Evidence map›Paper›PMID 24687905›Full record

ArticleAmerican journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics2014

Testing the role of circadian genes in conferring risk for psychiatric disorders.

Enda M Byrne, Andrew C Heath, Pamela A F Madden, Michele L Pergadia, Ian B Hickie, Grant W Montgomery, Nicholas G Martin, Naomi R Wray

Open access · greenAbstract 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, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 2 pooled it
3.0field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 43 citations in OpenAlex.

  1. Pooled it
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  4. Analysis of the underlying mechanism ofPharmaceutical science advances · 2024
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  16. A PERIOD3 variant causes a circadian phenotype and is associated with a seasonal mood trait.Proceedings of the National Academy of Sciences of the United States of America · 2016
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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

8 authors at 4 institutions in 2 countries.

Enda M ByrneThe University of Queensland, Queensland Brain Institute, Queensland, Australia.
Andrew C Heath
Pamela A F Madden
Michele L Pergadia
Ian B Hickie
Grant W Montgomery
Nicholas G Martin
Naomi R Wray
Washington University in St. Louis · USQIMR Berghofer Medical Research Institute · AUUniversity of Queensland · AUUniversity of Sydney · AU

Funding

Resource CoreP60AA011998 · NIAAA · WASHINGTON UNIVERSITY · PI NELSON, ELLIOT C · 2009 to 2013
$8.8M
Refining Phenotypic Measures of Nicotine WithdrawalK08DA019951 · NIDA · WASHINGTON UNIVERSITY · PI PERGADIA, MICHELE L · 2005 to 2009
$659k
1/5-The Psychiatric GWAS Consortium: Integrated & Coordinated GWAS Meta-AnalysesU01MH085520 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SULLIVAN, PATRICK F · 2008 to 2008
$642k
Medical Research Council 613608NIAAA NIH HHS P60 AA011998NIDA NIH HHS DA019951NIDA NIH HHS K08 DA019951NIMH NIH HHS U01 MH085520
6 · The paper itself

Abstract

Disturbed sleep and disrupted circadian rhythms are a common feature of psychiatric disorders, and many groups have postulated an association between genetic variants in circadian clock genes and psychiatric disorders. Using summary data from the association analyses of the Psychiatric Genomics Consortia (PGC) for schizophrenia, bipolar disorder and major depressive disorder, we evaluated the evidence that common SNPs in genes encoding components of the molecular clock influence risk to psychiatric disorders. Initially, gene-based and SNP P-values were analyzed for 21 core circadian genes. Subsequently, an expanded list of genes linked to control of circadian rhythms was analyzed. After correcting for multiple comparisons, none of the circadian genes were significantly associated with any of the three disorders. Several genes previously implicated in the etiology of psychiatric disorders harbored no SNPs significant at the nominal level of P < 0.05, and none of the the variants identified in candidate studies of clock genes that were included in the PGC datasets were significant after correction for multiple testing. There was no evidence of an enrichment of associations in genes linked to control of circadian rhythms in human cells. Our results suggest that genes encoding components of the molecular clock are not good candidates for harboring common variants that increase risk to bipolar disorder, schizophrenia, or major depressive disorder.

Indexed as

Genetic Predisposition to DiseaseBipolar DisorderCircadian ClocksCLOCK ProteinsHumansMajor Depressive DisorderPolymorphism, Single NucleotideSchizophreniaCLOCK Proteinscircadianclockmood

Identifiers

PMID24687905
PMCPMC4397914
OpenAlexW2170705015

What OpenQuestion holds

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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.