Evidence map›Paper›PMID 27021818›Full record

ArticleMolecular psychiatry2016

Alzheimer disease: modeling an Aβ-centered biological network.

D Campion, C Pottier, G Nicolas, K Le Guennec, A Rovelet-Lecrux

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Functional genomics identify causal variant underlying the protective CTSH locus for Alzheimer's disease.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Physical Exercise-Induced Myokines in Neurodegenerative Diseases.International journal of molecular sciences · 2021
    Review
  12. Interaction between Aβ and Tau in the Pathogenesis of Alzheimer's Disease.International journal of biological sciences · 2021
    Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Protective Effects ofToxics · 2019
    Article
  19. Review
  20. 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 at 4 institutions in 1 country.

D CampionInserm U1079, Rouen University, Institute for Research and Innovation in Biomedicine, Normandie University, Rouen, France.
C PottierInserm U1079, Rouen University, Institute for Research and Innovation in Biomedicine, Normandie University, Rouen, France.
G NicolasInserm U1079, Rouen University, Institute for Research and Innovation in Biomedicine, Normandie University, Rouen, France.
K Le GuennecInserm U1079, Rouen University, Institute for Research and Innovation in Biomedicine, Normandie University, Rouen, France.
A Rovelet-LecruxInserm U1079, Rouen University, Institute for Research and Innovation in Biomedicine, Normandie University, Rouen, France.
Normandie Université · FRInserm · FRInstitute for Research and Innovation in Biomedicine · FRUniversité de Rouen Normandie · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In genetically complex diseases, the search for missing heritability is focusing on rare variants with large effect. Thanks to next generation sequencing technologies, genome-wide characterization of these variants is now feasible in every individual. However, a lesson from current studies is that collapsing rare variants at the gene level is often insufficient to obtain a statistically significant signal in case-control studies, and that network-based analyses are an attractive complement to classical approaches. In Alzheimer disease (AD), according to the prevalent amyloid cascade hypothesis, the pathology is driven by the amyloid beta (Aβ) peptide. In past years, based on experimental studies, several hundreds of proteins have been shown to interfere with Aβ production, clearance, aggregation or toxicity. Thanks to a manual curation of the literature, we identified 335 genes/proteins involved in this biological network and classified them according to their cellular function. The complete list of genes, or its subcomponents, will be of interest in ongoing AD genetic studies.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsDatabases, Nucleic AcidGene Regulatory NetworksHigh-Throughput Nucleotide SequencingHumansAmyloid beta-PeptidesAmyloid beta-Protein Precursor

Identifiers

PMID27021818
OpenAlexW2326098818

What OpenQuestion holds

Textmetadata
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.