Evidence map›Paper›PMID 22404658›Full record

ArticleThe world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry2014

Molecular genetic overlap in bipolar disorder, schizophrenia, and major depressive disorder.

Thomas G Schulze, Nirmala Akula, René Breuer, Jo Steele, Michael A Nalls, Andrew B Singleton, Franziska A Degenhardt, Markus M Nöthen, Sven Cichon, Marcella Rietschel and 2 more

Abstract read
In one paragraph

Article in The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 5 pooled it
–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

63 citing papers in PubMed, 5 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Trial
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Genetic Factors and Long-term Treatment-Related Neurocognitive Deficits, Anxiety, and Depression in Childhood Leukemia Survivors: An Exome-Wide Association Study.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2024
    Article
  15. Review
  16. The future of diagnosis in clinical neurosciences: Comparing multiple sclerosis and schizophrenia.European psychiatry : the journal of the Association of European Psychiatrists · 2023
    Review
  17. Article
  18. Article
  19. Article
  20. Article

3 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

12 authors.

Thomas G SchulzeDepartment of Psychiatry and Psychotherapy, University of Göttingen , Göttingen , Germany.
Nirmala Akula
René Breuer
Jo Steele
Michael A Nalls
Andrew B Singleton
Franziska A Degenhardt
Markus M Nöthen
Sven Cichon
Marcella Rietschel
Bipolar Genome Study
Francis J McMahon

Funding

Mapping genes that contribute to bipolar disorderZIAMH002810 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI MCMAHON, FRANCIS J · 2009 to 2025
$31.2M
Identification of Genes Involved in Major Mood DisordersZIAMH002843 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI MCMAHON, FRANCIS J · 2009 to 2025
$24.5M
Characterization of Normal Genomic VariabilityZ01AG000932 · NIA · NATIONAL INSTITUTE ON AGING · PI SINGLETON, ANDREW · 2008 to 2008
$658k
REDUCING SERVICE USE IN OLDER PRIMARY CARE PATIENTSK23AG000932 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI KLAPOW, JOSHUA C · 1999 to 2003
$493k
Intramural NIH HHS Z01 AG000932Intramural NIH HHS Z99 MH999999NIA NIH HHS K23 AG000932NIA NIH HHS Z01 AG000932 - 02Wellcome Trust
6 · The paper itself

Abstract

objectivesGenome-wide association studies (GWAS) in complex phenotypes, including psychiatric disorders, have yielded many replicated findings, yet individual markers account for only a small fraction of the inherited differences in risk. We tested the performance of polygenic models in discriminating between cases and healthy controls and among cases with distinct psychiatric diagnoses.

methodsGWAS results in bipolar disorder (BD), major depressive disorder (MDD), schizophrenia (SZ), and Parkinson's disease (PD) were used to assign weights to individual alleles, based on odds ratios. These weights were used to calculate allele scores for individual cases and controls in independent samples, summing across many single nucleotide polymorphisms (SNPs). How well allele scores discriminated between cases and controls and between cases with different disorders was tested by logistic regression.

resultsLarge sets of SNPs were needed to achieve even modest discrimination between cases and controls. The most informative SNPs were overlapping in BD, SZ, and MDD, with correlated effect sizes. Little or no overlap was seen between allele scores for psychiatric disorders and those for PD.

conclusionsBD, SZ, and MDD all share a similar polygenic component, but the polygenic models tested lack discriminative accuracy and are unlikely to be useful for clinical diagnosis.

Indexed as

Bipolar DisorderCase-Control StudiesFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansLogistic ModelsMajor Depressive DisorderMaleModels, GeneticMultifactorial InheritanceOdds RatioParkinson DiseasePolymorphism, Single NucleotideSchizophrenia

Identifiers

PMID22404658
PMCPMC3406228

What OpenQuestion holds

Textmetadata
LicenceTDM
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.