Evidence map›Paper›PMID 22761806›Full record

ArticlePloS one2012

A gene co-expression network in whole blood of schizophrenia patients is independent of antipsychotic-use and enriched for brain-expressed genes.

Simone de Jong, Marco P M Boks, Tova F Fuller, Eric Strengman, Esther Janson, Carolien G F de Kovel, Anil P S Ori, Nancy Vi, Flip Mulder, Jan Dirk Blom and 6 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 4 pooled it
8.7field-weighted citation impact, top 2% 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

88 citing papers in PubMed, 4 syntheses or guidelines pooled it, 153 citations in OpenAlex.

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  17. Altered estradiol-dependent cellular CaMolecular psychiatry · 2021
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28 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

16 authors at 4 institutions in 3 countries.

Simone de JongDepartment of Medical Genetics, University Medical Center Utrecht, Utrecht, The Netherlands.
Marco P M Boks
Tova F Fuller
Eric Strengman
Esther Janson
Carolien G F de Kovel
Anil P S Ori
Nancy Vi
Flip Mulder
Jan Dirk Blom
Birte Glenthøj
Chris D Schubart
Wiepke Cahn
René S Kahn
Steve Horvath
Roel A Ophoff
University Medical Center Utrecht · NLUniversity of California, Los Angeles · USGlostrup Hospital · DKParnassia Groep · NL

Funding

Training Grant in Genomic Analysis and InterpretationT32HG002536 · NHGRI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Valerie A Arboleda, Harold Pimentel · 2002 to 2026
$8.6M
High-density Genome-wide Association Study SchizophreniaR01MH078075 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI OPHOFF, ROEL A · 2006 to 2009
$3.7M
Genetics of Gene Expression and Gene Mapping for Amytrophic Lateral SclerosisR01NS058980 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI OPHOFF, ROEL A · 2008 to 2012
$1.6M
NHGRI NIH HHS T32 HG002536NIMH NIH HHS MH078075NIMH NIH HHS R01 MH078075NINDS NIH HHS NS058980NINDS NIH HHS R01 NS058980
6 · The paper itself

Abstract

Despite large-scale genome-wide association studies (GWAS), the underlying genes for schizophrenia are largely unknown. Additional approaches are therefore required to identify the genetic background of this disorder. Here we report findings from a large gene expression study in peripheral blood of schizophrenia patients and controls. We applied a systems biology approach to genome-wide expression data from whole blood of 92 medicated and 29 antipsychotic-free schizophrenia patients and 118 healthy controls. We show that gene expression profiling in whole blood can identify twelve large gene co-expression modules associated with schizophrenia. Several of these disease related modules are likely to reflect expression changes due to antipsychotic medication. However, two of the disease modules could be replicated in an independent second data set involving antipsychotic-free patients and controls. One of these robustly defined disease modules is significantly enriched with brain-expressed genes and with genetic variants that were implicated in a GWAS study, which could imply a causal role in schizophrenia etiology. The most highly connected intramodular hub gene in this module (ABCF1), is located in, and regulated by the major histocompatibility (MHC) complex, which is intriguing in light of the fact that common allelic variants from the MHC region have been implicated in schizophrenia. This suggests that the MHC increases schizophrenia susceptibility via altered gene expression of regulatory genes in this network.

Indexed as

Gene Expression ProfilingAdultAllelesAntipsychotic AgentsATP-Binding Cassette TransportersBrainFemaleGene ExpressionGenetic Predisposition to DiseaseGenetic VariationGenotypeHumansMaleMiddle AgedSchizophreniaABCF1 protein, humanAntipsychotic AgentsATP-Binding Cassette Transporters

Identifiers

PMID22761806
PMCPMC3384650
OpenAlexW2166722062

What OpenQuestion holds

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Registered trials

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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.