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 emotion regulation network (ERN) in the brain provides a framework for understanding the neuropathology of affective disorders. Although previous neuroimaging studies have investigated the neurobiological correlates of the ERN in major depressive disorder (MDD), whether patients with MDD exhibit abnormal functional connectivity (FC) patterns in the ERN and whether the abnormal FC in the ERN can serve as a therapeutic response signature remain unclear.

A large functional magnetic resonance imaging dataset comprising 709 patients with MDD and 725 healthy controls (HCs) recruited across five sites was analyzed. Using a seed-based FC approach, we first investigated the group differences in whole-brain resting-state FC of the 14 ERN seeds between participants with and without MDD. Furthermore, an independent sample (45 MDD patients) was used to evaluate the relationship between the aforementioned abnormal FC in the ERN and symptom improvement after 8 weeks of antidepressant monotherapy.

Compared to the HCs, patients with MDD exhibited aberrant FC between 7 ERN seeds and several cortical and subcortical areas, including the bilateral middle temporal gyrus, bilateral occipital gyrus, right thalamus, calcarine cortex, middle frontal gyrus, and the bilateral superior temporal gyrus. In an independent sample, these aberrant FCs in the ERN were negatively correlated with the reduction rate of the HAMD17 score among MDD patients.

These results might extend our understanding of the neurobiological underpinnings underlying unadaptable or inflexible emotional processing in MDD patients and help to elucidate the mechanisms of therapeutic response.

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are widely used due to their profound efficacy in glycemic control and weight management. Real-world observations have revealed potential neuropsychiatric adverse events (AEs) associated with GLP-1RAs. This study aimed to comprehensively investigate and characterize these neuropsychiatric AEs with GLP-1RAs.

We analyzed GLP-1RA adverse reaction reports using the FDA Adverse Event Reporting System database. Disproportionality analysis using reporting odds ratio (ROR) identified eight categories of neuropsychiatric AEs associated with GLP-1RAs. We conducted descriptive and time-to-onset (TTO) analyses and explored neuropsychiatric AE signals among individual GLP-1RAs for weight loss and diabetes mellitus (DM) indications.

We identified 25,110 cases of GLP-1RA-related neuropsychiatric AEs. GLP-1RAs showed an association with headache (ROR 1.74, 95% confidence interval [CI] 1.65–1.84), migraine (ROR 1.28, 95%CI 1.06–1.55), and olfactory and sensory nerve abnormalities (ROR 2.44, 95%CI 1.83–3.25; ROR 1.69, 95%CI 1.54–1.85). Semaglutide showed a moderate suicide-related AEs signal in the weight loss population (ROR 2.55, 95%CI 1.97–3.31). The median TTO was 16 days (interquartile range: 3–66 days).

In this study, we identified eight potential neuropsychiatric adverse events (AEs) associated with GLP-1RAs and, for the first time, detected positive signals for migraine, olfactory abnormalities, and sensory abnormalities. We also observed positive suicide-related signals of semaglutide, in weight loss population. This study provides a reliable basis for further investigation of GLP-1RA-related neuropsychiatric AEs. However, as an exploratory study, our findings require confirmation through large-scale prospective studies.

Mild cognitive deficits (MCD) emerge before the first episode of psychosis (FEP) and persist in the clinical high-risk (CHR) stage. This study aims to refine risk prediction by developing MCD models optimized for specific early psychosis stages and target populations.

A comprehensive neuropsychological battery assessed 1059 individuals with FEP, 794 CHR, and 774 matched healthy controls (HCs). CHR subjects, followed up for 2 years, were categorized into converters (CHR-C) and non-converters (CHR-NC). The MATRICS Consensus Cognitive Battery standardized neurocognitive tests were employed.

Both the CHR and FEP groups exhibited significantly poorer performance compared to the HC group across all neurocognitive tests (all p < 0.001). The CHR-C group demonstrated poorer performance compared to the CHR-NC group on three sub-tests: visuospatial memory (p < 0.001), mazes (p = 0.005), and symbol coding (p = 0.023) tests. Upon adjusting for sex and age, the performance of the MCD model was excellent in differentiating FEP from HC, as evidenced by an Area Under the Receiver Operating Characteristic Curve (AUC) of 0.895 (p < 0.001). However, when applied in the CHR group for predicting CHR-C (AUC = 0.581, p = 0.008), the performance was not satisfactory. To optimize the efficiency of psychotic risk assessment, three distinct MCD models were developed to distinguish FEP from HC, predict CHR-C from CHR-NC, and identify CHR from HC, achieving accuracies of 89.3%, 65.6%, and 80.2%, respectively.

The MCD exhibits variations in domains, patterns, and weights across different stages of early psychosis and diverse target populations. Emphasizing precise risk assessment, our findings highlight the importance of tailored MCD models for different stages and risk levels.

