ArticleCurrent neuropharmacology2024
Inflammation in Posttraumatic Stress Disorder: Dysregulation or Recalibration?
Article in Current neuropharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Dynamic immune and metabolic dysregulation in women with post-traumatic stress disorder: Longitudinal transcriptomic insights following sexual assault.Molecular psychiatry · 2026Article
- Neuroimmune mechanisms in PTSD: inflammatory heterogeneity, circuit dysfunction, and biomarker-based subtypes.Molecular biology reports · 2026Review
- The gut microbiota-immune-brain axis in post-traumatic stress disorder: mechanistic integration and translational prospects.Frontiers in immunology · 2026Review
- Neuroimmune Interactions in Stress and Depression: Exploring the Molecular and Cellular Mechanisms within the Neuroinflammation-depression Nexus.Current medicinal chemistry · 2026Review
- Neurobiology of Chronic Pain, Posttraumatic Stress Disorder, and Mild Traumatic Brain Injury.Biology · 2025Review
- Effects of social dominance and acute social stress on morphology of microglia and structural integrity of the medial prefrontal cortex.Brain, behavior, and immunity · 2024Article
- Microglia-mediated neuroimmune suppression in PTSD is associated with anhedonia.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Thematic Selection: Stress and Stress-related Disorders Posttraumatic Stress Disorder (Part 2).Current neuropharmacology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite ample experimental data indicating a role of inflammatory mediators in the behavioral and neurobiological manifestations elicited by exposure to physical and psychologic stressors, causative associations between systemic low-grade inflammation and central nervous system inflammatory processes in posttraumatic stress disorder (PTSD) patients remain largely conceptual. As in other stress-related disorders, pro-inflammatory activity may play an equivocal role in PTSD pathophysiology, one that renders indiscriminate employment of anti-inflammatory agents of questionable relevance. In fact, as several pieces of preclinical and clinical research convergingly suggest, timely and targeted potentiation rather than inhibition of inflammatory responses may actually be beneficial in patients who are characterized by suppressed microglia function in the face of systemic low-grade inflammation. The deleterious impact of chronic stress-associated inflammation on the systemic level may, thus, need to be held in context with the - often not readily apparent - adaptive payoffs of low-grade inflammation at the tissue level.
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Registered trials
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.