Evidence map›Paper›PMID 23751484›Full record

ReviewAgeing research reviews2013

Calcium dysregulation and neuroinflammation: discrete and integrated mechanisms for age-related synaptic dysfunction.

Diana M Sama, Christopher M Norris

Abstract readReview
In one paragraph

Review in Ageing research reviews, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 5% 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

76 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Article
  7. Genome-wide pleiotropy analysis of longitudinal blood pressure and harmonized cognitive performance measures.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  8. Review
  9. Article
  10. Article
  11. ERG1A KScientific reports · 2025
    Article
  12. Review
  13. Article
  14. Underneath the Gut-Brain Axis in IBD-Evidence of the Non-Obvious.International journal of molecular sciences · 2024
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. International journal of molecular sciences · 2023
    Article

16 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

2 authors at 1 institution in 1 country.

Diana M SamaDepartment of Physiology, University of Kentucky College of Medicine, Lexington, KY 40536, USA; Spinal Cord and Brain Injury Research Center, University of Kentucky College of Medicine, Lexington, KY 40536, USA. Electronic address: diana.mathis@uky.edu.
Christopher M Norris
University of Kentucky · US

Funding

THE MOLECULAR AND CELLULAR BASIS OF BRAIN AGINGT32AG000242 · NIA · UNIVERSITY OF KENTUCKY · PI GERHARDT, GREG A. · 1994 to 2013
$3.4M
Calcineurin and inflammatory signaling processes in aging and Alzheimer's DiseaseR01AG027297 · NIA · UNIVERSITY OF KENTUCKY · PI NORRIS, CHRISTOPHER MARK · 2006 to 2018
$3.2M
Calcineurin and Biobehavioral Markers of Brain AgingK01AG024190 · NIA · UNIVERSITY OF KENTUCKY · PI NORRIS, CHRISTOPHER MARK · 2004 to 2008
$430k
NIA NIH HHS AG000242NIA NIH HHS AG02729NIA NIH HHS K01 AG024190NIA NIH HHS R01 AG027297NIA NIH HHS T32 AG000242
6 · The paper itself

Abstract

Some of the best biomarkers of age-related cognitive decline are closely linked to synaptic function and plasticity. This review highlights several age-related synaptic alterations as they relate to Ca(2+) dyshomeostasis, through elevation of intracellular Ca(2+), and neuroinflammation, through production of pro-inflammatory cytokines including interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α). Though distinct in many ways, Ca(2+) and neuroinflammatory signaling mechanisms exhibit extensive cross-talk and bidirectional interactions. For instance, cytokine production in glial cells is strongly dependent on the Ca(2+) dependent protein phosphatase calcineurin, which shows elevated activity in animal models of aging and disease. In turn, pro-inflammatory cytokines, such as TNF, can augment the expression/activity of L-type voltage sensitive Ca(2+) channels in neurons, leading to Ca(2+) dysregulation, hyperactive calcineurin activity, and synaptic depression. Thus, in addition to discussing unique contributions of Ca(2+) dyshomeostasis and neuroinflammation, this review emphasizes how these processes interact to hasten age-related synaptic changes.

Indexed as

AgingAnimalsCalciumHumansInflammationInflammation MediatorsLong-Term PotentiationLong-Term Synaptic DepressionNeuronal PlasticityNeuronsSignal TransductionSynapsesCalciumInflammation MediatorsAgingCa(2+)CytokineNeuroinflammationPlasticitySynapse

Identifiers

PMID23751484
PMCPMC3834216
OpenAlexW2000495890

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.