Evidence map›Paper›PMID 19078961›Full record

ArticleMolecular psychiatry2010

Strong genetic evidence for a selective influence of GABAA receptors on a component of the bipolar disorder phenotype.

N Craddock, L Jones, I R Jones, G Kirov, E K Green, D Grozeva, V Moskvina, I Nikolov, M L Hamshere, D Vukcevic and 17 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Molecular psychiatry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 65 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 3 pooled it
9.2field-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

65 citing papers in PubMed, 3 syntheses or guidelines pooled it, 134 citations in OpenAlex.

  1. Use of Drugs Affecting GABAMolecular neurobiology · 2025
    Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. The Regulatory Potential of Long Non-Coding RNAs in Bipolar Disorder.International journal of molecular sciences · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. GABAIUPHAR/BPS guide to pharmacology CITE · 2021
    Article
  10. GABAJournal, genetic engineering & biotechnology · 2021
    Review
  11. Article
  12. Article
  13. Structural basis of GABARAP-mediated GABANature communications · 2021
    Article
  14. Article
  15. Article
  16. Epidemiology and risk factors for bipolar disorder.Therapeutic advances in psychopharmacology · 2018
    Review
  17. Article
  18. Cortical Alpha Activity in Schizoaffective Patients.Iranian journal of psychiatry · 2017
    Article
  19. Article
  20. Innovative approaches to bipolar disorder and its treatment.Annals of the New York Academy of Sciences · 2016
    Review

5 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

27 authors at 7 institutions in 2 countries.

N CraddockDepartment of Psychological Medicine, School of Medicine, Cardiff University, Cardiff, UK. craddockn@cardiff.ac.uk
L Jones
I R Jones
G Kirov
E K Green
D Grozeva
V Moskvina
I Nikolov
M L Hamshere
D Vukcevic
S Caesar
K Gordon-Smith
C Fraser
E Russell
N Norton
G Breen
D St Clair
D A Collier
A H Young
I N Ferrier
A Farmer
P McGuffin
P A Holmans
Wellcome Trust Case Control Consortium (WTCCC)
P Donnelly
M J Owen
M C O'Donovan
Cardiff University · GBKing's College London · GBUniversity of Birmingham · GBRoyal Victoria Infirmary · GBUniversity of Aberdeen · GBStatistical Service · CYUniversity of Oxford · GB

Funding

Medical Research Council G0000934Medical Research Council G0801418Wellcome Trust 079643
6 · The paper itself

Abstract

Despite compelling evidence for a major genetic contribution to risk of bipolar mood disorder, conclusive evidence implicating specific genes or pathophysiological systems has proved elusive. In part this is likely to be related to the unknown validity of current phenotype definitions and consequent aetiological heterogeneity of samples. In the recent Wellcome Trust Case Control Consortium genome-wide association analysis of bipolar disorder (1868 cases, 2938 controls) one of the most strongly associated polymorphisms lay within the gene encoding the GABA(A) receptor beta1 subunit, GABRB1. Aiming to increase biological homogeneity, we sought the diagnostic subset that showed the strongest signal at this polymorphism and used this to test for independent evidence of association with other members of the GABA(A) receptor gene family. The index signal was significantly enriched in the 279 cases meeting Research Diagnostic Criteria for schizoaffective disorder, bipolar type (P=3.8 x 10(-6)). Independently, these cases showed strong evidence that variation in GABA(A) receptor genes influences risk for this phenotype (independent system-wide P=6.6 x 10(-5)) with association signals also at GABRA4, GABRB3, GABRA5 and GABRR3. [corrected] Our findings have the potential to inform understanding of presentation, pathogenesis and nosology of bipolar disorders. Our method of phenotype refinement may be useful in studies of other complex psychiatric and non-psychiatric disorders.

Indexed as

Genetic Predisposition to DiseasePhenotypeAdolescentAdultAgedBipolar DisorderChromosomes, Human, Pair 4FemaleGene FrequencyGenome-Wide Association StudyHumansMaleMiddle AgedPolymorphism, Single NucleotideReceptors, GABA-AStatistics as TopicReceptors, GABA-A

Identifiers

PMID19078961
PMCPMC3967096
OpenAlexW2075492585

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.