University · US

Funding

Aging, Inflammatory Challenge, and BDNF-Dependent Synaptic Plasticity ProcessesR01AG041944 · NIA · UNIVERSITY OF COLORADO · PI PATTERSON, SUSAN · 2012 to 2018
$1.6M
Effects of Aging and Inflammatory Challenge on BDNF-Dependent Synaptic PlasticityR21AG031467 · NIA · UNIVERSITY OF COLORADO · PI PATTERSON, SUSAN · 2008 to 2009
$347k
NIA NIH HHS R01 AG041944NIA NIH HHS R01AG041944NIA NIH HHS R21 AG031467NIA NIH HHS R21AG031467
6 · The paper itself

Abstract

Older individuals often experience declines in cognitive function after events (e.g. infection, or injury) that trigger activation of the immune system. This occurs at least in part because aging sensitizes the response of microglia (the brain's resident immune cells) to signals triggered by an immune challenge. In the aging brain, microglia respond to these signals by producing more pro-inflammatory cytokines (e.g. interleukin-1beta or IL-1β) and producing them for longer than microglia in younger brains. This exaggerated inflammatory response can compromise processes critical for optimal cognitive functioning. Interleukin-1β is central to the inflammatory response and is a key mediator and modulator of an array of associated biological functions; thus its production and release is usually very tightly regulated. This review will focus on the impact of dysregulated production of IL-1β on hippocampus dependent-memory systems and associated synaptic plasticity processes. The neurotrophin brain-derived neurotrophic factor (BNDF) helps to protect neurons from damage caused by infection or injury, and it plays a critical role in many of the same memory and hippocampal plasticity processes compromised by dysregulated production of IL-1β. This suggests that an exaggerated brain inflammatory response, arising from aging and a secondary immune challenge, may erode the capacity to provide the BDNF needed for memory-related plasticity processes at hippocampal synapses. This article is part of a Special Issue entitled 'Neuroimmunology and Synaptic Function'.

Indexed as

AgingAnimalsBrainBrain-Derived Neurotrophic FactorCognition DisordersHippocampusHumansInflammation MediatorsInterleukin-1betaMicrogliaNeuronal PlasticityBrain-Derived Neurotrophic FactorInflammation MediatorsInterleukin-1betaAgingBDNFCognitive vulnerabilityIL-1βInfectionInflammationMemoryMicrogliaSynaptic plasticity

Identifiers

PMID25549562
PMCPMC4475415
OpenAlexW1992256029

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.