Symptoms of complex post-traumatic stress disorder (cPTSD) may play a role in the maintenance of psychotic symptoms. Network analyses have shown interrelationships between post-traumatic sequelae and psychosis, but the temporal dynamics of these relationships in people with psychosis and a history of trauma remain unclear. We aimed to explore, using network analysis, the temporal order of relationships between symptoms of cPTSD (i.e. core PTSD and disturbances of self-organization [DSOs]) and psychosis in the flow of daily life.

Participants with psychosis and comorbid PTSD (N = 153) completed an experience-sampling study involving multiple daily assessments of psychosis (paranoia, voices, and visions), core PTSD (trauma-related intrusions, avoidance, hyperarousal), and DSOs (emotional dysregulation, interpersonal difficulties, negative self-concept) over six consecutive days. Multilevel vector autoregressive modeling was used to estimate three complementary networks representing different timescales.

Our between-subjects network suggested that, on average over the testing period, most cPTSD symptoms related to at least one positive psychotic symptom. Many average relationships persist in the contemporaneous network, indicating symptoms of cPTSD and psychosis co-occur, especially paranoia with hyperarousal and negative self-concept. The temporal network suggested that paranoia reciprocally predicted, and was predicted by, hyperarousal, negative self-concept, and emotional dysregulation from moment to moment. cPTSD did not directly relate to voices in the temporal network.

cPTSD and positive psychosis symptoms mutually maintain each other in trauma-exposed people with psychosis via the maintenance of current threat, consistent with cognitive models of PTSD. Current threat, therefore, represents a valuable treatment target in phased-based trauma-focused psychosis interventions.

Loneliness is a risk factor for late-life dementia. There is less consistent evidence of its association with cognitive performance. This study examined the replicability of the association between loneliness and overall and domain-specific cognitive function and informant-rated cognitive decline in cohorts from seven countries: the United States, England, India, China, South Africa, Mexico, and Chile.

Data were from the Harmonized Cognitive Assessment Protocol administered in seven population-based studies (total N > 20,000). Participants reported their loneliness, completed a battery of cognitive tests, and nominated a knowledgeable informant to rate their cognitive decline. Random-effect meta-analyses were used to summarize the associations from each cohort.

Loneliness was associated with poor overall cognitive performance and informant-rated cognitive decline controlling for sociodemographic factors (meta-analytic correlation for overall cognition = −.10 [95% CI = −.13, −.06] and informant-rated decline = .16 [95% CI = .14, .17]). Despite some heterogeneity, the associations were significant across samples from Africa, Asia, Europe, North, Central, and South America. The meta-analysis also indicated an association with specific cognitive domains: episodic memory, speed-attention, visuospatial abilities, numeric reasoning, and verbal fluency. The associations were attenuated but persisted when depressive symptoms were added as a covariate. Depression, cognitive impairment, and sociodemographic factors did not consistently moderate the associations across samples.

Loneliness is associated with poor performance across multiple domains of cognition and observer-rated cognitive decline, associations that replicated across diverse world regions and cultures.

Major depressive disorder (MDD) is a heterogeneous condition characterized by significant intersubject variability in clinical presentations. Recent neuroimaging studies have indicated that MDD involves altered brain connectivity across widespread regions. However, the variability in abnormal connectivity among MDD patients remains understudied.

Utilizing a large, multi-site dataset comprising 1,276 patients with MDD and 1,104 matched healthy controls, this study aimed to investigate the intersubject variability of structural covariance (IVSC) and functional connectivity (IVFC) in MDD.

Patients with MDD demonstrated higher IVSC in the precuneus and lingual gyrus, but lower IVSC in the medial frontal gyrus, calcarine, cuneus, and cerebellum anterior lobe. Conversely, they exhibited an overall increase in IVFC across almost the entire brain, including the middle frontal gyrus, anterior cingulate cortex, hippocampus, insula, striatum, and precuneus. Correlation and mediation analyses revealed that abnormal IVSC was positively correlated with gray matter atrophy and mediated the relationship between abnormal IVFC and gray matter atrophy. As the disease progressed, IVFC increased in the left striatum, insula, right lingual gyrus, posterior cingulate, and left calcarine. Pharmacotherapy significantly reduced IVFC in the right insula, superior temporal gyrus, and inferior parietal lobule. Furthermore, we found significant but distinct correlations between abnormal IVSC and IVFC and the distribution of neurotransmitter receptors, suggesting potential molecular underpinnings. Further analysis confirmed that abnormal patterns of IVSC and IVFC were reproducible and MDD specificity.

