Evidence map›Paper›PMID 40925676›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2025

Presenilin Loss Impairs Synaptic Transmission and Causes Axonal Degeneration through Ryanodine Receptor Dysfunction, Independent of γ-Secretase Activity.

Xinran Du, Longgang Niu, Michal Ragan, Zuzanna Fracz, Zhao-Wen Wang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

5 authors.

Xinran DuDepartment of Neuroscience, University of Connecticut School of Medicine, Farmington, Connecticut 06030.
Longgang NiuDepartment of Neuroscience, University of Connecticut School of Medicine, Farmington, Connecticut 06030.
Michal RaganDepartment of Neuroscience, University of Connecticut School of Medicine, Farmington, Connecticut 06030.
Zuzanna FraczDepartment of Neuroscience, University of Connecticut School of Medicine, Farmington, Connecticut 06030.
Zhao-Wen WangDepartment of Neuroscience, University of Connecticut School of Medicine, Farmington, Connecticut 06030 zwwang@uchc.edu.ORCID 0000-0003-3574-8556

Funding

Synaptic function of BK channel-interacting proteinsR01MH085927 · NIMH · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI ZHAO-WEN WANG · 2010 to 2026
$6.7M
NIMH NIH HHS R01 MH085927
6 · The paper itself

Abstract

Presenilin mutations are the most common cause of familial Alzheimer's disease (FAD), but the mechanisms by which they disrupt neuronal function remain unresolved, particularly in relation to γ-secretase activity. Using

Indexed as

Amyloid Precursor Protein SecretasesAxonsCaenorhabditis elegans ProteinsNerve DegenerationPresenilinsRyanodine Receptor Calcium Release ChannelSynaptic TransmissionAnimalsAnimals, Genetically ModifiedCaenorhabditis elegansHumansPresenilin-1Amyloid Precursor Protein SecretasesCaenorhabditis elegans ProteinsPresenilin-1PresenilinsRyanodine Receptor Calcium Release Channelneurodegenerationneurotransmitter releasepresenilinryanodine receptorsel-12γ-secretase

Identifiers

PMID40925676
PMCPMC12548705

What OpenQuestion holds

Textmetadata
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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.