Evidence map›Paper›PMID 26075270›Full record

ReviewBioMed research international2015

Bridging the gap between statistical and biological epistasis in Alzheimer's disease.

Mark T W Ebbert, Perry G Ridge, John S K Kauwe

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Interaction between variants in CLU and MS4A4E modulates Alzheimer's disease risk.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2016
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. A Novel Multitasking Ant Colony Optimization Method for Detecting Multiorder SNP Interactions.Interdisciplinary sciences, computational life sciences · 2022
    Article
  8. Article
  9. Genetic Bases of Complex Traits: From Quantitative Trait Loci to Prediction.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  10. Article
  11. Review
  12. Article
  13. Incomplete penetrance in familial Alzheimer's disease with PSEN1 Ala260Gly mutation.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2020
    Article
  14. The MUC6/AP2A2 Locus and Its Relevance to Alzheimer's Disease: A Review.Journal of neuropathology and experimental neurology · 2020
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

3 authors at 1 institution in 1 country.

Mark T W EbbertDepartment of Biology, Brigham Young University, Provo, UT, USA.
Perry G RidgeDepartment of Biology, Brigham Young University, Provo, UT, USA.
John S K KauweDepartment of Biology, Brigham Young University, Provo, UT, USA.
Brigham Young University · US

Funding

Research Supplements to Promote Diversity in Health-Related ResearchR01AG042611 · NIA · BRIGHAM YOUNG UNIVERSITY · PI KAUWE, JOHN SAI KEONG · 2012 to 2017
$1.5M
NIA NIH HHS R01 AG042611
6 · The paper itself

Abstract

Alzheimer's disease affects millions of people worldwide and incidence is expected to rise as the population ages, but no effective therapies exist despite decades of research and more than 20 known disease markers. Research has shown that Alzheimer's disease's missing heritability remains extensive with an estimated 25% of phenotypic variance unexplained by known variants. The missing heritability may be explained by missing variants or by epistasis. Researchers often focus on individual loci rather than epistatic interactions, which is likely an oversimplification of the underlying biology since most phenotypes are affected by multiple genes. Focusing research efforts on epistasis will be critical to resolving Alzheimer's disease etiology, and a major key to identifying and properly interpreting key epistatic interactions will be bridging the gap between statistical and biological epistasis. This review covers the current state of epistasis research in Alzheimer's disease and how researchers can bridge the gap between statistical and biological epistasis to help resolve Alzheimer's disease etiology.

Indexed as

Epistasis, GeneticAgingAlzheimer DiseaseHumans

Identifiers

PMID26075270
PMCPMC4449899
OpenAlexW2114099412

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.