ArticleMolecular psychiatry2026
Multimodal associations between posterior hippocampus glutamate metabolism, visual cortex connectivity, and intrusive trauma reexperiencing symptoms.
Article in Molecular psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Hippocampal dysfunction is implicated in posttraumatic stress disorder (PTSD), particularly intrusive reexperiencing symptoms, and may be mediated by glutamatergic excitotoxicity. Markers of glutamate dysfunction (higher glutamate to N-acetyl aspartate levels; Glu/NAA) in the hippocampus (HPC) have been linked to reexperiencing symptoms. However, the HPC demonstrates heterogeneity along its anterior-posterior axis, with different functional connectivity patterns and PTSD symptom associations, motivating investigations into glutamate metabolism in anterior and posterior HPC subregions (a/pHPC). To this end, 121 symptomatic trauma-exposed adults with current trauma reexperiencing symptoms completed magnetic resonance spectroscopy and resting-state functional magnetic resonance imaging to examine the regional specificity of HPC Glu/NAA associations with reexperiencing symptoms and the link to a/pHPC functional connectivity. PTSD symptoms were assessed with the Clinician-Administered PTSD Scale for DSM-5. Reexperiencing symptom severity was associated with greater Glu/NAA in the pHPC, but not aHPC. pHPC Glu/NAA was further linked to stronger functional connectivity between the pHPC and visual cortex (VC), which in turn correlated with more severe reexperiencing symptoms. This strengthened pHPC-VC connectivity explained the shared variance between pHPC Glu/NAA and reexperiencing severity, suggesting dysregulated glutamate metabolism in the pHPC may contribute to reexperiencing symptoms through functional connectivity with the VC. These findings replicate prior work linking HPC Glu/NAA to trauma reexperiencing symptoms and provide novel evidence of this association in the pHPC, but not aHPC, which is mediated by its functional connectivity with the VC. This multimodal investigation supports translational models of glutamatergic dysfunction in trauma-related disorders and highlights new targets for pharmacological and neuromodulatory interventions.
Identifiers
42919836What OpenQuestion holds
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.