Inflammation might play a role in bipolar disorder (BD), but it remains unclear the relationship between inflammation and brain structural and functional abnormalities in patients with BD. In this study, we focused on the alterations of functional connectivity (FC), peripheral pro-inflammatory cytokines and their correlations to investigate the role of inflammation in FC in BD depression.

In this study, 42 unmedicated patients with BD II depression and 62 healthy controls (HCs) were enrolled. Resting-state-functional magnetic resonance imaging was performed in all participants and independent component analysis was used. Serum levels of Interleukin-6 (IL-6) and Interleukin-8 (IL-8) were measured in all participants. Correlation between FC values and IL-6 and IL-8 levels in BD was calculated.

Compared with the HCs, BD II patients showed decreased FC in the left orbitofrontal cortex (OFC) implicating the limbic network and the right precentral gyrus implicating the somatomotor network. BD II showed increased IL-6 (p = 0.039), IL-8 (p = 0.002) levels. Moreover, abnormal FC in the right precentral gyrus were inversely correlated with the IL-8 (r = −0.458, p = 0.004) levels in BD II. No significant correlation was found between FC in the left OFC and cytokines levels.

Our findings that serum IL-8 levels are associated with impaired FC in the right precentral gyrus in BD II patients suggest that inflammation might play a crucial role in brain functional abnormalities in BD.

To evaluate the effects of dietary Ca intake and Ca supplementation during pregnancy on low birth weight (LBW) and small for gestational age (SGA) infants.

A birth cohort study was conducted in 2010–2012 at the Gansu Provincial Maternity and Child Care Hospital in Lanzhou, China.

A birth cohort study.

Totally, 9595 pregnant women who came to the hospital for delivery at 20 weeks of gestation or more, and who were 18 years of age or older.

Compared with non-users, Ca supplement users had a reduced risk of LBW infants (OR = 0·77, 95 % CI: 0·63, 0·95) and a reduced risk of nulliparous women giving birth to LBW infants (OR = 0·75, 95 % CI: 0·58, 0·98) (P < 0·05). More specifically, both the use of Ca supplement before conception and during pregnancy (OR = 0·44, 95 % CI: 0·19, 0·99) and during pregnancy only (OR = 0·80, 95 % CI: 0·65, 0·99) had the main effect of reducing risk of nulliparous women giving birth to LBW infants (P < 0·05). There was no association between Ca supplementation and SGA (OR = 0·87, 95 % CI: 0·75, 1·01) (P > 0·05). However, higher dietary Ca intake during pregnancy decreases the risk of both LBW (quartile 2: OR = 0·72, 95 % CI: 0·55, 0·94; quartile 3: OR = 0·68, 95 % CI: 0·50, 0·62) and SGA infants (quartile 2: OR = 0·77, 95 % CI: 0·63, 0·95; quartile 3: OR = 0·71, 95 % CI: 0·57, 0·88, quartile 4: OR = 0·71, 95 % CI: 0·57, 0·88) (P < 0·05).

Ca supplementation and adequate dietary intake of Ca during pregnancy are associated with a decreased risk of LBW infants born to nulliparous women.

Understanding the patterns of treatment response is critical for the treatment of patients with schizophrenia; one way to achieve this is through using a longitudinal dynamic process study design.

This study aims to explore the response trajectory of antipsychotics and compare the treatment responses of seven different antipsychotics over 6 weeks in patients with schizoprenia (trial registration: Chinese Clinical Trials Registry Identifier: ChiCTR-TRC-10000934).

Data were collected from a multicentre, randomised open-label clinical trial. Patients were evaluated with the Positive and Negative Syndrome Scale (PANSS) at baseline and follow-up at weeks 2, 4 and 6. Trajectory groups were classified by the method of k-means cluster modelling for longitudinal data. Trajectory analyses were also employed for the seven antipsychotic groups.

The early treatment response trajectories were classified into a high-trajectory group of better responders and a low-trajectory group of worse responders. The results of trajectory analysis showed differences compared with the classification method characterised by a 50% reduction in PANSS scores at week 6. A total of 349 patients were inconsistently grouped by the two methods, with a significant difference in the composition ratio of treatment response groups using these two methods (χ2 = 43.37, P < 0.001). There was no differential contribution of high- and low trajectories to different drugs (χ2 = 12.52, P = 0.051); olanzapine and risperidone, which had a larger proportion in the >50% reduction at week 6, performed better than aripiprazole, quetiapine, ziprasidone and perphenazine.

The trajectory analysis of treatment response to schizophrenia revealed two distinct trajectories. Comparing the treatment responses to different antipsychotics through longitudinal analysis may offer a new perspective for evaluating antipsychotics.