Evidence map›Paper›PMID 26663532›Full record

ArticleAmerican journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics2016

Genome-wide association study reveals greater polygenic loading for schizophrenia in cases with a family history of illness.

Tim B Bigdeli, Stephan Ripke, Silviu-Alin Bacanu, Sang Hong Lee, Naomi R Wray, Pablo V Gejman, Marcella Rietschel, Sven Cichon, David St Clair, Aiden Corvin and 14 more

Abstract read
In one paragraph

Article in American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Familial and socioeconomic contributions to premorbid functioning in psychosis: Impact on age at onset and treatment response.European psychiatry : the journal of the Association of European Psychiatrists · 2020
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Use of schizophrenia and bipolar disorder polygenic risk scores to identify psychotic disorders.The British journal of psychiatry : the journal of mental science · 2018
    Article
  13. Article
  14. Observational
  15. Review
  16. 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

24 authors.

Tim B BigdeliVirginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry, Virginia Commonwealth University, Richmond, Virginia.
Stephan RipkeAnalytic and Translational Genetics Unit, Massachusetts General Hospital, Boston, Massachusetts.
Silviu-Alin BacanuVirginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry, Virginia Commonwealth University, Richmond, Virginia.
Sang Hong LeeQueensland Brain Institute, The University of Queensland, Brisbane, Queensland, Australia.
Naomi R WrayQueensland Brain Institute, The University of Queensland, Brisbane, Queensland, Australia.
Pablo V GejmanDepartment of Psychiatry and Behavioral Sciences, NorthShore University HealthSystem, Evanston, Illinois.
Marcella RietschelDepartment of Genetic Epidemiology in Psychiatry, Central Institute of Mental Health, Medical Faculty Mannheim, University of Heidelberg, Heidelberg, Germany.
Sven CichonDivision of Medical Genetics, Department of Biomedicine, University of Basel, Basel, Switzerland.
David St ClairUniversity of Aberdeen, Institute of Medical Sciences, Aberdeen, Scotland, United Kingdom.
Aiden CorvinNeuropsychiatric Genetics Research Group, Department of Psychiatry, Trinity College Dublin, Ireland.
George KirovMRC Centre for Neuropsychiatric Genetics and Genomics, Institute of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, United Kingdom.
Andrew McQuillinMolecular Psychiatry Laboratory, Division of Psychiatry, University College London, United Kingdom.
Hugh GurlingMolecular Psychiatry Laboratory, Division of Psychiatry, University College London, United Kingdom.
Dan RujescuDepartment of Psychiatry, University of Halle, Halle, Germany.
Ole A AndreassenNORMENT, KG Jebsen Centre for Psychosis Research, Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Thomas WergeInstitute of Biological Psychiatry, MHC Sct. Hans, Mental Health Services Copenhagen, Denmark.
Douglas H R BlackwoodDivision of Psychiatry, University of Edinburgh, Edinburgh, United Kingdom.
Carlos N PatoDepartment of Psychiatry, Keck School of Medicine at University of Southern California, Los Angeles, California.
Michele T PatoDepartment of Psychiatry, Keck School of Medicine at University of Southern California, Los Angeles, California.
Anil K MalhotraThe Zucker Hillside Hospital, Glen Oaks, New York.
Michael C O'DonovanMRC Centre for Neuropsychiatric Genetics and Genomics, Institute of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, United Kingdom.
Kenneth S KendlerVirginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry, Virginia Commonwealth University, Richmond, Virginia.
Ayman H FanousVirginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry, Virginia Commonwealth University, Richmond, Virginia.
Schizophrenia Working Group of the Psychiatric Genomics Consortium

Funding

Genomic Psychiatry CohortR01MH085548 · NIMH · UNIVERSITY OF SOUTHERN CALIFORNIA · PI PATO, CARLOS N, PATO, MICHELE T · 2008 to 2012
$16.3M
1/4 Psychiatric GWAS Consortium: Genomic Follow-up Next-Gen Sequencing & GenotypiU01MH094421 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SULLIVAN, PATRICK F · 2012 to 2015
$1.9M
Convergent Genetic and Genomic Analyses of SchizophreniaI01CX000278 · VA · U.S. DEPT/VETS AFFAIRS MEDICAL CENTER · PI FANOUS, AYMAN H · 2011 to 2014
–
CSRD VA I01 CX000278Department of Health PDA/02/06/016Medical Research Council G0800509Medical Research Council G0901310Medical Research Council G1000708Medical Research Council MR/L010305/1Medical Research Council MR/P005748/1NIMH NIH HHS R01 MH085548NIMH NIH HHS U01 MH094421
6 · The paper itself

Abstract

Genome-wide association studies (GWAS) of schizophrenia have yielded more than 100 common susceptibility variants, and strongly support a substantial polygenic contribution of a large number of small allelic effects. It has been hypothesized that familial schizophrenia is largely a consequence of inherited rather than environmental factors. We investigated the extent to which familiality of schizophrenia is associated with enrichment for common risk variants detectable in a large GWAS. We analyzed single nucleotide polymorphism (SNP) data for cases reporting a family history of psychotic illness (N = 978), cases reporting no such family history (N = 4,503), and unscreened controls (N = 8,285) from the Psychiatric Genomics Consortium (PGC1) study of schizophrenia. We used a multinomial logistic regression approach with model-fitting to detect allelic effects specific to either family history subgroup. We also considered a polygenic model, in which we tested whether family history positive subjects carried more schizophrenia risk alleles than family history negative subjects, on average. Several individual SNPs attained suggestive but not genome-wide significant association with either family history subgroup. Comparison of genome-wide polygenic risk scores based on GWAS summary statistics indicated a significant enrichment for SNP effects among family history positive compared to family history negative cases (Nagelkerke's R(2 ) = 0.0021; P = 0.00331; P-value threshold <0.4). Estimates of variability in disease liability attributable to the aggregate effect of genome-wide SNPs were significantly greater for family history positive compared to family history negative cases (0.32 and 0.22, respectively; P = 0.031). We found suggestive evidence of allelic effects detectable in large GWAS of schizophrenia that might be specific to particular family history subgroups. However, consideration of a polygenic risk score indicated a significant enrichment among family history positive cases for common allelic effects. Familial illness might, therefore, represent a more heritable form of schizophrenia, as suggested by previous epidemiological studies.

Indexed as

Genetic Predisposition to DiseaseGenome-Wide Association StudyBipolar DisorderCase-Control StudiesFamilyHumansInheritance PatternsMajor Depressive DisorderModels, GeneticMultifactorial InheritancePolymorphism, Single NucleotideSchizophreniafamily historyGWASpolygenicschizophrenia

Identifiers

PMID26663532
PMCPMC5816590

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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.