Post-traumatic stress disorder (PTSD) is a mental health condition caused by the dysregulation or overgeneralization of memories related to traumatic events. Investigating the interplay between explicit narrative and implicit emotional memory contributes to a better understanding of the mechanisms underlying PTSD.

This case–control study focused on two groups: unmedicated patients with PTSD and a trauma-exposed control (TEC) group who did not develop PTSD. Experiments included real-time measurements of blood oxygenation changes using functional near-infrared spectroscopy during trauma narration and processing of emotional and linguistic data through natural language processing (NLP).

Real-time fNIRS monitoring showed that PTSD patients (mean [SD] Oxy-Hb activation, 0.153 [0.084], 95% CI 0.124 to 0.182) had significantly higher brain activity in the left anterior medial prefrontal cortex (L-amPFC) within 10 s after expressing negative emotional words compared with the control group (0.047 [0.026], 95% CI 0.038 to 0.056; p < 0.001). In the control group, there was a significant time-series correlation between the use of negative emotional memory words and activation of the L-amPFC (latency 3.82 s, slope = 0.0067, peak value = 0.184, difference = 0.273; Spearman’s r = 0.727, p < 0.001). In contrast, the left anterior cingulate prefrontal cortex of PTSD patients remained in a state of high activation (peak value = 0.153, difference = 0.084) with no apparent latency period.

PTSD patients display overactivity in pathways associated with rapid emotional responses and diminished regulation in cognitive processing areas. Interventions targeting these pathways may alleviate symptoms of PTSD.

The association between executive dysfunction, brain dysconnectivity, and inflammation is a prominent feature across major psychiatric disorders (MPDs), schizophrenia, bipolar disorder, and major depressive disorder. A dimensional approach is warranted to delineate their mechanistic interplay across MPDs.

This single site study included a total of 1543 participants (1058 patients and 485 controls). In total, 1169 participants underwent diffusion tensor and resting-state functional magnetic resonance imaging (745 patients and 379 controls completed the Wisconsin Card Sorting Test). Fractional anisotropy (FA) and regional homogeneity (ReHo) assessed structural and functional connectivity, respectively. Pro-inflammatory cytokine levels [interleukin (IL)-1β, IL-6, and tumor necrosis factor-α] were obtained in 325 participants using blood samples collected with 24 h of scanning. Group differences were determined for main measures, and correlation and mediation analyses and machine learning prediction modeling were performed.

Executive deficits were associated with decreased FA, increased ReHo, and elevated IL-1β and IL-6 levels across MPDs, compared to controls. FA and ReHo alterations in fronto-limbic-striatal regions contributed to executive deficits. IL-1β mediated the association between FA and cognition, and IL-6 mediated the relationship between ReHo and cognition. Executive cognition was better predicted by both brain connectivity and cytokine measures than either one alone for FA-IL-1β and ReHo-IL-6.

Transdiagnostic associations among brain connectivity, inflammation, and executive cognition exist across MPDs, implicating common neurobiological substrates and mechanisms for executive deficits in MPDs. Further, inflammation-related brain dysconnectivity within fronto-limbic-striatal regions may represent a transdiagnostic dimension underlying executive dysfunction that could be leveraged to advance treatment.

Schizophrenia is considered a polygenic disorder. People with schizophrenia and those with genetic high risk of schizophrenia (GHR) have presented with similar neurodevelopmental deficits in hemispheric asymmetry. The potential associations between neurodevelopmental abnormalities and schizophrenia-related risk genes in both schizophrenia and those with GHR remains unclear.

To investigate the shared and specific alternations to the structural network in people with schizophrenia and those with GHR. And to identify an association between vulnerable structural network alternation and schizophrenia-related risk genes.

A total of 97 participants with schizophrenia, 79 participants with GHR and 192 healthy controls, underwent diffusion tensor imaging (DTI) scans at a single site. We used graph theory to characterise hemispheric and whole-brain structural network topological metrics. For 26 people in the schizophrenia group and 48 in the GHR group with DTI scans we also calculated their schizophrenia-related polygenic risk scores (SZ-PRSs). The correlations between alterations to the structural network and SZ-PRSs were calculated. Based on the identified genetic–neural association, bioinformatics enrichment was explored.

There were significant hemispheric asymmetric deficits of nodal efficiency, global and local efficiency in the schizophrenia and GHR groups. Hemispheric asymmetric deficit of local efficiency was significantly positively correlated with SZ-PRSs in the schizophrenia and GHR groups. Bioinformatics enrichment analysis showed that these risk genes may be linked to signal transduction, neural development and neuron structure. The schizophrenia group showed a significant decrease in the whole-brain structural network.

The shared asymmetric deficits in people with schizophrenia and those with GHR, and the association between anomalous asymmetry and SZ-PRSs suggested a vulnerability imaging marker regulated by schizophrenia-related risk genes. Our findings provide new insights into asymmetry regulated by risk genes and provides a better understanding of the genetic–neural pathological underpinnings of schizophrenia.