Evidence map›Paper›PMID 16631129›Full record

SynthesisBiological psychiatry2006

Evaluation of a susceptibility gene for schizophrenia: genotype based meta-analysis of RGS4 polymorphisms from thirteen independent samples.

Michael E Talkowski, Howard Seltman, Anne S Bassett, Linda M Brzustowicz, Xiangning Chen, Kodavali V Chowdari, David A Collier, Quirino Cordeiro, Aiden P Corvin, Smita N Deshpande and 26 more

Open access · greenAbstract readMeta-AnalysisReview
In one paragraph

Synthesis in Biological psychiatry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
10.1field-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

29 citing papers in PubMed, 99 citations in OpenAlex.

  1. Trial
  2. Review
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  4. Article
  5. Association Analysis Between SNPs in the Promoter Region ofNeuropsychiatric disease and treatment · 2020
    Article
  6. Association between RGS4 variants and psychotic-like experiences in nonclinical individuals.European archives of psychiatry and clinical neuroscience · 2017
    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

36 authors at 17 institutions in 7 countries.

Michael E TalkowskiDepartment of Human Genetics, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, USA.
Howard Seltman
Anne S Bassett
Linda M Brzustowicz
Xiangning Chen
Kodavali V Chowdari
David A Collier
Quirino Cordeiro
Aiden P Corvin
Smita N Deshpande
Michael F Egan
Michael Gill
Kenneth S Kendler
George Kirov
Leonard L Heston
Pat Levitt
David A Lewis
Tao Li
Karoly Mirnics
Derek W Morris
Nadine Norton
Michael C O'Donovan
Michael J Owen
Christian Richard
Prachi Semwal
Janet L Sobell
David St Clair
Richard E Straub
B K Thelma
Homero Vallada
Daniel R Weinberger
Nigel M Williams
Joel Wood
Feng Zhang
Bernie Devlin
Vishwajit L Nimgaonkar
University of Pittsburgh · USUniversity of Wales · GBNational Institute of Mental Health · USTrinity College Dublin · IEUniversidade de São Paulo · BRUniversity of Aberdeen · GBUniversity of Delhi · INUniversity of Southern California · USVirginia Commonwealth University · USAtal Bihari Vajpayee Institute of Medical Sciences and Dr. Ram Manohar Lohia Hospital · INCarnegie Mellon University · USCentre for Addiction and Mental Health · CAPsychiatry Research Trust · GBRutgers, The State University of New Jersey · USUniversity of Washington · USVanderbilt University · USWest China Hospital of Sichuan University · CN

Funding

GENETIC ASSOCIATION IN SCHIZOPHRENIA AND OTHER DISORDERSR01MH057881 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DEVLIN, BERNIE · 1998 to 2012
$4.8M
Molecular Genetics of Schizophrenia SusceptibilityR01MH062440 · NIMH · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI BRZUSTOWICZ, LINDA M · 2001 to 2008
$3.4M
Genetic Susceptibility in SchizophreniaR01MH056242 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI NIMGAONKAR, VISHWAJIT LAXMIKANT · 2002 to 2007
$2.9M
GENETIC SUSCEPTIBILITY IN SCHIZOPHRENIAR10MH056242 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI NIMGAONKAR, VISHWAJIT LAXMIKANT · 1997 to 2001
$1.2M
Uncovering complex expression patterns in schizophreniaK02MH070786 · NIMH · VANDERBILT UNIVERSITY · PI MIRNICS, KAROLY · 2004 to 2008
$527k
SCHIZOPHRENIA--GENETIC ASSOCIATIONS IN AFRICAN-AMERICANSR29MH053459 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI NIMGAONKAR, VISHWAJIT LAXMIKANT · 1995 to 1999
–
CIHR 53216Intramural NIH HHSMedical Research Council G9309834Medical Research Council G9810900NIMH NIH HHS K02 MH070786NIMH NIH HHS K02 MH07086NIMH NIH HHS MH051456NIMH NIH HHS MH53459NIMH NIH HHS MH56242NIMH NIH HHS MH62440NIMH NIH HHS R01 MH056242NIMH NIH HHS R01 MH057881NIMH NIH HHS R01 MH062440NIMH NIH HHS R10 MH056242Wellcome Trust
6 · The paper itself

Abstract

backgroundAssociations between schizophrenia (SCZ) and polymorphisms at the regulator of G-protein signaling 4 (RGS4) gene have been reported (single nucleotide polymorphisms [SNPs] 1, 4, 7, and 18). Yet, similar to other SCZ candidate genes, studies have been inconsistent with respect to the associated alleles.

methodsIn an effort to resolve the role for RGS4 in SCZ susceptibility, we undertook a genotype-based meta-analysis using both published and unpublished family-based and case-control samples (total n = 13,807).

resultsThe family-based dataset consisted of 10 samples (2160 families). Significant associations with individual SNPs/haplotypes were not observed. In contrast, global analysis revealed significant transmission distortion (p = .0009). Specifically, analyses suggested overtransmission of two common haplotypes that account for the vast majority of all haplotypes. Separate analyses of 3486 cases and 3755 control samples (eight samples) detected a significant association with SNP 4 (p = .01). Individual haplotype analyses were not significant, but evaluation of test statistics from individual samples suggested significant associations.

conclusionsOur collaborative meta-analysis represents one of the largest SCZ association studies to date. No individual risk factor arose from our analyses, but interpretation of these results is not straightforward. Our analyses suggest risk due to at least two common haplotypes in the presence of heterogeneity. Similar analysis for other putative susceptibility genes is warranted.

Indexed as

Case-Control StudiesDatabases, GeneticFamilyGenotypeHumansLinkage DisequilibriumPolymorphism, GeneticPublication BiasQuality ControlSchizophrenia

Identifiers

PMID16631129
PMCPMC3133764
OpenAlexW2068260880

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.