Evidence map›Paper›PMID 20091797›Full record

ArticleGenetic epidemiology2010

Joint linkage and segregation analysis under multiallelic trait inheritance: simplifying interpretations for complex traits.

Elisabeth A Rosenthal, Ellen M Wijsman

Abstract read
In one paragraph

Article in Genetic epidemiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–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

6 citing papers in PubMed.

  1. Genome scan in familial late-onset Alzheimer's disease: a locus on chromosome 6 contributes to age-at-onset.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2013
    Article
  2. Genome scan of age-at-onset in the NIMH Alzheimer disease sample uncovers multiple loci, along with evidence of both genetic and sample heterogeneity.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2011
    Article
  3. Article
  4. Article
  5. Article
  6. A gene frequency model for QTL mapping using Bayesian inference.Genetics, selection, evolution : GSE · 2010
    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

2 authors.

Elisabeth A RosenthalDivision of Medical Genetics and Department of Biostatistics, University of Washington, Seattle, WA 98195-7720, USA.
Ellen M Wijsman

Funding

THERAPEUTIC EFFECTS OF INTRA-NASAL INSULIN DETEMIRP50AG005136 · NIA · UNIVERSITY OF WASHINGTON · PI GRABOWSKI, THOMAS J. · 1985 to 2019
$57.2M
INTERDISCIPLINARY TRAINING IN GENOMIC SCIENCEST32HG000035 · NHGRI · UNIVERSITY OF WASHINGTON · PI Bruce Colston Trapnell · 1995 to 2026
$24.2M
Serum Amyloid and Inflammation in AtherogenesisP01HL030086 · NHLBI · UNIVERSITY OF WASHINGTON · PI JARVIK, GAIL PAIRITZ · 1985 to 2009
$14.7M
Methods for the Genetic Epidemiology of Complex TraitsR37GM046255 · NIGMS · UNIVERSITY OF WASHINGTON · PI THOMPSON, ELIZABETH ALISON · 2008 to 2017
$4.2M
NHGRI NIH HHS T32 HG000035NHGRI NIH HHS T32 HG00035NHLBI NIH HHS P01 HL030086NHLBI NIH HHS P01 HL30086NIA NIH HHS P50 AG005136NIA NIH HHS P50 AG05136NIGMS NIH HHS R37 GM046255NIGMS NIH HHS R37 GM46255
6 · The paper itself

Abstract

Identification of the genetic basis of common traits may be hindered by underlying complex genetic architectures that are inadequately captured by existing models, including both multiallelic and multilocus modes of inheritance (MOI). One useful approach for localizing genes underlying continuous complex traits is the joint oligogenic linkage and segregation analysis implemented in the package Loki. The method uses reversible jump Markov chain Monte Carlo to eliminate the need to prespecify the number of quantitative trait loci (QTLs) in the trait model, thus providing posterior distributions for the number of QTLs in a Bayesian framework. The current implementation assumes QTLs are diallelic, and therefore can overestimate the number of linked QTLs in the presence of a multiallelic QTL. To address the possibility of multiple alleles, we extended the QTL model to allow for a variable number of additive alleles at each locus. Application to simulated data shows that, under a diallelic MOI, the multiallelic and diallelic analysis models give similar results. Under a multiallelic MOI, the multiallelic analysis model provides better mixing and improved convergence, and leads to a more accurate estimate of the underlying trait MOI and model parameter values, than does the diallelic model. Application to real data shows the multiallelic model results in fewer estimated linked QTLs and that the predominant QTL model is similar to one of two predominant models estimated from the diallelic analysis. Our results indicate that use of a multiallelic analysis model can lead to better understanding of the genetic architecture underlying complex traits.

Indexed as

AllelesGenetic LinkageBayes TheoremComputer SimulationGenotypeHumansMarkov ChainsModels, GeneticModels, StatisticalMonte Carlo MethodPhenotypeQuantitative Trait LociSoftware

Identifiers

PMID20091797
PMCPMC2914272

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Registered trials

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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.