Cited by 105Posttraumatic Stress Disorder ResearchStress Responses and CortisolChild Abuse and Trauma

New translational perspectives for blood-based biomarkers of PTSD: From glucocorticoid to immune mediators of stress susceptibility

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Daskalakis, Nikolaos P., Cohen, Hagit, Nievergelt, Caroline M., Baker, Dewleen G., Buxbaum, Joseph D., Russo, Scott J., Yehuda, Rachel·2016·Experimental Neurology

Abstract

Although biological systems have evolved to promote stress-resilience, there is variation in stress-responses. Understanding the biological basis of such individual differences has implications for understanding Posttraumatic Stress Disorder (PTSD) etiology, which is a maladaptive response to trauma occurring only in a subset of vulnerable individuals. PTSD involves failure to reinstate physiological homeostasis after traumatic events and is due to either intrinsic or trauma-related alterations in physiological systems across the body. Master homeostatic regulators that circulate and operate throughout the organism, such as stress hormones (e.g., glucocorticoids) and immune mediators (e.g., cytokines), are at the crossroads of peripheral and central susceptibility pathways and represent promising functional biomarkers of stress-response and target for novel therapeutics.

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Crossref · 10.1016/j.expneurol.2016.07.024

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  • HPA axis dysregulation in ELS/CT affects GR-mediated transcriptional and post-transcriptional responses of immune-related genes with lower recovery ability.

    “On the other hand, HPA axis dysregulation in ELS/CT affects GR-mediated transcriptional and post-transcriptional responses of immune-related genes with lower recovery ability (89, 207).”

    From Developmental Trajectories of Early Life Stress and Trauma: A Narrative Review on Neurobiological Aspects Beyond Stress System Dysregulation (2019) · cites this paper as [207]

    In “Glucocorticoids (GCs) and peripheral inflammation in PTSD” (page unavailable), the paper says low glucocorticoid tone in PTSD compromises GR-mediated transcriptional responses of stress-sensitive genes, resulting in a lack of recovery from stress-induced alterations. It also links early trauma to possible HPA-axis vulnerability, but does not establish the claimed post-transcriptional effects or specifically show this recovery mechanism in people with early-life stress or childhood trauma. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • HPA axis dysfunction is strongly implicated in the etiopathology of affective disorders.

    “HPA axis dysfunction is strongly implicated in the etiopathology of affective disorders (93–95)”

    From Higher Circulating Cortisol in the Follicular vs. Luteal Phase of the Menstrual Cycle: A Meta-Analysis (2020) · cites this paper as [93]

    The “Glucocorticoids (GCs) and peripheral inflammation in PTSD” section says converging data make HPA-axis functioning relevant to the pathophysiology of stress-related psychiatric disorders, and describes HPA-axis changes in PTSD. It does not establish the broader claim about affective disorders as a group or state that HPA-axis dysfunction is strongly implicated in their etiopathology. No page number is available in our copy. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

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References 95 · Cited by 105

Authors
Daskalakis, N. P., Cohen, H., Nievergelt, C. M., Baker, D. G., Buxbaum, J. D., Russo, S. J., & Yehuda, R.
Affiliations
  • James J. Peters VA Medical Center (US)
  • Ben-Gurion University of the Negev (IL)
  • University of California San Diego (US)
  • Icahn School of Medicine at Mount Sinai (US)
Corresponding author
Daskalakis, Nikolaos P.
Venue
Experimental Neurology
Publisher
Elsevier BV
Published
2016-10
Volume
284
Issue
Pt B
Pages
133-140
ISSN
0014-4886 (ISSN-L)
OpenAlex
W2493197369
Cited by
105
References
95
Citations by year
2026: 6 · 2025: 4 · 2024: 11 · 2023: 11 · 2022: 14 · 2021: 10 · 2020: 9 · 2019: 10 · 2018: 19 · 2017: 11
FWCI
1.94
Type
journal article
Language
en
Open access
Locations
  • Experimental Neurology (acceptedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • eScholarship (California Digital Library) (submittedVersion)
Funders
  • U.S. Army Medical Research and Materiel Command (W81XWH-08-2-0021, W81XWH-13-1-0071)
  • Brain & Behavior Research Foundation (NARSAD 23670)
  • US National Institute of Mental Health (RO1 MH090264, RO1 MH104559)
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, blood-based biomarkers, glucocorticoids, stress hormones, immune mediators, cytokines, stress resilience, individual differences in stress response, trauma vulnerability, translational research
MeSH terms
Disease Susceptibility, Glucocorticoids, Humans, Stress Disorders, Post-Traumatic, Biomarkers, Cytokines

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