Evidence map›Paper›PMID 11356894›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

Calcineurin links Ca2+ dysregulation with brain aging.

T C Foster, K M Sharrow, J R Masse, C M Norris, A Kumar

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

106 citing papers in PubMed, 214 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Calcineurin inhibition may prevent Alzheimer disease in people with Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Likelihood ratio tests for a large directed acyclic graph.Journal of the American Statistical Association · 2020
    Article
  16. Article
  17. The Puzzling Role of Neuron-Specific PMCA Isoforms in the Aging Process.International journal of molecular sciences · 2019
    Review
  18. Senescent neurophysiology: CaNeurobiology of learning and memory · 2019
    Review
  19. Review
  20. Review

46 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

5 authors at 1 institution in 1 country.

T C FosterDepartment of Molecular and Biomedical Pharmacology, University of Kentucky, College of Medicine, Lexington, Kentucky 40536, USA. tfoster@pop.uky.edu
K M Sharrow
J R Masse
C M Norris
A Kumar
University of Kentucky · US

Funding

ROLE OF CALCIUM, CALPAINS, AND CASPASES IN NEURODEGENERATIONP01AG010836 · NIA · UNIVERSITY OF KENTUCKY · PI GEDDES, JAMES W. · 1992 to 2008
$12.4M
MECHANISMS FOR ALTERED SYNAPTIC FUNCTION DURING AGINGR01AG014979 · NIA · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI FOSTER, THOMAS C · 1998 to 2011
$2.5M
ESTROGEN AND COGNITION OVER THE LIFESPANR01MH059891 · NIMH · UNIVERSITY OF KENTUCKY · PI FOSTER, THOMAS C · 2000 to 2009
$2.2M
CALCINEURIN IN CALCIUM CHANNEL REGULATION DURING AGING.F32AG005903 · NIA · UNIVERSITY OF KENTUCKY · PI NORRIS, CHRISTOPHER MARK · 2000 to 2002
$128k
NIA NIH HHS AG10836NIA NIH HHS AG/NS14979NIA NIH HHS F32 AG005903NIA NIH HHS P01 AG010836NIA NIH HHS R01 AG014979NIMH NIH HHS MH59891NIMH NIH HHS R01 MH059891
6 · The paper itself

Abstract

Brain aging is associated with altered Ca(2+) regulation. However, many Ca(2+) signal transduction mechanisms have not been explored in the aged brain. Here, we report that cytosolic expression and activity of the Ca(2+)-dependent protein phosphatase calcineurin (CaN) increases in the hippocampus during aging. CaN changes were paralleled by increased activation, but not expression, of CaN-regulated protein phosphatase 1 and a reduction in the phosphorylation state of CaN substrates involved in cell survival (i.e., Bcl-2-associated death protein and cAMP response element-binding protein). The age-related increase in CaN activity was not attributable to the inability of CaN to translocate to the membrane and was reduced by blocking L-type Ca(2+) channels. Finally, increased CaN activity correlated with memory function as measured with the Morris water escape task. The results suggest that altered regulation of CaN is one of the processes that could link Ca(2+) dyshomeostasis to age-related changes in neural function and cognition.

Indexed as

AgingAnimalsbcl-Associated Death ProteinCalcineurinCalciumCalcium Channel BlockersCalcium Channels, L-TypeCarrier ProteinsCuesCyclic AMP Response Element-Binding ProteinCytosolEnzyme ActivationEscape ReactionHippocampusIn Vitro TechniquesMaleBad protein, ratbcl-Associated Death ProteinCalcineurinCalciumCalcium Channel BlockersCalcium Channels, L-TypeCarrier ProteinsCyclic AMP Response Element-Binding ProteinPhosphoprotein PhosphatasesProtein Phosphatase 1

Identifiers

PMID11356894
PMCPMC1201477
OpenAlexW2120258938

What OpenQuestion holds

Textmetadata
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.