Blood-based gene-expression biomarkers of post-traumatic stress disorder among deployed marines: A pilot study
Open accessAbstract
The etiology of post-traumatic stress disorder (PTSD) likely involves the interaction of numerous genes and environmental factors. Similarly, gene-expression levels in peripheral blood are influenced by both genes and environment, and expression levels of many genes show good correspondence between peripheral blood and brain tissues. In that context, this pilot study sought to test the following hypotheses: (1) post-trauma expression levels of a gene subset in peripheral blood would differ between Marines with and without PTSD; (2) a diagnostic biomarker panel of PTSD among high-risk individuals could be developed based on gene-expression in readily assessable peripheral blood cells; and (3) a diagnostic panel based on expression of individual exons would surpass the accuracy of a model based on expression of full-length gene transcripts. Gene-expression levels in peripheral blood samples from 50 U.S. Marines (25 PTSD cases and 25 non-PTSD comparison subjects) were determined by microarray following their return from deployment to war-zones in Iraq or Afghanistan. The original sample was carved into training and test subsets for construction of support vector machine classifiers. The panel of peripheral blood biomarkers achieved 80% prediction accuracy in the test subset based on the expression of just two full-length transcripts (GSTM1 and GSTM2). A biomarker panel based on 20 exons attained an improved 90% accuracy in the test subset. Though further refinement and replication of these biomarker profiles are required, these preliminary results provide proof-of-principle for the diagnostic utility of blood-based mRNA-expression in PTSD among trauma-exposed individuals.
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Several recent human gene expression studies show accumulating evidence for innate immune dysregulation after trauma and a particular and specific (i.e., comorbidity-independent) role of cytokines.
“Respectively, several recent human gene expression studies show accumulating evidence for innate immune dysregulation after trauma and a particular and specific (i.e., comorbidity-independent) role of cytokines (211–215).”
From Developmental Trajectories of Early Life Stress and Trauma: A Narrative Review on Neurobiological Aspects Beyond Stress System Dysregulation (2019) · cites this paper as [214]
The Discussion (page not provided) reports that combining gene-expression results across studies yielded enrichment of cytokine-signaling and other immune-cell terms, supporting an immune-dysregulation link in PTSD. It does not establish a specific role for cytokines independent of comorbid conditions; the Discussion also says the individual studies showed no common enriched terms. (LLM, conf=0.86)
Experimental — accuracy not yet measuredTranscripts of genes encoding enzymes involved in metabolism of reactive oxygen species such as GSTM1 and GSTM2 are altered in chronic PTSD and have been associated with risk for PTSD development in a prospective manner.
“In addition, transcripts of genes encoding enzymes involved in metabolism of reactive oxygen species (ROS) such as GSTM1 and GSTM2 (glutathione S-transferase mu 1 and 2) are altered in chronic PTSD (Neylan et al, 2011) and have been associated with risk for PTSD development in a prospective manner (Glatt et al, 2013;Tylee et al, 2015).”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Tylee et al, 2015
The Discussion reports that pre-deployment GSTM1 expression was associated with subsequent PTSD diagnosis, supporting a prospective association for GSTM1. It identifies GSTM1 and GSTM2 together as predictors of current PTSD, but does not report a prospective association for GSTM2. (LLM, conf=0.87)
Experimental — accuracy not yet measured
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- Authors
- Tylee, D. S., Chandler, S. D., Nievergelt, C. M., Liu, X., Pazol, J., Woelk, C. H., Lohr, J. B., Kremen, W. S., Baker, D. G., Glatt, S. J., & Tsuang, M. T.
- Affiliations
- SUNY Upstate Medical University (US)
- University of California San Diego (US)
- Shanghai Jiao Tong University (CN)
- Harvard University (US)
- Corresponding author
- Glatt, Stephen J.
- ORCID
- Venue
- Psychoneuroendocrinology
- Publisher
- Elsevier BV
- Published
- 2015-01
- Volume
- 51
- Pages
- 472-494
- ISSN
- 0306-4530 (ISSN-L)
- PMC
- PMC4199086
- OpenAlex
- W2155023794
- Cited by
- 65
- References
- 42
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 5 · 2023: 6 · 2022: 10 · 2021: 7 · 2020: 8 · 2019: 6 · 2018: 4 · 2017: 8 · 2016: 4 · 2015: 2
- FWCI
- 5.51
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Psychoneuroendocrinology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- ePrints Soton (University of Southampton) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institute of Mental Health (R21MH085240, R01MH093500)
- Topics
- Social Sciences › Psychology › Clinical Psychology › Posttraumatic Stress Disorder Research
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Keywords
- post-traumatic stress disorder, blood-based biomarkers, gene expression, Marines, GSTM1, GSTM2, exon expression, diagnostic biomarker panel, support vector machine classification, trauma exposure, gene-environment interaction
- MeSH terms
- Adolescent, Adult, Combat Disorders, Humans, Life Change Events, Male, Military Personnel, Pilot Projects, Stress Disorders, Post-Traumatic, Biomarkers, Gene Expression, Iraq War, 2003-2011, Young Adult, Afghan Campaign 2001-
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