Evidence map›Paper›PMID 20185149›Full record

ArticleJournal of psychiatric research2010

Gene variants associated with schizophrenia in a Norwegian genome-wide study are replicated in a large European cohort.

Lavinia Athanasiu, Morten Mattingsdal, Anna K Kähler, Andrew Brown, Omar Gustafsson, Ingrid Agartz, Ina Giegling, Pierandrea Muglia, Sven Cichon, Marcella Rietschel and 12 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of psychiatric research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed, 6 pooled it
15.5field-weighted citation impact, top 1% 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

98 citing papers in PubMed, 6 syntheses or guidelines pooled it, 215 citations in OpenAlex.

  1. Celiac disease poses significant risk in developing depression, anxiety, headache, epilepsy, panic disorder, dysthymia: A meta-analysis.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2021
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  17. Journal of personalized medicine · 2023
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  19. Polymodal Control of TMEM16x Channels and Scramblases.International journal of molecular sciences · 2022
    Review
  20. Article

38 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

22 authors at 12 institutions in 7 countries.

Lavinia AthanasiuInstitute of Psychiatry, University of Oslo, P.O. 1130, Blindern, N-0318 Oslo, Norway
Morten Mattingsdal
Anna K Kähler
Andrew Brown
Omar Gustafsson
Ingrid Agartz
Ina Giegling
Pierandrea Muglia
Sven Cichon
Marcella Rietschel
Olli P H Pietiläinen
Leena Peltonen
Elvira Bramon
David Collier
David St Clair
Engilbert Sigurdsson
Hannes Petursson
Dan Rujescu
Ingrid Melle
Vidar M Steen
Srdjan Djurovic
Ole A Andreassen
Oslo University Hospital · NOLudwig-Maximilians-Universität München · DEKing's College London · GBUniversity of Oslo · NOBroad Institute · USGlaxoSmithKline (Italy) · ITHaukeland University Hospital · NOHeidelberg University · DEInstitute for Molecular Medicine Finland · FIUniversity of Aberdeen · GBUniversity of Bonn · DEUniversity of Iceland · IS

Funding

Department of Health PDA/02/06/016Medical Research Council G0901310Wellcome Trust 089061
6 · The paper itself

Abstract

We have performed a genome-wide association study (GWAS) of schizophrenia in a Norwegian discovery sample of 201 cases and 305 controls (TOP study) with a focused replication analysis in a larger European sample of 2663 cases and 13,780 control subjects (SGENE-plus study). Firstly, the discovery sample was genotyped with Affymetrix Genome-Wide Human SNP Array 6.0 and 572,888 markers were tested for schizophrenia association. No SNPs in the discovery sample attained genome-wide significance (P<8.7 x 10(-8)). Secondly, based on the GWAS data, we selected 1000 markers with the lowest P values in the discovery TOP sample, and tested these (or HapMap-based surrogates) for association in the replication sample. Sixteen loci were associated with schizophrenia (nominal P value<0.05 and concurring OR) in the replication sample. As a next step, we performed a combined analysis of the findings from these two studies, and the strongest evidence for association with schizophrenia was provided for markers rs7045881 on 9p21, rs433598 on 16p12 and rs10761482 on 10q21. The markers are located in PLAA, ACSM1 and ANK3, respectively. PLAA has not previously been described as a susceptibility gene, but 9p21 is implied as a schizophrenia linkage region. ACSM1 has been identified as a susceptibility gene in a previous schizophrenia GWAS study. The association of ANK3 with schizophrenia is intriguing in light of recent associations of ANK3 with bipolar disorder, thereby supporting the hypothesis of an overlap in genetic susceptibility between these psychopathological entities.

Indexed as

Genome-Wide Association StudyAnkyrinsCoenzyme A LigasesCohort StudiesEuropeFemaleHumansLinkage DisequilibriumMaleNorwayPolymorphism, Single NucleotideProteinsReference ValuesRetrospective StudiesSchizophreniaWhite PeopleACSM1 protein, humanANK3 protein, humanAnkyrinsCoenzyme A Ligasesphospholipase A2-activating proteinProteins

Identifiers

PMID20185149
PMCPMC3224994
OpenAlexW2158991820

What OpenQuestion holds

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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.