Evidence map›Paper›PMID 19358880›Full record

ReviewNeuroscience2009

The genetics of bipolar disorder.

J H Barnett, J W Smoller

Registry-linked trialAbstract readReview
In one paragraph

Review in Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04797351 (Acceptability and Feasibility of a DBT Skills Group Intervention for Bipolar Disorder - a Randomized Pilot Trial), which is not on this map. Cited by 142 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed, 5 pooled it
12.7field-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.

NCT04797351 nacompletednot on this mapstarted 2020, after this paper: background citation

Acceptability and Feasibility of a DBT Skills Group Intervention for Bipolar Disorder - a Randomized Pilot Trial

TypeinterventionalSponsorJulieta AzevedoRan2020 to 2022Enrolled109ConditionsBipolar DisorderArmsDialectical Behavior Therapy - Skills
3 · Its place in the literature

Who cites it

142 citing papers in PubMed, 5 syntheses or guidelines pooled it, 397 citations in OpenAlex.

  1. Pooled it
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  20. Association of Human Endogenous Retrovirus HERV-K18 Variant with Bipolar Disorder Type I.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2025
    Article

82 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

2 authors at 1 institution in 2 countries.

J H BarnettCenter for Human Genetic Research, Department of Psychiatry, Massachusetts General Hospital, Boston, MA 02114, USA.
J W Smoller
Massachusetts General Hospital · US

Funding

Using Genetics to Dissect Schizhoprenia, Bipolar Disorder, and DepressionR01MH079799 · NIMH · MASSACHUSETTS GENERAL HOSPITAL · PI SMOLLER, JORDAN W · 2007 to 2011
$2.9M
NIMH NIH HHS R01 MH079799
6 · The paper itself

Abstract

Bipolar disorder is a mood disorder characterized by impairing episodes of mania and depression. Twin studies have established that bipolar disorder is among the most heritable of medical disorders and efforts to identify specific susceptibility genes have intensified over the past two decades. The search for genes influencing bipolar disorder has been complicated by a paucity of animal models, limited understanding of pathogenesis, and the genetic and phenotypic complexity of the syndrome. Linkage studies have implicated several chromosomal regions as harboring relevant genes, but results have been inconsistent. It is now widely accepted that the genetic liability to bipolar disorder reflects the action of many genes of individually small effect, a scenario for which linkage studies are poorly suited. Thus, association studies, which are more powerful for the detection of modest effect loci, have become the focus of gene-finding research. A large number of candidate genes, including biological candidates derived from hypotheses about the pathogenesis of the disorder and positional candidates derived from linkage and cytogenetic studies, have been evaluated. Several of these genes have been associated with the disorder in independent studies (including BDNF, DAOA, DISC1, GRIK4, SLC6A4, and TPH2), but none has been established. The clinical heterogeneity of bipolar disorder and its phenotypic and genetic overlap with other disorders (especially schizophrenia, schizoaffective disorder, and major depressive disorder) have raised questions about the optimal phenotype definition for genetic studies. Nevertheless, genomewide association analysis, which has successfully identified susceptibility genes for a variety of complex disorders, has begun to implicate specific genes for bipolar disorder (DGKH, CACNA1C, ANK3). The polygenicity of the disorder means that very large samples will be needed to detect the modest effect loci that likely contribute to bipolar disorder. Detailed genetic dissection of the disorder may provide novel targets (both pharmacologic and psychosocial) for intervention.

Indexed as

AnimalsBipolar DisorderGenetic Predisposition to DiseaseHumans

Identifiers

PMID19358880
PMCPMC3637882
OpenAlexW2008741245

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.