Evidence map›Paper›PMID 26455952›Full record

ArticleNeurobiology of aging2015

Reduction of increased calcineurin activity rescues impaired homeostatic synaptic plasticity in presenilin 1 M146V mutant.

Seonil Kim, Caroline J Violette, Edward B Ziff

Abstract read
In one paragraph

Article in Neurobiology of aging, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.0field-weighted citation impact, top 16% 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

36 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Ketamine Reverses Chronic Stress-Induced Behavioral Changes via the Expression of CaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  6. Article
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  8. Review
  9. Article
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  16. Article
  17. IGeroScience · 2021
    Article
  18. Calmodulin and Its Binding Proteins in Parkinson's Disease.International journal of molecular sciences · 2021
    Review
  19. Review
  20. Review
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

3 authors at 2 institutions in 1 country.

Seonil KimDepartment of Biochemistry and Molecular Pharmacology, New York University Langone Medical Center, New York, NY, USA. Electronic address: seonil.kim@nyumc.org.
Caroline J VioletteBucknell University, PA, USA.
Edward B ZiffDepartment of Biochemistry and Molecular Pharmacology, New York University Langone Medical Center, New York, NY, USA. Electronic address: edward.ziff@nyumc.org.
NYU Langone Health · USBucknell University · US

Funding

Calcium Permeable AMPA Receptors: Signaling, Toxicity and ControlR01NS061920 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ZIFF, EDWARD B · 2009 to 2013
$1.9M
NINDS NIH HHS 5R01NS061920NINDS NIH HHS R01 NS061920
6 · The paper itself

Abstract

Alzheimer's disease (AD) is one of the most common neurodegenerative diseases characterized by memory loss and cognitive impairment. Whereas most AD cases are sporadic, some are caused by mutations in early-onset familial AD (FAD) genes. One FAD gene encodes presenilin 1 (PS1), and a PS1 mutation in methionine 146 impairs homeostatic synaptic plasticity (HSP). We have previously shown that Ca(2+) and calcineurin activity are critical regulators of HSP. Here, we confirm that endoplasmic reticulum-mediated Ca(2+) signals are increased in mutant PS1 neurons. We further show that calcineurin activity is abnormally elevated in the mutant and that inhibition of increased calcineurin activity stabilizes GluA1 phosphorylation, promoting synaptic trafficking of Ca(2+)-permeable α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, contributing to the recovery of impaired HSP found in the mutant. Because HSP is suggested to have roles during learning and memory formation, increased calcineurin activity-induced impairment of HSP can cause cognitive decline in FAD. Thus, reducing abnormally increased calcineurin activity in AD brain may be beneficial for improving AD-related cognitive decline.

Indexed as

MutationAlzheimer DiseaseAnimalsCalcineurinCalciumCalcium SignalingCells, CulturedCognitionEndoplasmic ReticulumHippocampusHomeostasisHumansLearningMemoryMethionineMice, Inbred C57BLCalcineurinCalciumMethioninePresenilin-1Receptors, AMPATacrolimusAlzheimer’s diseaseAMPA receptorCalcineurinHomeostatic synaptic plasticityPresenilin 1

Identifiers

PMID26455952
PMCPMC4641803
OpenAlexW1706913129

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.