Gene Expression Patterns Associated with Posttraumatic Stress Disorder Following Exposure to the World Trade Center Attacks
Open accessAbstract
Background Although genetic risk factors for posttraumatic stress disorder (PTSD) in similarly traumatized cohorts can be confounded with risk for type of exposure, the primary risk for exposure to the 9/11 attack on New York City was proximity, allowing study of PTSD risk in a sample that is not confounded by exposure-related risk.Methods Thirty-five Caucasians (15 with PTSD, stratified for exposure, age, and gender) were selected from a population-representative sample of persons exposed to the attack from which longitudinal data had been collected in four previous waves. Whole blood gene expression and cortisol levels were obtained.Results Seventeen probe sets were differentially expressed in PTSD. Identified genes were generally involved in hypothalamic-pituitary-adrenal (HPA) axis, signal transduction, or brain and immune cell function. FKBP5, a modulator of glucocorticoid receptor (GR) sensitivity, showed reduced expression in PTSD, consistent with enhanced GR responsiveness. FKBP5 expression was predicted by cortisol when entered with PTSD severity in regression analysis. Quantitative polymerase chain reaction confirmed significant reductions in FKBP5. Also less expressed in PTSD were STAT5B, a direct inhibitor of GR, and major histocompatibility complex (MHC) Class II.Conclusions Consistent with observations of HPA axis dysfunction in PTSD, several genes involved in glucocorticoid signaling are differentially expressed among those with current PTSD.
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Reduced expression of FKBP5, a regulator of glucocorticoid signaling, has also been reported following prenatal psychological stress.
“Reduced expression of FKBP5, a regulator of glucocorticoid signaling, has also been reported following prenatal psychological stress (38).”
From Epigenetic changes associated with multi-generational trauma: characterization, mechanisms, and therapeutics (2026) · cites this paper as [38]
The Results and Discussion report significantly reduced FKBP5 expression in people with PTSD after exposure to the World Trade Center attacks, and the Discussion identifies FKBP5 as an inhibitor of glucocorticoid receptor activity. The paper does not report reduced FKBP5 expression following prenatal psychological stress; that condition is not the one studied. (LLM, conf=0.88)
Experimental — accuracy not yet measuredFKBP5 methylation differences have been reported across multiple trauma contexts in both survivors and offspring, raising the possibility that stress-response regulatory genes may help distinguish individuals more likely to benefit from specific interventions.
“FKBP5 methylation differences have been reported across multiple trauma contexts in both survivors and offspring, raising the possibility that stress-response regulatory genes may help distinguish individuals more likely to benefit from specific interventions (38, 66, 83, 84, 136).”
From Epigenetic changes associated with multi-generational trauma: characterization, mechanisms, and therapeutics (2026) · cites this paper as [38]
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Experimental — accuracy not yet measuredAlterations in the transcriptional patterns of expression for genes involved in inflammatory pathways have been associated with PTSD.
“Alterations in the transcriptional patterns of expression for genes involved in inflammatory pathways have also been associated with PTSD (Segman et al, 2005;Yehuda et al, 2009;Zieker et al, 2007).”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Yehuda et al, 2009
The Results report genes differentially expressed between participants with and without PTSD, and the Discussion identifies immune-cell function and reduced MHC Class II expression among the findings (page not available). The paper does not characterize these changes as involving inflammatory pathways, so that specific part of the claim is not established by our copy. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThe reciprocal association between decreased levels of FKBP5-mRNA and enhanced GR sensitivity is characteristic of PTSD in trauma survivors.
“The reciprocal association between decreased levels of FKBP5-mRNA and enhanced GR sensitivity is characteristic of PTSD in trauma survivors (Yehuda et al, 2009).”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Yehuda et al, 2009
The Abstract and Results report reduced FKBP5 expression in participants with PTSD after exposure to the World Trade Center attacks, and describe it as consistent with enhanced GR responsiveness. The Discussion says the association *suggests* a possible link; it does not establish enhanced GR sensitivity directly or show that this pattern is characteristic of trauma survivors generally. (LLM, conf=0.85)
Experimental — accuracy not yet measuredHuman sample sizes are frequently modest, with many studies enrolling fewer than 100 participants.
“Human sample sizes are frequently modest, with many studies enrolling fewer than 100 participants (38, 81, 114).”
From Epigenetic changes associated with multi-generational trauma: characterization, mechanisms, and therapeutics (2026) · cites this paper as [38]
FKBP5 gene expression has been shown to be altered in PTSD and major depression.
“FKBP5 gene expression has been shown to be altered in PTSD and major depression (32)(33)(34)(35).”
From Holocaust Exposure Induced Intergenerational Effects on FKBP5 Methylation (2016) · cites this paper as [35]
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References 18 · Cited by 294
Research works printed but not linked: 1
- [3]3. Yehuda R (in press): Status of glucocorticoid alterations in posttrau- matic stress disorder. Ann N Y Acad Sci .
- Authors
- Yehuda, R., Cai, G., Golier, J. A., Sarapas, C., Galea, S., Ising, M., Rein, T., Schmeidler, J., Müller-Myhsok, B., Holsboer, F., & Buxbaum, J. D.
- Affiliations
- James J. Peters VA Medical Center (US)
- Icahn School of Medicine at Mount Sinai (US)
- University of Michigan (US)
- Max Planck Society (DE)
- Corresponding author
- Yehuda, Rachel
- ORCID
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2009-10
- Volume
- 66
- Issue
- 7
- Pages
- 708-711
- ISSN
- 0006-3223 (ISSN-L)
- OpenAlex
- W2088677979
- Cited by
- 294
- References
- 18
- Citations by year
- 2026: 3 · 2025: 9 · 2024: 12 · 2023: 7 · 2022: 13 · 2021: 11 · 2020: 25 · 2019: 17 · 2018: 16 · 2017: 20 · 2016: 25 · 2015: 23 · 2014: 15 · 2013: 27 · 2012: 26
- FWCI
- 25.07
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Deep Blue (University of Michigan) (submittedVersion)
- Max Planck Institute for Plasma Physics (submittedVersion)
- Funders
- National Institute of Mental Health (R56MH077321)
- National Center for Research Resources (5MO1 RR00071, M01RR000071)
- Topics
- Social Sciences › Psychology › Clinical Psychology › Posttraumatic Stress Disorder Research
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Social Sciences › Psychology › Clinical Psychology › Child Abuse and Trauma
- Keywords
- post-traumatic stress disorder, September 11 attacks, gene expression, FKBP5, glucocorticoid receptor, HPA axis dysregulation, cortisol, STAT5B, MHC class II, whole blood, genetic risk factors, trauma exposure
- MeSH terms
- Tacrolimus Binding Protein 5, Adult, Aged, Analysis of Variance, Histocompatibility Antigens Class II, Female, Gene Expression Regulation, Humans, Male, Middle Aged, Receptors, Glucocorticoid, Stress Disorders, Post-Traumatic, Tacrolimus Binding Proteins, September 11 Terrorist Attacks, STAT5 Transcription Factor
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