Evidence map›Paper›PMID 34475508›Full record

ArticleScientific reports2021

Overexpression of wild-type human amyloid precursor protein alters GABAergic transmission.

Anna Kreis, Jana Desloovere, Nuria Suelves, Nathalie Pierrot, Xavier Yerna, Farah Issa, Olivier Schakman, Roberta Gualdani, Marie de Clippele, Nicolas Tajeddine and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 9% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

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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

14 authors at 2 institutions in 1 country.

Anna KreisLaboratory of Cell Physiology, Institute of Neuroscience, Université Catholique de Louvain, av. Mounier 53/B1.53.17, 1200, Brussels, Belgium.
Jana DesloovereFaculty of Medicine and Health Sciences, Universiteit Gent, C. Heymanslaan 10, 9000, Gent, Belgium.
Nuria SuelvesAlzheimer Dementia Group, Institute of Neuroscience, Université Catholique de Louvain, av. Mounier 53, 1200, Brussels, Belgium.
Nathalie PierrotAlzheimer Dementia Group, Institute of Neuroscience, Université Catholique de Louvain, av. Mounier 53, 1200, Brussels, Belgium.
Xavier YernaLaboratory of Cell Physiology, Institute of Neuroscience, Université Catholique de Louvain, av. Mounier 53/B1.53.17, 1200, Brussels, Belgium.
Farah IssaLaboratory of Cell Physiology, Institute of Neuroscience, Université Catholique de Louvain, av. Mounier 53/B1.53.17, 1200, Brussels, Belgium.
Olivier SchakmanLaboratory of Cell Physiology, Institute of Neuroscience, Université Catholique de Louvain, av. Mounier 53/B1.53.17, 1200, Brussels, Belgium.
Roberta GualdaniLaboratory of Cell Physiology, Institute of Neuroscience, Université Catholique de Louvain, av. Mounier 53/B1.53.17, 1200, Brussels, Belgium.
Marie de ClippeleLaboratory of Cell Physiology, Institute of Neuroscience, Université Catholique de Louvain, av. Mounier 53/B1.53.17, 1200, Brussels, Belgium.
Nicolas TajeddineLaboratory of Cell Physiology, Institute of Neuroscience, Université Catholique de Louvain, av. Mounier 53/B1.53.17, 1200, Brussels, Belgium.
Pascal Kienlen-CampardAlzheimer Dementia Group, Institute of Neuroscience, Université Catholique de Louvain, av. Mounier 53, 1200, Brussels, Belgium.
Robrecht RaedtFaculty of Medicine and Health Sciences, Universiteit Gent, C. Heymanslaan 10, 9000, Gent, Belgium.
Jean-Noël OctaveAlzheimer Dementia Group, Institute of Neuroscience, Université Catholique de Louvain, av. Mounier 53, 1200, Brussels, Belgium.
Philippe GaillyLaboratory of Cell Physiology, Institute of Neuroscience, Université Catholique de Louvain, av. Mounier 53/B1.53.17, 1200, Brussels, Belgium. philippe.gailly@uclouvain.be.
UCLouvain · BEGhent University · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The function of the amyloid precursor protein (APP) is not fully understood, but its cleavage product amyloid beta (Aβ) together with neurofibrillary tangles constitute the hallmarks of Alzheimer's disease (AD). Yet, imbalance of excitatory and inhibitory neurotransmission accompanied by loss of synaptic functions, has been reported much earlier and independent of any detectable pathological markers. Recently, soluble APP fragments have been shown to bind to presynaptic GABA

Indexed as

Up-RegulationAmyloid beta-Protein PrecursorAnimalsCognitive Dysfunctiongamma-Aminobutyric AcidHumansMaleMiceNeuronal PlasticityReceptors, GlutamateSynapsesSynaptic TransmissionAmyloid beta-Protein PrecursorAPP protein, humangamma-Aminobutyric AcidReceptors, Glutamate

Identifiers

PMID34475508
PMCPMC8413381
OpenAlexW3196959953

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.