These results elucidate the heterogeneity of abnormal connectivity in MDD, underscoring the importance of addressing this heterogeneity in future research.

According to the aberrant salience proposal, reward processing abnormality, specifically erroneous reward prediction error (RPE) signaling due to stimulus-independent release of dopamine, underlies delusions in schizophrenia. However, no studies to date have examined RPE-associated brain activations in relation to this symptom.

Seventy-eight patients with a DSM-5 diagnosis of schizophrenia/schizoaffective disorder and 43 healthy individuals underwent fMRI while they performed a probabilistic monetary reward task designed to generate a measure of RPE. Ratings of delusions and referentiality were made in the patients.

Using whole-brain, voxel-based analysis, schizophrenia patients showed only minor differences in RPE-associated activation compared to healthy controls. Within the patient group, however, severity of delusions was inversely associated with RPE-associated activation in areas including the caudate nucleus, the thalamus and the left pallidum, as well as the lateral frontal cortex bilaterally, the pre- and postcentral gyrus and supplementary motor area, the middle cingulate gyrus, and parts of the temporal and parietal cortex. A broadly similar pattern of association was seen for referentiality.

According to this study, while patients with schizophrenia as a group do not show marked alterations in RPE signaling, delusions and referentiality are associated with reduced activation in parts of the prefrontal cortex and the basal ganglia, though not specifically the ventral striatum. The direction of the changes is on the face of it contrary to that predicted by aberrant salience theory.

Impulsivity is a multidimensional trait associated with substance use disorders (SUDs), but the relationship between distinct impulsivity facets and stages of substance use involvement remains unclear.

We used genomic structural equation modeling and genome-wide association studies (N = 79,729–903,147) to examine the latent genetic architecture of nine impulsivity traits and seven substance use (SU) and SUD traits.

We found that the SU and SUD factors were strongly genetically inter-correlated (rG=0.77) but their associations with impulsivity facets differed. Lack of premeditation, negative and positive urgency were equally positively genetically correlated with both the SU (rG=.0.30–0.50) and SUD (rG=0.38–0.46) factors; sensation seeking was more strongly genetically correlated with the SU factor (rG=0.27 versus rG=0.10); delay discounting was more strongly genetically correlated with the SUD factor (rG=0.31 versus rG=0.21); and lack of perseverance was only weakly genetically correlated with the SU factor (rG=0.10). After controlling for the genetic correlation between SU/SUD, we found that lack of premeditation was independently genetically associated with both the SU (β=0.42) and SUD factors (β=0.21); sensation seeking and positive urgency were independently genetically associated with the SU factor (β=0.48, β=0.33, respectively); and negative urgency and delay discounting were independently genetically associated with the SUD factor (β=0.33, β=0.36, respectively).

Our findings show that specific impulsivity facets confer risk for distinct stages of substance use involvement, with potential implications for SUDs prevention and treatment.

Cognitive behavioural therapy for insomnia (CBT-I) is the recommended first-line treatment for insomnia. However, scaling this proven effective intervention to areas of high need remains a challenge, necessitating sensitive adaptation and evaluation.

A randomised waitlist-controlled trial evaluated the efficacy of a hybrid digital CBT-I and emotion regulation (dCBT-I + ER) intervention delivered through workplaces. Participants with at least mild insomnia and depression or anxiety symptoms were randomised to the intervention or waitlist control groups. The intervention was delivered via a web-based platform and four video-conferencing therapy sessions. Participants tracked their sleep using actigraphy and a sleep diary that was used to pace the intervention delivered. Assessments occurred at baseline and 8 weeks post-randomisation, measuring insomnia, depression, anxiety, psychological well-being, quality of life, and work productivity.

Of the 159 participants (mean age 43.6 ± 9.4 years, 76.7% female, 80.5% white), 80 received the intervention and 79 were in the control group. The intervention group showed significant improvements in insomnia (F1, 134 = 71.46, p < .0001); depression (F1, 134 = 35.67, p < .0001); and anxiety (F1, 134 = 17.63, p < .0001), with large effect sizes (d = 0.7–1.5). Sleep diary data supported these findings, whereas actigraphy data did not. Improvements in psychological well-being were significant (F1, 132.13 = 10.64, p < 0.001), whereas quality of life, work productivity, and satisfaction outcomes were not.

