Evidence map›Paper›PMID 41794826›Full record

ArticleNature communications2026

Selective weakening of population-coupled synaptic activity in vivo in a mouse model of amyloid-beta pathology.

Leire Melgosa-Ecenarro, Carola I Radulescu, Nazanin Doostdar, Joe Airey, Francesca A Chaloner, Nawal Zabouri, Giada Pedretti, Francesca Osso, Leire Garrido Perez, Kjara S Pilch and 6 more

Abstract read
In one paragraph

Article in Nature communications, 2026. 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. 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

16 authors.

Leire Melgosa-Ecenarro *UK Dementia Research Institute Centre, Department of Brain Sciences, Imperial College London, Hammersmith Hospital Campus, London, UK.ORCID http://orcid.org/0000-0003-2740-7356
Carola I Radulescu *UK Dementia Research Institute Centre, Department of Brain Sciences, Imperial College London, Hammersmith Hospital Campus, London, UK.ORCID http://orcid.org/0000-0003-4089-9295
Nazanin Doostdar *UK Dementia Research Institute Centre, Department of Brain Sciences, Imperial College London, Hammersmith Hospital Campus, London, UK.
Joe AireyUK Dementia Research Institute Centre, Department of Brain Sciences, Imperial College London, Hammersmith Hospital Campus, London, UK.
Francesca A ChalonerUK Dementia Research Institute Centre, Department of Brain Sciences, Imperial College London, Hammersmith Hospital Campus, London, UK.ORCID http://orcid.org/0000-0003-2707-4539
Nawal ZabouriDepartment of Biomedical Engineering, Imperial College London, South Kensington Campus, London, UK.
Giada PedrettiUK Dementia Research Institute Centre, Department of Brain Sciences, Imperial College London, Hammersmith Hospital Campus, London, UK.
Francesca OssoUK Dementia Research Institute Centre, Department of Brain Sciences, Imperial College London, Hammersmith Hospital Campus, London, UK.
Leire Garrido PerezUK Dementia Research Institute Centre, Department of Brain Sciences, Imperial College London, Hammersmith Hospital Campus, London, UK.ORCID http://orcid.org/0009-0004-4160-0923
Kjara S PilchUK Dementia Research Institute Centre, Department of Brain Sciences, Imperial College London, Hammersmith Hospital Campus, London, UK.ORCID http://orcid.org/0000-0003-2145-2535
Xingjian WangUK Dementia Research Institute Centre, Department of Brain Sciences, Imperial College London, Hammersmith Hospital Campus, London, UK.
Anna MallachUK Dementia Research Institute Centre, Department of Brain Sciences, Imperial College London, Hammersmith Hospital Campus, London, UK.ORCID http://orcid.org/0000-0001-7181-3429
Sadra SadehCentre for Developmental Neurobiology, King's College London, New Hunt's House, Guy's Campus, London, UK.
Johanna JacksonUK Dementia Research Institute Centre, Department of Brain Sciences, Imperial College London, Hammersmith Hospital Campus, London, UK.ORCID http://orcid.org/0000-0002-8459-0591
Paul M MatthewsUK Dementia Research Institute Centre, Department of Brain Sciences, Imperial College London, Hammersmith Hospital Campus, London, UK.ORCID http://orcid.org/0000-0002-1619-8328
Samuel J BarnesUK Dementia Research Institute Centre, Department of Brain Sciences, Imperial College London, Hammersmith Hospital Campus, London, UK. samuel.barnes@imperial.ac.uk.ORCID http://orcid.org/0000-0003-4030-6453

Funding

BrightFocus Foundation (BrightFocus) A2022030S
6 · The paper itself

Abstract

Synaptic dysfunction in Alzheimer's disease (AD) may drive synapse loss and cognitive impairment. Whether AD-related synaptic pathophysiology occurs globally, or in specific synapses, is unclear. We investigate in vivo AD-related synaptic dysfunction during early-stage amyloidosis in App

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesSynapsesAmyloid beta-Protein PrecursorAnimalsCalciumDendritic SpinesDisease Models, AnimalGABAergic NeuronsHumansMaleMiceMice, TransgenicParvalbuminsPresynaptic TerminalsSynaptic TransmissionAmyloid beta-PeptidesAmyloid beta-Protein PrecursorCalciumParvalbumins

Identifiers

PMID41794826
PMCPMC13096637

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.