Evidence map›Paper›PMID 23736218›Full record

ArticleEuropean journal of human genetics : EJHG2014

Accurate prediction of a minimal region around a genetic association signal that contains the causal variant.

Zoltán Bochdanovits, Javier Simón-Sánchez, Marianne Jonker, Witte J Hoogendijk, Aad van der Vaart, Peter Heutink

Abstract read
In one paragraph

Article in European journal of human genetics : EJHG, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. New Genetic Approaches to AD: Lessons from APOE-TOMM40 Phylogenetics.Current neurology and neuroscience reports · 2016
    Review
  3. 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

6 authors.

Zoltán BochdanovitsDepartment of Clinical Genetics, VU University Medical Center, Amsterdam, The Netherlands.
Javier Simón-SánchezDepartment of Clinical Genetics, VU University Medical Center, Amsterdam, The Netherlands.
Marianne JonkerSection Stochastics, Department of Mathematics, Faculty of Sciences, Vrije Universiteit, Amsterdam, The Netherlands.
Witte J Hoogendijk1] Department of Psychiatry, VU University Medical Center, Amsterdam, The Netherlands [2] Department of Psychiatry, Erasmus Medical Center, Rotterdam, The Netherlands.
Aad van der VaartSection Stochastics, Department of Mathematics, Faculty of Sciences, Vrije Universiteit, Amsterdam, The Netherlands.
Peter HeutinkDepartment of Clinical Genetics, VU University Medical Center, Amsterdam, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In recent years, genome-wide association studies have been very successful in identifying loci for complex traits. However, typically these findings involve noncoding and/or intergenic SNPs without a clear functional effect that do not directly point to a gene. Hence, the challenge is to identify the causal variant responsible for the association signal. Typically, the first step is to identify all genetic variation in the locus region, usually by resequencing a large number of case chromosomes. Among all variants, the causal one needs to be identified in further functional studies. Because the experimental follow up can be very laborious, restricting the number of variants to be scrutinized can yield a great advantage. An objective method for choosing the size of the region to be followed up would be highly valuable. Here, we propose a simple method to call the minimal region around a significant association peak that is very likely to contain the causal variant. We model linkage disequilibrium (LD) in cases from the observed single SNP association signals, and predict the location of the causal variant by quantifying how well this relationship fits the data. Simulations showed that our approach identifies genomic regions of on average ∼50 kb with up to 90% probability to contain the causal variant. We apply our method to two genome-wide association data sets and localize both the functional variant REP1 in the α-synuclein gene that conveys susceptibility to Parkinson's disease and the APOE gene responsible for the association signal in the Alzheimer's disease data set.

Indexed as

Models, Geneticalpha-SynucleinApolipoproteins EGene FrequencyGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansLinkage DisequilibriumParkinson DiseasePolymorphism, Single Nucleotidealpha-SynucleinApolipoproteins ESNCA protein, human

Identifiers

PMID23736218
PMCPMC3895635

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.