Evidence map›Paper›PMID 25849665›Full record

ArticlePLoS genetics2015

Simultaneous discovery, estimation and prediction analysis of complex traits using a bayesian mixture model.

Gerhard Moser, Sang Hong Lee, Ben J Hayes, Michael E Goddard, Naomi R Wray, Peter M Visscher

Abstract read
In one paragraph

Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 226 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
226citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

226 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
  4. An introduction to polygenic scores - methodological basics and recent advances.Medizinische Genetik : Mitteilungsblatt des Berufsverbandes Medizinische Genetik e.V · 2026
    Article
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  6. Principled measures and estimates of trait polygenicity.American journal of human genetics · 2026
    Article
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166 more citing papers are in PubMed but not listed here.

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

6 authors.

Gerhard MoserQueensland Brain Institute, University of Queensland, Brisbane, Australia.
Sang Hong LeeQueensland Brain Institute, University of Queensland, Brisbane, Australia.
Ben J HayesDepartment of Primary Industries, Biosciences Research Division, Bundoora, Australia; Dairy Futures Cooperative Research Centre, Bundoora, Australia.
Michael E GoddardDepartment of Primary Industries, Biosciences Research Division, Bundoora, Australia; Faculty of Land and Food Resources, University of Melbourne, Melbourne, Australia.
Naomi R WrayQueensland Brain Institute, University of Queensland, Brisbane, Australia.
Peter M VisscherQueensland Brain Institute, University of Queensland, Brisbane, Australia; University of Queensland Diamantina Institute, University of Queensland, Translational Research Institute (TRI), Brisbane, Australia.

Funding

Statistical Methods for X-Chromosome Genetic DataP01GM099568 · NIGMS · UNIVERSITY OF WASHINGTON · PI WEIR, BRUCE S. · 2012 to 2016
$7.3M
NIGMS NIH HHS P01 GM 099568NIGMS NIH HHS P01 GM099568
6 · The paper itself

Abstract

Gene discovery, estimation of heritability captured by SNP arrays, inference on genetic architecture and prediction analyses of complex traits are usually performed using different statistical models and methods, leading to inefficiency and loss of power. Here we use a Bayesian mixture model that simultaneously allows variant discovery, estimation of genetic variance explained by all variants and prediction of unobserved phenotypes in new samples. We apply the method to simulated data of quantitative traits and Welcome Trust Case Control Consortium (WTCCC) data on disease and show that it provides accurate estimates of SNP-based heritability, produces unbiased estimators of risk in new samples, and that it can estimate genetic architecture by partitioning variation across hundreds to thousands of SNPs. We estimated that, depending on the trait, 2,633 to 9,411 SNPs explain all of the SNP-based heritability in the WTCCC diseases. The majority of those SNPs (>96%) had small effects, confirming a substantial polygenic component to common diseases. The proportion of the SNP-based variance explained by large effects (each SNP explaining 1% of the variance) varied markedly between diseases, ranging from almost zero for bipolar disorder to 72% for type 1 diabetes. Prediction analyses demonstrate that for diseases with major loci, such as type 1 diabetes and rheumatoid arthritis, Bayesian methods outperform profile scoring or mixed model approaches.

Indexed as

Models, GeneticPolymorphism, Single NucleotideQuantitative Trait, HeritableAnimalsBayes TheoremGenetic Diseases, InbornHumans

Identifiers

PMID25849665
PMCPMC4388571

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.