Evidence map›Paper›PMID 37967663›Full record

ArticleBrain, behavior, and immunity2024

Longitudinal study of traumatic-stress related cellular and cognitive aging.

Erika J Wolf, Mark W Miller, Sage E Hawn, Xiang Zhao, Sara E Wallander, Beth McCormick, Christine Govan, Ann Rasmusson, Annjanette Stone, Steven A Schichman and 1 more

Abstract read
In one paragraph

Article in Brain, behavior, and immunity, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
–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

18 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
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  4. Review
  5. A longitudinal study of CLDN5 DNA methylation and PTSD.Journal of behavioral medicine · 2026
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  9. Trauma Exposure, PTSD, and Methylation of the Blood Brain Barrier Claudin-5 Gene.medRxiv : the preprint server for health sciences · 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

11 authors.

Erika J WolfNational Center for PTSD at VA Boston Healthcare System, Boston, MA, USA; Boston University Chobanian & Avedisian School of Medicine, Department of Psychiatry, Boston, MA, USA. Electronic address: Erika.Wolf@va.gov.
Mark W MillerNational Center for PTSD at VA Boston Healthcare System, Boston, MA, USA; Boston University Chobanian & Avedisian School of Medicine, Department of Psychiatry, Boston, MA, USA.
Sage E HawnNational Center for PTSD at VA Boston Healthcare System, Boston, MA, USA; Old Dominion University, Department of Psychology, Norfolk, VA, USA.
Xiang ZhaoNational Center for PTSD at VA Boston Healthcare System, Boston, MA, USA; Boston University School of Public Health, Department of Biostatistics, Boston, MA, USA.
Sara E WallanderNational Center for PTSD at VA Boston Healthcare System, Boston, MA, USA; Boston University Chobanian & Avedisian School of Medicine, Department of Psychiatry, Boston, MA, USA.
Beth McCormickNational Center for PTSD at VA Boston Healthcare System, Boston, MA, USA; Boston University Chobanian & Avedisian School of Medicine, Department of Psychiatry, Boston, MA, USA.
Christine GovanMAVERIC Central Biorepository, VA Boston Healthcare System, Boston, MA, USA.
Ann RasmussonNational Center for PTSD at VA Boston Healthcare System, Boston, MA, USA; Boston University Chobanian & Avedisian School of Medicine, Department of Psychiatry, Boston, MA, USA.
Annjanette StonePharmacogenomics Analysis Laboratory, Research Service, Central Arkansas Veterans Healthcare System, Little Rock, AR, USA.
Steven A SchichmanPathology and Laboratory Medicine Service, Central Arkansas Veterans Healthcare System, USA; Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
Mark W LogueNational Center for PTSD at VA Boston Healthcare System, Boston, MA, USA; Boston University Chobanian & Avedisian School of Medicine, Department of Psychiatry, Boston, MA, USA; Boston University School of Public Health, Department of Biostatistics, Boston, MA, USA; Boston University School of Medicine, Department of Medicine, Biomedical Genetics, Boston, MA, USA.

Funding

Postdoctoral Training Program in Stress and TraumaT32MH019836 · NIMH · TUFTS UNIVERSITY BOSTON · PI DENISE M. SLOAN · 1996 to 2026
$4.7M
Longitudinal Neurometabolic Outcomes of Traumatic Stress-Related Accelerated Cellular AgingRF1AG068121 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WOLF, ERIKA J · 2020 to 2020
$1.7M
PTSD-Related Accelerated Aging in DNA Methylation and Risk for Metabolic SyndromeI01CX001276 · VA · VA BOSTON HEALTH CARE SYSTEM · PI WOLF, ERIKA J · 2016 to 2021
–
CSRD VA I01 CX001276NIA NIH HHS RF1 AG068121NIMH NIH HHS T32 MH019836
6 · The paper itself

Abstract

Traumatic stress is associated with both accelerated epigenetic age and increased risk for dementia. Accelerated epigenetic age might link symptoms of traumatic stress to dementia-associated biomarkers, such as amyloid-beta (Aβ) proteins, neurofilament light (NFL), and inflammatory molecules. We tested this hypothesis using longitudinal data obtained from 214 trauma-exposed military veterans (85 % male, mean age at baseline: 53 years, 75 % White) who were assessed twice over the course of an average of 5.6 years. Cross-lagged panel mediation models evaluated measures of lifetime posttraumatic stress disorder and internalizing and externalizing comorbidity (assessed at Time 1; T1) in association with T1 epigenetic age (per the GrimAge algorithm) and T1 plasma markers of neuropathology along with bidirectional temporal paths between T1 and T2 epigenetic age and the plasma markers. Results revealed that a measure of externalizing comorbidity was associated with accelerated epigenetic age (β = 0.30, p <.01), which in turn, was associated with subsequent increases in Aβ-40 (β = 0.20, p <.001), Aβ-42 (β = 0.18, p <.001), and interleukin-6 (β = 0.18, p <.01). T1 advanced epigenetic age and the T1 neuropathology biomarkers NFL and glial fibrillary acidic protein predicted worse performance on T2 neurocognitive tasks assessing working memory, executive/attentional control, and/or verbal memory (ps = 0.03 to 0.009). Results suggest that advanced GrimAge is predictive of subsequent increases in neuropathology and inflammatory biomarkers as well as worse cognitive function, highlighting the clinical significance of this biomarker with respect to cognitive aging and brain health over time. The finding that advanced GrimAge mediated the association between psychiatric comorbidity and future neuropathology is important for understanding potential pathways to neurodegeneration and early identification of those at greatest risk.

Indexed as

Cognitive AgingCognitive DysfunctionDementiaAgingAmyloid beta-PeptidesBiomarkersFemaleHumansLongitudinal StudiesMaleMiddle AgedAmyloid beta-PeptidesBiomarkersAccelerated agingAmyloid-betaGrimAgeInflammationNeurocognitionPTSDSimoa

Identifiers

PMID37967663
PMCPMC10843744

What OpenQuestion holds

Textmetadata
LicenceTDM
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.