Evidence map›Paper›PMID 31877058›Full record

ArticleMolecular biology of the cell2020

PI3K activation prevents Aβ42-induced synapse loss and favors insoluble amyloid deposit formation.

Mercedes Arnés, Ninovska Romero, Sergio Casas-Tintó, Ángel Acebes, Alberto Ferrús

Open access · bronzeAbstract read
In one paragraph

Article in Molecular biology of the cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. QBP1 Peptide as a Potential Anti-Amyloidogenic Therapy for Type 2 Diabetes: An In Vitro Study.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. A renaissance in targeting the PI3K/AKT/mTOR pathway.Nature reviews. Drug discovery · 2026
    Review
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  10. Circadian GeneInternational journal of molecular sciences · 2022
    Article
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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

5 authors at 2 institutions in 1 country.

Mercedes ArnésCajal Institute (CSIC), Madrid 28002, Spain.
Ninovska RomeroDepartment of Basic Medical Sciences, Institute of Biomedical Technologies, University of La Laguna, Tenerife 38200, Spain.
Sergio Casas-TintóCajal Institute (CSIC), Madrid 28002, Spain.
Ángel AcebesCajal Institute (CSIC), Madrid 28002, Spain.
Alberto FerrúsCajal Institute (CSIC), Madrid 28002, Spain.
Instituto Cajal · ESUniversidad de La Laguna · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excess of Aβ42 peptide is considered a hallmark of the disease. Here we express the human Aβ42 peptide to assay the neuroprotective effects of PI3K in adult

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAnimals, Genetically ModifiedAxonal TransportBrainCarrier ProteinsCell Line, TumorDisease Models, AnimalDrosophila melanogasterDrosophila ProteinsHumansIntracellular Signaling Peptides and ProteinsLongevityNeuronsOlfactory PerceptionAmyloid beta-Peptidesamyloid beta-protein (1-42)BRP protein, DrosophilaCarrier ProteinsDrosophila ProteinsIntracellular Signaling Peptides and ProteinsLiprin-alpha protein, Drosophilaliprin-beta protein, DrosophilaPeptide FragmentsPhosphatidylinositol 3-KinasesProtein AggregatesR-SNARE Proteins

Identifiers

PMID31877058
PMCPMC7183762
OpenAlexW2996877320

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.