The transition to university and resultant social support network disruption can be detrimental to the mental health of university students. As the need for mental health support is becoming increasingly prevalent in students, identification of factors associated with poorer outcomes is a priority. Changes in social functioning have a bi-directional relationship with mental health, however it is not clear how such measures may be related to effectiveness of psychological treatments.

Growth mixture models were estimated on a sample of 5221 students treated in routine mental health services to identify different trajectories of change in self-rated impairment in social leisure activities and close relationships during the course of treatment. Multinomial regression explored associations between trajectory classes and treatment outcomes.

Five trajectory classes were identified for social leisure activity impairment while three classes were identified for close relationship impairment. In both measures most students remained mildly impaired. Other trajectories included severe impairment with limited improvement, severe impairment with delayed improvement, and, in social leisure activities only, rapid improvement, and deterioration. Trajectories of improvement were associated with positive treatment outcomes while trajectories of worsening or stable severe impairment were associated with negative treatment outcomes.

Changes in social functioning impairment are associated with psychological treatment outcomes in students, suggesting that these changes may be associated with treatment effectiveness as well as recovery experiences. Future research should seek to establish whether a causal link exists to understand whether integrating social support within psychological treatment may bring additional benefit for students.

Cognitive Processing Therapy (CPT) and Prolonged Exposure (PE) are first-line treatments for posttraumatic stress disorder (PTSD). There have been few direct comparisons of CPT and PE intended to determine their comparative effectiveness, none of which have examined outcomes among military veterans receiving these treatments in a residential setting such as the Department of Veterans Affairs (VA) residential rehabilitation treatment programs (RRTPs). Such work is essential given that these veterans are among the most complex and severely symptomatic patients with PTSD treated in VA. In this study we compared changes in PTSD and depressive symptoms across admission, discharge, four months and 12 months following discharge among veterans who received CPT or PE within VA RRTPs.

Using linear mixed models conducted on program evaluation data derived from the electronic medical record and follow-up surveys, we compared self-reported PTSD and depressive symptom outcomes among 1130 veterans with PTSD who were treated with individual CPT (n = 832, 73.5%) or PE (n = 297, 26.5%) in VA PTSD RRTPs in fiscal years 2018–2020.

PTSD and depressive symptom severity did not significantly differ at any time points. The CPT and PE groups both showed large-sized reductions in PTSD (CPT d = 1.41, PE d = 1.51) and depression (CPT d = 1.01, PE d = 1.09) from baseline to 12-month follow-up.

Outcomes for PE and CPT do not differ among a highly complex population of veterans with severe PTSD and several comorbid conditions that can make it difficult to engage in treatment.

To identify risk genes whose expression are regulated by the reported risk variants and to explore the potential regulatory mechanism in schizophrenia (SCZ).

We systematically integrated three independent brain expression quantitative traits (eQTLs) (CommonMind, GTEx, and BrainSeq Phase 2, a total of 1039 individuals) and GWAS data (56 418 cases and 78 818 controls), with the use of transcriptome-wide association study (TWAS). Diffusion magnetic resonance imaging was utilized to quantify the integrity of white matter bundles and determine whether polygenic risk of novel genes linked to brain structure was present in patients with first-episode antipsychotic SCZ.

TWAS showed that eight risk genes (CORO7, DDAH2, DDHD2, ELAC2, GLT8D1, PCDHA8, THOC7, and TYW5) reached transcriptome-wide significance (TWS) level. These findings were confirmed by an independent integrative approach (i.e. Sherlock). We further conducted conditional analyses and identified the potential risk genes that driven the TWAS association signal in each locus. Gene expression analysis showed that several TWS genes (including CORO7, DDAH2, DDHD2, ELAC2, GLT8D1, THOC7 and TYW5) were dysregulated in the dorsolateral prefrontal cortex of SCZ cases compared with controls. TWS genes were mainly expressed on the surface of glutamatergic neurons, GABAergic neurons, and microglia. Finally, SCZ cases had a substantially greater TWS genes-based polygenic risk (PRS) compared to controls, and we showed that fractional anisotropy of the cingulum-hippocampus mediates the influence of TWS genes PRS on SCZ.

Our findings identified novel SCZ risk genes and highlighted the importance of the TWS genes in frontal-limbic dysfunctions in SCZ, indicating possible therapeutic targets.

Studies that examined sex differences in first-episode patients consistently show that males compared to females have poor premorbid adjustment, earlier age of onset, worse clinical characteristics, and poorer outcomes. However, little is known about potential mediators that could explain these sex differences.

Our sample consisted of 137 individuals with first episode schizophrenia (males, n = 105; 77%) with a mean age of 22.1(s.d. = 4.1) years and mean education of 12.5(s.d. = 1.7) years. At entry, patients were within 2 years of their first psychotic episode onset. Baseline assessments were conducted for premorbid adjustment, symptoms, cognitive functioning, insight, and at 6-months for role and social functioning.

Males as compared to females had poorer premorbid adjustment across several key developmental periods (p < 0.01), an earlier age of onset [M = 20.3(3.3) v. 22.8(5.6), p = 0.002], more negative symptoms (p = 0.044), poorer insight (p = 0.031), and poorer baseline and 6-month role (p = 0.002) and social functioning (p = 0.034). Several of these variables in which males showed impairment were significant predictors of 6-month role and social functioning. Premorbid adjustment and insight mediated the relationship between sex and role and social functioning at 6-months, but not negative symptoms.

Males compared to females were at lower levels across several key premorbid and clinical domains which are strongly associated with functional outcome supporting the hypothesis that males might have a more disabling form of schizophrenia. The relationship between sex with role and social functioning was mediated through premorbid adjustment and insight suggesting pathways for understanding why females might have a less disabling form of schizophrenia.

