Evidence map›Paper›PMID 23872402›Full record

ReviewEuropean journal of pharmacology2013

Hippocampal calcium dysregulation at the nexus of diabetes and brain aging.

Olivier Thibault, Katie L Anderson, Chris DeMoll, Lawrence D Brewer, Philip W Landfield, Nada M Porter

Abstract readReview
In one paragraph

Review in European journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

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

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  20. Caloric restriction improves diabetes-induced cognitive deficits by attenuating neurogranin-associated calcium signaling in high-fat diet-fed mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016
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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

6 authors.

Olivier ThibaultDepartment of Molecular and Biomedical Pharmacology, MS 313, 800 Rose Street, University of Kentucky Medical Center, Lexington, KY 40536, United States. Electronic address: othibau@uky.edu.
Katie L AndersonDepartment of Molecular and Biomedical Pharmacology, MS 313, 800 Rose Street, University of Kentucky Medical Center, Lexington, KY 40536, United States.
Chris DeMollDepartment of Molecular and Biomedical Pharmacology, MS 313, 800 Rose Street, University of Kentucky Medical Center, Lexington, KY 40536, United States.
Lawrence D BrewerDepartment of Molecular and Biomedical Pharmacology, MS 313, 800 Rose Street, University of Kentucky Medical Center, Lexington, KY 40536, United States.
Philip W LandfieldDepartment of Molecular and Biomedical Pharmacology, MS 313, 800 Rose Street, University of Kentucky Medical Center, Lexington, KY 40536, United States.
Nada M PorterDepartment of Molecular and Biomedical Pharmacology, MS 313, 800 Rose Street, University of Kentucky Medical Center, Lexington, KY 40536, United States.

Funding

HIPPOCAMPAL SYNAPTIC STRUCTURE--PHYSIOLOGY DURING AGINGR37AG004542 · NIA · UNIVERSITY OF KENTUCKY · PI LANDFIELD, PHILIP W. · 1998 to 2020
$7.1M
Metabolic syndrome and hippocampal Ca2+ dysregulation in aging-related memory decR01AG033649 · NIA · UNIVERSITY OF KENTUCKY · PI THIBAULT, OLIVIER · 2009 to 2019
$3.4M
NIA NIH HHS AG020268NIA NIH HHS AG033649NIA NIH HHS R01 AG033649NIA NIH HHS R37 AG004542
6 · The paper itself

Abstract

Recently it has become clear that conditions of insulin resistance/metabolic syndrome, obesity and diabetes, are linked with moderate cognitive impairment in normal aging and elevated risk of Alzheimer's disease. It appears that a common feature of these conditions is impaired insulin signaling, affecting the brain as well as peripheral target tissues. A number of studies have documented that insulin directly affects brain processes and that reduced insulin signaling results in impaired learning and memory. Several studies have also shown that diabetes induces Ca(2+) dysregulation in neurons. Because brain aging is associated with substantial Ca(2+) dyshomeostasis, it has been proposed that impaired insulin signaling exacerbates or accelerates aging-related Ca(2+) dyshomeostasis. However, there have been few studies examining insulin interactions with Ca(2+) regulation in aging animals. We have been testing predictions of the Ca(2+) dysregulation/diabetes/brain aging hypothesis and have found that insulin and insulin-sensitizers (thiazolidinediones) target several hippocampal Ca(2+)-related processes affected by aging. The drugs appear able to reduce the age-dependent increase in Ca(2+) transients and the Ca(2+) -sensitive afterhyperpolarization. Thus, while additional testing is needed, the results to date are consistent with the view that strategies that enhance insulin signaling can counteract the effect of aging on Ca(2+) dysregulation.

Indexed as

AgingAnimalsCalciumCognitionDiabetes MellitusHippocampusHumansInsulinCalciumInsulinAfterhyperpolarizationAgingCognitionImagingLearningThiazolidinediones

Identifiers

PMID23872402
PMCPMC3838483

What OpenQuestion holds

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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.