Evidence map›Paper›PMID 22265986›Full record

ArticleBiochimica et biophysica acta2012

Reduction in neuronal L-type calcium channel activity in a double knock-in mouse model of Alzheimer's disease.

Olivier Thibault, Tristano Pancani, Philip W Landfield, Christopher M Norris

Abstract read
In one paragraph

Article in Biochimica et biophysica acta, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–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

28 citing papers in PubMed.

  1. Astrovascular decoupling in awake 5×FAD mice is associated with reduced astrocytic calcium.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
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  4. Article
  5. Review
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  13. Article
  14. Article
  15. Review
  16. FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  17. Calcium's role as nuanced modulator of cellular physiology in the brain.Biochemical and biophysical research communications · 2017
    Review
  18. From Molecular Circuit Dysfunction to Disease: Case Studies in Epilepsy, Traumatic Brain Injury, and Alzheimer's Disease.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2016
    Review
  19. Article
  20. Article
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

4 authors.

Olivier ThibaultDepartment of Molecular and Biomedical Pharmacology, University of Kentucky College of Medicine, Lexington, KY 40536, USA. othibau@uky.edu
Tristano Pancani
Philip W Landfield
Christopher M Norris

Funding

ROLE OF CALCIUM, CALPAINS, AND CASPASES IN NEURODEGENERATIONP01AG010836 · NIA · UNIVERSITY OF KENTUCKY · PI LANDFIELD, PHILIP W. · 1992 to 2008
$12.4M
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
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 inflammatory signaling processes in aging and Alzheimer's DiseaseRF1AG027297 · NIA · UNIVERSITY OF KENTUCKY · PI NORRIS, CHRISTOPHER MARK · 2018 to 2022
$2.6M
HIPPOCAMPAL SYNAPTIC STUCTURE-PHYSIOLOGY DURING AGINGR01AG004542 · NIA · WAKE FOREST UNIVERSITY · PI LANDFIELD, PHILIP W. · 1985 to 1995
–
NIA NIH HHS AG004542NIA NIH HHS AG010836NIA NIH HHS AG027297NIA NIH HHS AG033649NIA NIH HHS P01 AG010836NIA NIH HHS R01 AG027297NIA NIH HHS R01 AG033649NIA NIH HHS R37 AG004542NIA NIH HHS RF1 AG027297
6 · The paper itself

Abstract

Increased function of neuronal L-type voltage-sensitive Ca(2+) channels (L-VSCCs) is strongly linked to impaired memory and altered hippocampal synaptic plasticity in aged rats. However, no studies have directly assessed L-VSCC function in any of the common mouse models of Alzheimer's disease where neurologic deficits are typically more robust. Here, we used cell-attached patch-clamp recording techniques to measure L-VSCC activity in CA1 pyramidal neurons of partially dissociated hippocampal "zipper" slices prepared from 14-month-old wild-type mice and memory-impaired APP/PS1 double knock-in mice. Surprisingly, the functional channel density of L-VSCCs was significantly reduced in the APP/PS1 group. No differences in voltage dependency and unitary conductance of L-VSCCs were observed. The results suggest that mechanisms for Ca(2+) dysregulation can differ substantially between animal models of normal aging and models of pathological aging.

Indexed as

Disease Models, AnimalAlzheimer DiseaseAnimalsCalcium Channels, L-TypeMaleMiceMice, TransgenicNeuronsCalcium Channels, L-Type

Identifiers

PMID22265986
PMCPMC3293940

What OpenQuestion holds

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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.