Postpartum depression (PPD) affects up to one in five mothers and birthing parents, yet as few as 10% access evidence-based treatment. One-day cognitive behavioral therapy (CBT)-based workshops for PPD have the potential to reach large numbers of sufferers and be integrated into stepped models of care.

This randomized controlled trial of 461 mothers and birthing parents in Ontario, Canada with Edinburgh Postnatal Depression Scale (EPDS) scores ⩾10, age ⩾18 years, and an infant <12 months of age compared the effects of a 1-day CBT-based workshop plus treatment as usual (TAU; i.e. care from any provider(s) they wished) to TAU alone at 12-weeks post-intervention on PPD, anxiety, the mother–infant relationship, offspring behavior, health-related quality of life, and cost-effectiveness. Data were collected via REDCap.

Workshops led to meaningful reductions in EPDS scores (m = 15.77 to 11.22; b = −4.6, p < 0.01) and were associated with three times higher odds of a clinically significant decrease in PPD [odds ratio (OR) 3.00, 95% confidence interval (CI) 1.93–4.67]. Anxiety also decreased and participants had three times the odds of clinically significant improvement (OR 3.20, 95% CI 2.03–5.04). Participants reported improvements in mother–infant bonding, infant-focused rejection and anger, and effortful control in their toddlers. The workshop plus TAU achieved similar quality-adjusted life-years at lower costs than TAU alone.

One-day CBT-based workshops for PPD can lead to improvements in depression, anxiety, and the mother–infant relationship and are cost-saving. This intervention could represent a perinatal-specific option that can treat larger numbers of individuals and be integrated into stepped care approaches at reasonable cost.

Social anxiety symptoms are most likely to emerge during adolescence, a developmental window marked by heightened concern over peer evaluation. However, the neurocognitive mechanism(s) underlying adolescent social anxiety remain unclear. Emerging work points to the error-related negativity (ERN) as a potential neural marker of exaggerated self/error-monitoring in social anxiety, particularly for errors committed in front of peers. However, social anxiety symptoms are marked by heterogeneity and it remains unclear exactly what domain(s) of social anxiety symptoms are associated with ERN variation in peer presence, particularly within the adolescent period.

To advance and deepen the mechanistic understanding of the ERN's putative role as a neural marker for social anxiety in adolescence, we leveraged a social manipulation procedure and assessed a developmentally salient domain of social anxiety during adolescence – fear of negative evaluation (FNE). Adolescents residing in Hanzhong, a small city in the southwestern region of mainland China, had EEG recorded while performing a flanker task, twice (peer presence/absence); FNE, as well as global social anxiety symptoms, was assessed.

Overall ERN increases in peer presence. FNE specifically, but not global levels of social anxiety symptoms, predicted ERN in peer presence.

These data are the first demonstration that the ERN relates to a specific domain of social anxiety in adolescents, as well as the first evidence of such relations within a non-WEIRD (Western, Educated, Industrialized, Rich and Democratic) sample. Results have important implications for theory and research into adolescent social anxiety.

Adolescent internalizing symptoms and trauma exposure have been linked with altered reward learning processes and decreased ventral striatal responses to rewarding cues. Recent computational work on decision-making highlights an important role for prospective representations of the imagined outcomes of different choices. This study tested whether internalizing symptoms and trauma exposure among youth impact the generation of prospective reward representations during decision-making and potentially mediate altered behavioral strategies during reward learning.

Sixty-one adolescent females with varying exposure to interpersonal violence exposure (n = 31 with histories of physical or sexual assault) and severity of internalizing symptoms completed a social reward learning task during fMRI. Multivariate pattern analyses (MVPA) were used to decode neural reward representations at the time of choice.

MVPA demonstrated that rewarding outcomes could accurately be decoded within several large-scale distributed networks (e.g. frontoparietal and striatum networks), that these reward representations were reactivated prospectively at the time of choice in proportion to the expected probability of receiving reward, and that youth with behavioral strategies that favored exploiting high reward options demonstrated greater prospective generation of reward representations. Youth internalizing symptoms, but not trauma exposure characteristics, were negatively associated with both the behavioral strategy of exploiting high reward options as well as the prospective generation of reward representations in the striatum.

These data suggest diminished prospective mental simulation of reward as a mechanism of altered reward learning strategies among youth with internalizing symptoms.

The neurobiological pathogenesis of major depression disorder (MDD) remains largely controversial. Previous literatures with limited sample size utilizing group-level structural covariance networks (SCN) commonly generated mixed findings regarding the topology of brain networks.

We analyzed T1 images from a high-powered multisite sample including 1173 patients with MDD and 1019 healthy controls (HCs). We used regional gray matter volume to construct individual SCN by utilizing a novel approach based on the interregional effect size difference. We further investigated MDD-related structural connectivity alterations using topological metrics.

Compared to HCs, the MDD patients showed a shift toward randomization characterized by increased integration. Further subgroup analysis of patients in different stages revealed this randomization pattern was also observed in patients with recurrent MDD, while the first-episode drug naïve patients exhibited decreased segregation. Altered nodal properties in several brain regions which have a key role in both emotion regulation and executive control were also found in MDD patients compared with HCs. The abnormalities in inferior temporal gyrus were not influenced by any specific site. Moreover, antidepressants increased nodal efficiency in the anterior ventromedial prefrontal cortex.

The MDD patients at different stages exhibit distinct patterns of randomization in their brain networks, with increased integration during illness progression. These findings provide valuable insights into the disruption in structural brain networks that occurs in patients with MDD and might be useful to guide future therapeutic interventions.