Evidence map›Paper›PMID 37761004›Full record

ArticleBiomedicines2023

Amyloid-Beta Peptides Trigger Premature Functional and Gene Expression Alterations in Human-Induced Neurons.

Ana Raquel Melo de Farias, Alexandre Pelletier, Lukas Cruz Carvalho Iohan, Orthis Saha, Amélie Bonnefond, Philippe Amouyel, Fabien Delahaye, Jean-Charles Lambert, Marcos R Costa

Open access · goldAbstract read
In one paragraph

Article in Biomedicines, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. 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

9 authors at 3 institutions in 2 countries.

Ana Raquel Melo de FariasUniversité de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1167-RID-AGE Facteurs de Risque et Déterminants Moléculaires des Maladies Liées au Vieillissement, DISTALZ, 1 rue du Professeur Calmette, 59019 Lille, France.ORCID 0000-0003-4324-6759
Alexandre PelletierUniversité de Lille, Inserm, CNRS, CHU Lille, Institut Pasteur de Lille, U1283-UMR 8199 EGID, Pôle Recherche, 1 Place de Verdun, CEDEX, 59045 Lille, France.
Lukas Cruz Carvalho IohanBioinformatics Multidisciplinary Environment, Federal University of Rio Grande do Norte, Natal 59078-970, Brazil.
Orthis SahaUniversité de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1167-RID-AGE Facteurs de Risque et Déterminants Moléculaires des Maladies Liées au Vieillissement, DISTALZ, 1 rue du Professeur Calmette, 59019 Lille, France.ORCID 0000-0003-2459-060X
Amélie BonnefondUniversité de Lille, Inserm, CNRS, CHU Lille, Institut Pasteur de Lille, U1283-UMR 8199 EGID, Pôle Recherche, 1 Place de Verdun, CEDEX, 59045 Lille, France.ORCID 0000-0001-9976-3005
Philippe AmouyelUniversité de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1167-RID-AGE Facteurs de Risque et Déterminants Moléculaires des Maladies Liées au Vieillissement, DISTALZ, 1 rue du Professeur Calmette, 59019 Lille, France.ORCID 0000-0001-9088-234X
Fabien DelahayeUniversité de Lille, Inserm, CNRS, CHU Lille, Institut Pasteur de Lille, U1283-UMR 8199 EGID, Pôle Recherche, 1 Place de Verdun, CEDEX, 59045 Lille, France.ORCID 0000-0002-9921-8653
Jean-Charles LambertUniversité de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1167-RID-AGE Facteurs de Risque et Déterminants Moléculaires des Maladies Liées au Vieillissement, DISTALZ, 1 rue du Professeur Calmette, 59019 Lille, France.
Marcos R CostaUniversité de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1167-RID-AGE Facteurs de Risque et Déterminants Moléculaires des Maladies Liées au Vieillissement, DISTALZ, 1 rue du Professeur Calmette, 59019 Lille, France.ORCID 0000-0002-4928-2163
Inserm · FRCentre National de la Recherche Scientifique · FRUniversidade Federal do Rio Grande do Norte · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most prevalent cause of dementia in the elderly, characterized by the presence of amyloid-beta (Aβ) plaques, neurofibrillary tangles, neuroinflammation, synapse loss and neurodegeneration in the brain. The amyloid cascade hypothesis postulates that deposition of Aβ peptides is the causative agent of AD pathology, but we still lack comprehensive understanding of the molecular mechanisms connecting Aβ peptides to neuronal dysfunctions in AD. In this work, we investigate the early effects of Aβ peptide accumulation on the functional properties and gene expression profiles of human-induced neurons (hiNs). We show that hiNs acutely exposed to low concentrations of both cell-secreted Aβ peptides or synthetic Aβ

Indexed as

amyloid-beta peptidescalcium imaginghuman-induced neuronsinter-cellular communicationsingle-nucleus RNA sequencing

Identifiers

PMID37761004
PMCPMC10526858
OpenAlexW4386848292

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.