Evidence map›Paper›PMID 26211730›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2016

An Integrative Genomic Study Implicates the Postsynaptic Density in the Pathogenesis of Bipolar Disorder.

Nirmala Akula, Jens R Wendland, Kwang H Choi, Francis J McMahon

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
2.1field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Independent replications and integrative analyses confirm TRANK1 as a susceptibility gene for bipolar disorder.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Pooled it
  3. Genome-wide methylation biomarkers and biological aging in patients with bipolar disorder characterized for lithium response.European psychiatry : the journal of the Association of European Psychiatrists · 2025
    Article
  4. Article
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  6. Review
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  9. De novo variation in bipolar disorder.Molecular psychiatry · 2021
    Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. The genetics of bipolar disorder.Molecular psychiatry · 2020
    Review
  17. Article
  18. 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

4 authors at 2 institutions in 1 country.

Nirmala AkulaHuman Genetics Branch, National Institute of Mental Health Intramural Research Program (NIMH-IRP), National Institutes of Health, US Department of Health and Human Services, Bethesda, MD, USA.
Jens R WendlandHuman Genetics Branch, National Institute of Mental Health Intramural Research Program (NIMH-IRP), National Institutes of Health, US Department of Health and Human Services, Bethesda, MD, USA.
Kwang H ChoiDepartment of Psychiatry, Uniformed Services University of the Health Sciences, Bethesda, MD, USA.
Francis J McMahonHuman Genetics Branch, National Institute of Mental Health Intramural Research Program (NIMH-IRP), National Institutes of Health, US Department of Health and Human Services, Bethesda, MD, USA.
Uniformed Services University of the Health Sciences · USUnited States Department of Health and Human Services · US

Funding

Mapping genes that contribute to bipolar disorderZIAMH002810 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI MCMAHON, FRANCIS J · 2009 to 2025
$31.2M
Intramural NIH HHS ZIA MH002810PHS HHS ZIAMH002810
6 · The paper itself

Abstract

Genome-wide association studies (GWAS) have identified several common variants associated with bipolar disorder (BD), but the biological meaning of these findings remains unclear. Integrative genomics-the integration of GWAS signals with gene expression data-may illuminate genes and gene networks that have key roles in the pathogenesis of BD. We applied weighted gene co-expression network analysis (WGCNA), which exploits patterns of co-expression among genes, to brain transcriptome data obtained by sequencing of poly-A RNA derived from postmortem dorsolateral prefrontal cortex from people with BD, along with age- and sex-matched controls. WGCNA identified 33 gene modules. Many of the modules corresponded closely to those previously reported in human cortex. Three modules were associated with BD, enriched for genes differentially expressed in BD, and also enriched for signals in prior GWAS of BD. Functional analysis of genes within these modules revealed significant enrichment of several functionally related sets of genes, especially those involved in the postsynaptic density (PSD). These results provide convergent support for the hypothesis that dysregulation of genes involved in the PSD is a key factor in the pathogenesis of BD. If replicated in larger samples, these findings could point toward new therapeutic targets for BD.

Indexed as

TranscriptomeBipolar DisorderGene Expression ProfilingGenome-Wide Association StudyHumansMicroarray AnalysisPost-Synaptic DensityPrefrontal Cortex

Identifiers

PMID26211730
PMCPMC4707835
OpenAlexW1042281424

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.