This study suggests that a hybrid dCBT-I + ER intervention, delivered via workplaces, effectively improves insomnia, depression, and anxiety. It holds promise as a scalable solution, warranting further investigation into its long-term efficacy and economic impact.

We conducted a prospective study to advance knowledge of biological factors that predict the future onset of binge eating and compensatory weight control behaviors because few biological risk factors for eating pathology have been identified.

Adolescent girls free of binge eating or compensatory behaviors (N = 88; Mage = 14.5; [SD = 0.9]) completed functional magnetic resonance imaging tasks assessing individual differences in neural responsivity hypothesized to increase risk for onset of binge eating and compensatory behaviors, along with additional self-report measures, and were assessed over a 4-year follow-up.

Elevated responsivity of regions implicated in attention and valuation (dorsal anterior cingulate cortex; ventromedial prefrontal cortex) to thin models and lower responsivity of a reward valuation region (caudate) to anticipated milkshake tastes (which correlated with feeling fat) predicted the future onset of binge eating or compensatory behaviors over 4-year follow-up. Parental history of binge eating and compensatory behaviors, emotionality, weight/shape overvaluation, feeling fat, and elevated BMI also predicted the future onset of binge eating or compensatory behaviors.

The evidence that elevated attentional bias for, and valuation of the thin ideal, in combination with lower valuation of high-calorie foods, predicted the future onset of eating-disordered behaviors are novel findings. The evidence that weight/shape overvaluation, feeling fat, elevated body mass, emotionality, and parental history of eating pathology predicted the future onset of eating-disordered behaviors extend past findings.

The COVID-19 pandemic has had a significant impact on the health of millions of people worldwide, and many manifest new or persistent symptoms long after the initial onset of the infection. One of the leading symptoms of long-COVID is cognitive impairment, which includes memory loss, lack of concentration, and brain fog. Understanding the nature and underlying mechanisms of cognitive impairment in long-COVID is important for developing preventive and therapeutic interventions.

Our present study investigated functional connectivity (FC) changes in patients with long-COVID and their associations with cognitive impairment. Resting-state functional MRI data from 60 long-COVID patients and 52 age- and sex-matched healthy controls were analyzed using seed-based functional connectivity analysis.

We found increased FC between the right caudate nucleus and both the left and right precentral gyri in long-COVID patients compared with healthy controls. In addition, elevated FC was observed between the right anterior globus pallidus and posterior cingulate cortex as well as the right temporal pole in long-COVID patients. Importantly, the magnitude of FC between the caudate and the left precentral gyrus showed a significant negative correlation with Montreal Cognitive Assessment (MoCA) scores and a negative correlation with Trail Making Test B performance in the patient group.

Patients with long-COVID present enhanced FC between the caudate and the left precentral gyrus. Furthermore, those FC alterations are related to the severity of cognitive impairment, particularly in the domain of executive functions.

Recent research has demonstrated that domains of social determinants of health (SDOH) (e.g. air pollution and social context) are associated with psychosis. However, SDOHs have often been studied in isolation. This study investigated distinct exposure profiles, estimated their associations with persistent distressing psychotic-like experiences (PLE), and evaluated whether involvement in physical activity partially explains this association.

Analyses included 8,145 young adolescents from the Adolescent Brain and Cognitive Development Study. Data from the baseline and three follow-ups were included. Area-level geocoded variables spanning various domains of SDOH, including socioeconomic status, education, crime, built environment, social context, and crime, were clustered using a self-organizing map method to identify exposure profiles. Generalized linear mixed modeling tested the association between exposure profiles and persistent distressing PLE and physical activities (i.e. team and individual sports), adjusting for individual-level covariates including age, sex, race/ethnicity, highest level of parent education, family-relatedness, and study sites.

Five exposure profiles were identified. Compared to the reference Profile 1 (suburban affluent areas), Profile 3 (rural areas with low walkability and high ozone), and Profile 4 (urban areas with high SES deprivation, high crime, and high pollution) were associated with greater persistent distressing PLE. Team sports mediated 6.14% of the association for Profile 3.

This study found that neighborhoods characterized by rural areas with low walkability and urban areas with high socioeconomic deprivation, pollution concentrations, and crime were associated with persistent distressing PLE. Findings suggest that various social-environmental factors may differentially impact the development of psychosis.

Psychosis prediction has been a key focus of psychiatry research for over 20 years. The two dominant approaches to identifying psychosis risk have been the clinical high-risk (CHR) and the familial high-risk (FHR) approaches. To date, the real-world sensitivity of these approaches – that is, the proportion of all future psychotic disorders in the population that they identify – has not been systematically reviewed.

