Cited by 187Tryptophan and brain disordersTreatment of Major DepressionGenetic Associations and Epidemiology

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

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Mostafavi, S, Battle, A, Zhu, X, Potash, J B, Weissman, M M, Shi, J, Beckman, K, Haudenschild, C +15 more·2014·Molecular Psychiatry

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.

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  • Peripheral blood gene expression profiles consistent with a pro-inflammatory M1 macrophage phenotype and an over-representation of IL-6, IL-8 and type I IFN-induced signalling pathways have been described in depression.

    “Peripheral blood gene expression profiles consistent with a pro-inflammatory ‘M1’ macrophage phenotype and an over-representation of IL-6, IL-8 and type I IFN-induced signalling pathways have also been described18–20.”

    From The role of inflammation in depression: from evolutionary imperative to modern treatment target (2016) · cites this paper as [20]

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  1. [6]A mega-analysis of genome-wide association studies for major depressive disorder Molecular psychiatry 2012 Epub 2012/04/05 PMC3837431 22472876

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Authors
Mostafavi, S., Battle, A., Zhu, X., Potash, J. B., Weissman, M. M., Shi, J., Beckman, K., Haudenschild, C., McCormick, C., Mei, R., Gameroff, M. J., Gindes, H., Adams, P., Goes, F. S., Mondimore, F. M., MacKinnon, D. F., Notes, L., Schweizer, B., Furman, D., Montgomery, S. B., Urban, A. E., Koller, D., & Levinson, D. F.
Affiliations
  • Stanford University (US)
  • Stanford Medicine (US)
  • University of Iowa (US)
  • New York State Psychiatric Institute (US)
  • National Cancer Institute (US)
  • University of Minnesota (US)
  • Personalis (United States) (US)
  • Illumina (United States) (US)
  • Johns Hopkins University (US)
  • American University (US)
Corresponding author
Levinson, D F
Venue
Molecular Psychiatry
Published
2013-12-03
Volume
19
Issue
12
Pages
1267-1274
ISSN
  • 1359-4184 (ISSN-L)
  • 1476-5578
OpenAlex
W1969198439
Cited by
187
References
55
Citations by year
2026: 11 · 2025: 18 · 2024: 12 · 2023: 13 · 2022: 13 · 2021: 21 · 2020: 11 · 2019: 17 · 2018: 22 · 2017: 14 · 2016: 23 · 2015: 11 · 2014: 1
FWCI
3.61
Type
journal article
Language
en
Open access
Locations
  • Molecular Psychiatry (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
  • Columbia Academic Commons (Columbia University)
Funders
  • National Institutes of Health
  • National Institute of Mental Health (RC2MH089916, R01MH090941)
Topics
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
Keywords
major depressive disorder, recurrent depression, type I interferon signaling, gene expression, immune signaling, depression pathogenesis, single nucleotide polymorphisms
MeSH terms
Adult, Major Depressive Disorder, Female, Humans, Interferon Type I, Interviews as Topic, Male, Middle Aged, Recurrence, Signal Transduction, Gene Expression, Sequence Analysis, RNA, Polymorphism, Single Nucleotide, White People, Genome-Wide Association Study, Young Adult, Self Report

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