Evidence map›Paper›PMID 28944401›Full record

ReviewCurrent psychiatry reports2017

Molecular and Cellular Effects of Traumatic Stress: Implications for PTSD.

Matthew J Girgenti, Brendan D Hare, Sriparna Ghosal, Ronald S Duman

Abstract readReview
In one paragraph

Review in Current psychiatry reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
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

26 citing papers in PubMed.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Microglia-mediated neuroimmune suppression in PTSD is associated with anhedonia.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
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

4 authors.

Matthew J GirgentiDepartment of Psychiatry, Laboratory of Molecular Psychiatry, Center for Genes and Behavior, Yale University School of Medicine, New Haven, CT, 06508, USA.
Brendan D HareDepartment of Psychiatry, Laboratory of Molecular Psychiatry, Center for Genes and Behavior, Yale University School of Medicine, New Haven, CT, 06508, USA.
Sriparna GhosalDepartment of Psychiatry, Laboratory of Molecular Psychiatry, Center for Genes and Behavior, Yale University School of Medicine, New Haven, CT, 06508, USA.
Ronald S DumanDepartment of Psychiatry, Laboratory of Molecular Psychiatry, Center for Genes and Behavior, Yale University School of Medicine, New Haven, CT, 06508, USA. Ronald.duman@yale.edu.

Funding

Role of mTOR and Synaptogenesis in the Actions of Rapid-Acting AntidepressantsR01MH093897 · NIMH · YALE UNIVERSITY · PI DILEONE, RALPH J · 2011 to 2021
$5.0M
NIMH NIH HHS R01 MH093897
6 · The paper itself

Abstract

purpose of reviewPosttraumatic stress disorder (PTSD) is characterized by hyperarousal and recurrent stressful memories after an emotionally traumatic event. Extensive research has been conducted to identify the neurobiological determinants that underlie the pathophysiology of PTSD. In this review, we examine evidence regarding the molecular and cellular pathophysiology of PTSD focusing on two primary brain regions: the vmPFC and the amygdala. RECENT

findingsThis discussion includes a review of the molecular alterations related to PTSD, focusing mainly on changes to glucocorticoid receptor signaling. We also examine postmortem gene expression studies that have been conducted to date and the molecular changes that have been observed in peripheral blood studies of PTSD patients. Causal, mechanistic evidence is difficult to obtain in human studies, so we also review preclinical models of PTSD. Integration of peripheral blood and postmortem studies with preclinical models of PTSD has begun to reveal the molecular changes occurring in patients with PTSD. These findings indicate that the pathophysiology of PTSD includes disruption of glucocorticoid signaling and inflammatory systems and occurs at the level of altered gene expression. We will assess the impact of these findings on the future of PTSD molecular research.

Indexed as

AnimalsBrainGenomicsGlucocorticoidsHumansInflammationRatsSignal TransductionStress Disorders, Post-TraumaticGlucocorticoidsAnimal models of PTSDGenomicsGlucocorticoid signalingPrefrontal cortexPTSDTranscriptomics

Identifiers

PMID28944401
PMCPMC5907804

What OpenQuestion holds

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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.