We systematically reviewed and meta-analysed studies in MEDLINE, Embase, PsychINFO, and Web of Science (from inception until September 2024) that reported data on the sensitivity of CHR and FHR approaches – i.e., individuals with a psychosis diagnosis preceded by a CHR diagnosis or a history of parental psychosis (PROSPERO: CRD42024542268).

We identified four CHR studies and four FHR studies reporting relevant data. The pooled estimate of the sensitivity of the CHR approach was 6.7% (95% CI: 1.5–15.0%) and of the FHR approach was 6.5% (95% CI: 4.4–8.9%). There was a high level of heterogeneity between studies. Most FHR studies had a low risk of bias, but most CHR studies had a high risk of bias.

Pooled data suggest that CHR and FHR approaches, each, capture only about 6–7% of future psychotic disorders. These findings demonstrate the need for additional approaches to identify risk for psychosis.

Refugee experiences of trauma and displacement can significantly disrupt established social networks. While social functioning has been routinely associated with mental health, to our knowledge, no study has tested the direction of influence between social and psychological functioning within displaced refugee communities. This study investigated the temporal association between psychological symptoms (PTSD, depression, anger) and multiple facets of social functioning (including community connectedness, perceived social responsibility, positive social support and negative social support).

A culturally diverse sample of refugees (N = 1,235) displaced in Indonesia completed an online survey at four time-points, six months apart. Longitudinal structural equation modelling was used to investigate the temporal ordering between psychological symptoms and social functioning.

Findings revealed that greater psychological symptoms were associated with a subsequent deterioration in social functioning (decreased positive social support and community connectedness and increased negative social support and perceived social responsibility). Greater perceived social responsibility was also associated with subsequent increases in psychological symptoms, while positive social support and community connectedness were bi-directionally associated over-time.

These findings highlight the potential utility of mental health interventions for displaced refugees as a means to improve social functioning and inclusion with host communities. Findings have important implications in guiding the development of interventions and allocation of resources to support refugee engagement and wellbeing in displacement contexts.

Maternal perinatal mental health is essential for optimal brain development and mental health of the offspring. We evaluated whether maternal depression during the perinatal period and early life of the offspring might be selectively associated with altered brain function during emotion regulation and whether those may further correlate with physiological responses and the typical use of emotion regulation strategies.

Participants included 163 young adults (49% female, 28–30 years) from the ELSPAC prenatal birth cohort who took part in its neuroimaging follow-up and had complete mental health data from the perinatal period and early life. Maternal depressive symptoms were measured mid-pregnancy, 2 weeks, 6 months, and 18 months after birth. Regulation of negative affect was studied using functional magnetic resonance imaging, concurrent skin conductance response (SCR) and heart rate variability (HRV), and assessment of typical emotion regulation strategy.

Maternal depression 2 weeks after birth interacted with sex and showed a relationship with greater brain response during emotion regulation in a right frontal cluster in women. Moreover, this brain response mediated the relationship between greater maternal depression 2 weeks after birth and greater suppression of emotions in young adult women (ab = 0.11, SE = 0.05, 95% CI [0.016; 0.226]). The altered brain response during emotion regulation and the typical emotion regulation strategy were also as sociated with SCR and HRV.

These findings suggest that maternal depression 2 weeks after birth predisposes female offspring to maladaptive emotion regulation skills and particularly to emotion suppression in young adulthood.

Cannabis is one of the most commonly used drugs globally, although its legal status varies across regions. Public support for its decriminalization has increased, but gaps in our understanding of the health consequences of cannabis use remain, particularly related to its impact on mental health. This article provides an updated systematic review and meta-analysis (previous being Lev-Ran et al., 2014) looking at the relationship between cannabis and depression.

Literature available before March 2023 was screened for longitudinal studies that included cannabis use and depression. Cross-sectional studies and those only looking at special populations were excluded. Studies must have also controlled for depression at baseline to allow for investigation of a temporal relationship. Extracted data included cannabis measures, depression outcomes, adjusted odds ratios, and study settings. Meta-analysis employed a random effects model with multilevel meta-regression for effect size moderators.

