Evidence map›Paper›PMID 29594645›Full record

ReviewJournal of inherited metabolic disease2018

The role of suboptimal mitochondrial function in vulnerability to post-traumatic stress disorder.

Graeme Preston, Faisal Kirdar, Tamas Kozicz

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of inherited metabolic disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
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

17 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. The Emerging Role of Brain Mitochondria in Fear and Anxiety.Current topics in behavioral neurosciences · 2025
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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

3 authors at 2 institutions in 2 countries.

Graeme PrestonHayward Genetics Center, Tulane University School of Medicine, 1430 Tulane Ave, New Orleans, LA, 70112, USA. gpreston@tulane.edu.
Faisal KirdarHayward Genetics Center, Tulane University School of Medicine, 1430 Tulane Ave, New Orleans, LA, 70112, USA.
Tamas KoziczHayward Genetics Center, Tulane University School of Medicine, 1430 Tulane Ave, New Orleans, LA, 70112, USA.
Tulane University · USRadboud University Nijmegen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Post-traumatic stress disorder remains the most significant psychiatric condition associated with exposure to a traumatic event, though rates of traumatic event exposure far outstrip incidence of PTSD. Mitochondrial dysfunction and suboptimal mitochondrial function have been increasingly implicated in several psychopathologies, and recent genetic studies have similarly suggested a pathogenic role of mitochondria in PTSD. Mitochondria play a central role in several physiologic processes underlying PTSD symptomatology, including abnormal fear learning, brain network activation, synaptic plasticity, steroidogenesis, and inflammation. Here we outline several potential mechanisms by which inherited (genetic) or acquired (environmental) mitochondrial dysfunction or suboptimal mitochondrial function, may contribute to PTSD symptomatology and increase susceptibility to PTSD. The proposed pathogenic role of mitochondria in the pathophysiology of PTSD has important implications for prevention and therapy, as antidepressants commonly prescribed for patients with PTSD have been shown to inhibit mitochondrial function, while alternative therapies shown to improve mitochondrial function may prove more efficacious.

Indexed as

AllostasisFearGene-Environment InteractionGenetic Predisposition to DiseaseHumansHydrocortisoneInflammationLife Change EventsMitochondriaNeuronal PlasticityStress Disorders, Post-TraumaticHydrocortisone

Identifiers

PMID29594645
OpenAlexW2794982034

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.