Evidence map›Paper›PMID 29267373›Full record

ArticlePloS one2017

Combinations of genetic variants associated with bipolar disorder.

Erling Mellerup, Ole A Andreassen, Bente Bennike, Henrik Dam, Srdjan Djurovic, Martin Balslev Jorgensen, Lars Vedel Kessing, Pernille Koefoed, Ingrid Melle, Ole Mors and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.5field-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

2 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
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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

11 authors at 5 institutions in 2 countries.

Erling MellerupLaboratory of Neuropsychiatry, Department of Neuroscience and Pharmacology, University of Copenhagen, Copenhagen, Denmark.ORCID 0000-0001-7150-7755
Ole A AndreassenDepartment of Psychiatry, Oslo University Hospital and Institute of Psychiatry, University of Oslo, Oslo, Norway.
Bente BennikeLaboratory of Neuropsychiatry, Department of Neuroscience and Pharmacology, University of Copenhagen, Copenhagen, Denmark.
Henrik DamPsychiatric Centre Copenhagen, Department O, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
Srdjan DjurovicDepartment of Medical Genetics, Oslo University Hospital and Institute of Psychiatry, University of Oslo, Oslo, Norway.
Martin Balslev JorgensenPsychiatric Centre Copenhagen, Department O, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
Lars Vedel KessingPsychiatric Centre Copenhagen, Department O, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
Pernille KoefoedLaboratory of Neuropsychiatry, Department of Neuroscience and Pharmacology, University of Copenhagen, Copenhagen, Denmark.
Ingrid MelleDepartment of Psychiatry, Oslo University Hospital and Institute of Psychiatry, University of Oslo, Oslo, Norway.
Ole MorsCentre for Psyciatric Research, Aarhus University Hospital, Skovagervej 2, Risskov, Denmark.
Gert Lykke MoellerGenokey ApS, ScionDTU, Technical University Denmark, Agern Allé 3, Hoersholm, Denmark.
Copenhagen University Hospital · DKOslo University Hospital · NOUniversity of Copenhagen · DKAarhus University Hospital · DKTechnical University of Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The main objective of the study was to find genetic variants that in combination are significantly associated with bipolar disorder. In previous studies of bipolar disorder, combinations of three and four single nucleotide polymorphisms (SNP) genotypes taken from 803 SNPs were analyzed, and five clusters of combinations were found to be significantly associated with bipolar disorder. In the present study, combinations of ten SNP genotypes taken from the same 803 SNPs were analyzed, and one cluster of combinations was found to be significantly associated with bipolar disorder. Combinations from the new cluster and from the five previous clusters were identified in the genomes of 266 or 44% of the 607 patients in the study whereas none of the 1355 control participants had any of these combinations in their genome.The SNP genotypes in the smaller combinations were the normal homozygote, heterozygote or variant homozygote. In the combinations containing 10 SNP genotypes almost all the genotypes were the normal homozygote. Such a finding may indicate that accumulation in the genome of combinations containing few SNP genotypes may be a risk factor for bipolar disorder when those combinations contain relatively many rare SNP genotypes, whereas combinations need to contain many SNP genotypes to be a risk factor when most of the SNP genotypes are the normal homozygote.

Indexed as

Polymorphism, Single NucleotideBipolar DisorderCase-Control StudiesCluster AnalysisGenetic Predisposition to DiseaseGenotypeHumans

Identifiers

PMID29267373
PMCPMC5739413
OpenAlexW2777372086

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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.