The search yielded 1,599 titles from various databases, resulting in 22 studies for meta-analysis, including 14 from Lev-Ran et al. Eleven studies were US-based, with participants mostly under 18. Meta-analysis showed a higher risk of depression among cannabis users (OR: 1.29, 95% CI: 1.13–1.46). Risk of bias assessment showed medium risk across studies with exposure measurement being a key bias area. The funnel plot and Egger’s Sandwich test did not suggest publication bias.

This study underscores the association between cannabis use and depression but also emphasizes the need for further research, especially in understanding usage patterns, heavy use definitions, and long-term effects on depression risk amidst changing cannabis trends.

Impaired emotion regulation has been proposed as a putative endophenotype in bipolar disorder (BD). Functional magnetic resonance imaging (fMRI) studies investigating this in unaffected first-degree relatives (UR) have thus far yielded incongruent findings. Hence, the current paper examines neural subgroups among UR during emotion regulation.

71 UR of patients with BD and 66 healthy controls (HC) underwent fMRI scanning while performing an emotion regulation task. Hierarchical cluster analysis was performed on extracted signal change during emotion down-regulation in pre-defined regions of interest (ROIs). Identified subgroups were compared on neural activation, demographic, clinical, and cognitive variables.

Two subgroups of UR were identified: subgroup 1 (39 UR; 55%) was characterized by hypo-activity in the dorsolateral, dorsomedial, and ventrolateral prefrontal cortex and the bilateral amygdalae, but comparable activation to HC in the other ROIs; subgroup 2 (32 UR; 45%) was characterized by hyperactivity in all ROIs. Subgroup 1 had lower success in emotion regulation compared to HC and reported more childhood trauma compared to subgroup 2 and HC. Subgroup 2 reported more anxiety, lower functioning, and greater attentional vigilance toward fearful faces compared to HC. Relatives from both subgroups were poorer in recognizing positive faces compared to HC.

These findings may explain the discrepancy in earlier fMRI studies on emotion regulation in UR, showing two different subgroups of UR that both exhibited aberrant neural activity during emotion regulation, but in opposite directions. Furthermore, the results suggest that impaired recognition of positive facial expressions is a broad endophenotype of BD.

Previous research has shown abnormal functional network gradients in Alzheimer’s disease (AD). Structural network gradient is capable of capturing continuous changes in brain morphology and has the ability to elucidate the underlying processes of neurodevelopment. However, it remains unclear whether structural network gradients are altered in AD and what associations exist between these changes and cognitive function, and gene expression profiles.

By constructing an individualized structural network gradient decomposition framework, we calculated the morphological similarity network (MSN) gradients for 404 subjects (186 AD patients and 218 normal controls). We investigated AD-related alterations in MSN gradients, along with the associations between MSN gradients and cognitive function, MSN topological properties, and gene expression profiles.

Our findings indicated that the principal MSN gradient alterations in AD were primarily characterized by an increase in the primary and secondary sensory cortices and a decrease in the association cortex 1. The primary and higher-order cortices exhibited opposite associations with cognition, including executive function, language skills, and memory processes. Moreover, the principal MSN gradients were found to significantly predict cognitive function in AD. The altered gradient pattern was 14.8% attributable to gene expression profiles, and the genes demonstrating the highest correlation are involved in metabolic activity and synaptic signaling.

Our results offered novel insights into the underlying mechanisms of structural brain network impairment in AD patients, enhancing our understanding of the neurobiological processes responsible for impaired cognition in patients with AD, and offering a new dimensional structural biomarker for AD.

Based on facial expression experiments, childhood adversity may be associated with threat-related information processing bias. Yet, it is unclear whether this generalizes to other threat-related stimuli, such as social and non-social visual scenes.

We combined fast periodic visual stimulation with frequency-tagging electroencephalography (EEG) and eye-tracking to assess automatic and implicit neural discrimination, neural salience and preferential looking towards negative versus neutral social and non-social visual scenes in young adults aged 16–24 years (51 with childhood adversity and psychiatric symptoms and 43 controls).

Controls showed enhanced negative-neutral neural discrimination within a social versus non-social context. However, this facilitating effect of social content was absent in those with adversity, suggesting a selective alteration in social threat processing. Moreover, individual differences in adversity severity, and more specifically threat experiences (but not neglect experiences), were associated with decreased neural discrimination of negative versus neutral social scenes, corresponding to similar findings in facial expression processing, indicating the robustness of adversity-related deficits in threat-safety discrimination across social visual stimuli.

The adversity-related decreased threat-safety discrimination might impact individuals’ perception of social cues in daily life and relate to poor social functioning and future development of psychopathology.