Evidence map›Paper›PMID 41046731›Full record

ArticleCell calcium2025

Pathological calcium influx through amyloid beta pores disrupts synaptic function.

Temitope Adeoye, Ghanim Ullah

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell calcium, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

2 authors.

Temitope AdeoyeDepartment of Physics, University of South Florida, Tampa, FL 33620, USA.
Ghanim UllahDepartment of Physics, University of South Florida, Tampa, FL 33620, USA. Electronic address: gullah@usf.edu.

Funding

Investigating the aggregation of amyloid β during metabolic stress using multiscale modelingR21AG087910 · NIA · UNIVERSITY OF SOUTH FLORIDA · PI MUSCHOL, MARTIN, ULLAH, GHANIM · 2024 to 2025
$394k
NIA NIH HHS R21 AG087910
6 · The paper itself

Abstract

Alzheimer's disease (AD) is characterized by profound disruption of synaptic function, with mounting evidence suggesting that amyloid-β (Aβ) oligomers disrupt calcium (Ca

Indexed as

Amyloid beta-PeptidesCalciumSynapsesAlzheimer DiseaseAnimalsCalcium SignalingEndoplasmic ReticulumExocytosisHumansSynaptic TransmissionAmyloid beta-PeptidesCalciumAlzheimer’s diseaseAmyloid beta poresAsynchronous releaseNeuronal calcium signallingNeurotransmitter releaseSynchronous release

Identifiers

PMID41046731
PMCPMC13289046

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.