Evidence map›Paper›PMID 24296977›Full record

ArticleMolecular psychiatry2014

Type I interferon signaling genes in recurrent major depression: increased expression detected by whole-blood RNA sequencing.

S Mostafavi, A Battle, X Zhu, J B Potash, M M Weissman, J Shi, K Beckman, C Haudenschild, C McCormick, R Mei and 13 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed, 4 pooled it
3.1field-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

112 citing papers in PubMed, 4 syntheses or guidelines pooled it, 188 citations in OpenAlex.

  1. Pooled it
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  4. Genetic Contributions of Inflammation to Depression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017
    Pooled it
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52 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

23 authors at 11 institutions in 1 country.

S MostafaviDepartment of Computer Science, Stanford University, Stanford, CA, USA.
A BattleDepartment of Computer Science, Stanford University, Stanford, CA, USA.
X ZhuDepartment of Psychiatry and Behavioral Science, Stanford University School of Medicine, Stanford, CA, USA.
J B PotashDepartment of Psychiatry, University of Iowa Hospitals & Clinics, Iowa City, IA, USA.
M M WeissmanDepartment of Psychiatry, Columbia University and New York State Psychiatric Institute, New York, NY, USA.
J ShiDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA.
K BeckmanBiomedical Genomics Center, University of Minnesota, Minneapolis, MN, USA.
C HaudenschildPersonalis, Inc., Menlo Park, CA, USA.
C McCormickIllumina, Inc., La Jolla, CA, USA.
R MeiCentrillion Biosciences, Inc., Palo Alto, CA, USA.
M J GameroffDepartment of Psychiatry, Columbia University and New York State Psychiatric Institute, New York, NY, USA.
H GindesDepartment of Psychiatry, University of Iowa Hospitals & Clinics, Iowa City, IA, USA.
P AdamsDepartment of Psychiatry, Columbia University and New York State Psychiatric Institute, New York, NY, USA.
F S GoesDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University, Baltimore, MD, USA.
F M MondimoreDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University, Baltimore, MD, USA.
D F MacKinnonDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University, Baltimore, MD, USA.
L NotesDepatment of Clinical Psychology, American University, Washington DC, DC, USA.
B SchweizerDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University, Baltimore, MD, USA.
D FurmanDepartment of Microbiology & Immunology, School of Medicine, Stanford University, Stanford, CA, USA.
S B Montgomery1] Department of Genetics, Stanford University, Stanford, CA, USA [2] Department of Pathology, Stanford University, Stanford, CA, USA.
A E UrbanDepartment of Psychiatry and Behavioral Science, Stanford University School of Medicine, Stanford, CA, USA.
D KollerDepartment of Computer Science, Stanford University, Stanford, CA, USA.
D F LevinsonDepartment of Psychiatry and Behavioral Science, Stanford University School of Medicine, Stanford, CA, USA.
Stanford University · USJohns Hopkins University · USColumbia University · USUniversity of Iowa Hospitals and Clinics · USAmerican University · USDivision of Cancer Epidemiology and GeneticsFluxion Biosciences (United States) · USIllumina (United States) · USNew York Psychoanalytic Society and Institute · USPersonalis (United States) · USUniversity of Minnesota · US

Funding

Depression susceptibility genes and networks: expression, eQTL and GWAS analysisRC2MH089916 · NIMH · STANFORD UNIVERSITY · PI LEVINSON, DOUGLAS FREDERICK · 2009 to 2010
$3.4M
Methods for high-resolution analysis of genetic effects on gene expressionR01MH090941 · NIMH · UNIVERSITY OF GENEVA · PI DERMITZAKIS, EMMANOUIL, GUIGO, RODERIC · 2010 to 2012
$863k
NIMH NIH HHS 3R01MH090941NIMH NIH HHS 5RC2MH089916NIMH NIH HHS R01 MH090941NIMH NIH HHS RC2 MH089916
6 · The paper itself

Abstract

A study of genome-wide gene expression in major depressive disorder (MDD) was undertaken in a large population-based sample to determine whether altered expression levels of genes and pathways could provide insights into biological mechanisms that are relevant to this disorder. Gene expression studies have the potential to detect changes that may be because of differences in common or rare genomic sequence variation, environmental factors or their interaction. We recruited a European ancestry sample of 463 individuals with recurrent MDD and 459 controls, obtained self-report and semi-structured interview data about psychiatric and medical history and other environmental variables, sequenced RNA from whole blood and genotyped a genome-wide panel of common single-nucleotide polymorphisms. We used analytical methods to identify MDD-related genes and pathways using all of these sources of information. In analyses of association between MDD and expression levels of 13 857 single autosomal genes, accounting for multiple technical, physiological and environmental covariates, a significant excess of low P-values was observed, but there was no significant single-gene association after genome-wide correction. Pathway-based analyses of expression data detected significant association of MDD with increased expression of genes in the interferon α/β signaling pathway. This finding could not be explained by potentially confounding diseases and medications (including antidepressants) or by computationally estimated proportions of white blood cell types. Although cause-effect relationships cannot be determined from these data, the results support the hypothesis that altered immune signaling has a role in the pathogenesis, manifestation, and/or the persistence and progression of MDD.

Indexed as

AdultFemaleGene ExpressionGenome-Wide Association StudyHumansInterferon Type IInterviews as TopicMajor Depressive DisorderMaleMiddle AgedPolymorphism, Single NucleotideRecurrenceSelf ReportSequence Analysis, RNASignal TransductionWhite PeopleInterferon Type I

Identifiers

PMID24296977
PMCPMC5404932
OpenAlexW1969198439

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.