ArticleDepression and anxiety2022
Methylation of the AIM2 gene: An epigenetic mediator of PTSD-related inflammation and neuropathology plasma biomarkers.
Article in Depression and anxiety, 2022. 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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Who cites it
8 citing papers in PubMed, 24 citations in OpenAlex.
- Immune signaling as a determinant of cellular identity and tissue function.Frontiers in immunology · 2026Review
- Acute Stress and Autoimmune Markers: Evaluating the Psychoneuroimmunology Axis in Firefighter Recruits.International journal of molecular sciences · 2025Article
- Therapeutic potentials of natural products for post-traumatic stress disorder: A focus on epigenetics.Chinese herbal medicines · 2025Review
- Heparin as a Potential Therapeutic Substance for Post-Traumatic Stress Disorder.Bulletin of experimental biology and medicine · 2024Article
- Psychological and biological mechanisms linking trauma with cardiovascular disease risk.Translational psychiatry · 2023Review
- AIM2 and Psoriasis.Frontiers in immunology · 2023Review
- Advances in the molecular neurobiology of posttraumatic stress disorder from global contexts: A systematic review of longitudinal studies.Global mental health (Cambridge, England) · 2023Review
- Epigenetic Alterations in Post-Traumatic Stress Disorder: Comprehensive Review of Molecular Markers.Complex psychiatryReview
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundPosttraumatic stress disorder (PTSD) is associated with inflammation and various forms of chronic disease. The Absent in Melanoma 2 (AIM2) gene has been implicated in mechanisms of inflammation and anxiety, and methylation at a particular locus in this gene (cg10636246) has previously been shown to influence the association between PTSD and elevated C-reactive protein levels in blood.
methodWe tested if this association might extend to other indicators of inflammation and to plasma-based measures of neuropathology in a cohort of post-9/11 US military veterans. Using a Bayesian approach, mediation models were tested cross-sectionally (n = 478) and longitudinally (n = 298). Peripheral markers of inflammation and neuropathology were measured with ultra-sensitive Single Molecule Array (Simoa®) technology.
resultsAnalyses revealed indirect effects of PTSD symptom severity on peripheral indices of both inflammation (interleukin [IL]6, IL-10, tumor necrosis factor-α; indirect standardized [std.] ß range = 0.018-0.023, all p-values adjusted for multiple testing [p
conclusionsGiven that AIM2 methylation mediated the association between PTSD symptoms and multiple inflammatory and neuropathology markers, our results suggest that AIM2 methylation may offer clinical utility for indexing risk for adverse health outcomes associated with these peripheral indices of inflammation and neuropathology. Results also suggest a possible shared etiology underlying the frequent co-occurrence of inflammation and neuropathology.
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