Suicide is a leading cause of preventable death among youth worldwide. Improving the knowledge and skills of professionals who care for youth is imperative to lowering the suicide rate. The Assessing and Managing Suicide Risk (AMSR) training aims to enhance professionals' therapeutic skills and increase the use of best practices for those working with individuals at elevated suicide risk. Changes in suicide prevention-specific therapeutic skills and the utilization of recommended brief interventions were evaluated in the 3 months following participation in AMSR training. Participants were youth-serving professionals (N = 115) across varied practice settings (e.g., mental health, education, emergency services) who attended an AMSR training and completed a pre-training and a 3-month post-training evaluation. Wilcoxon signed-rank tests were used to examine changes across time. Professionals reported a significant increase in use of recommended therapeutic skills overall, specifically in validating youth's experience of suicidal thinking and conveying that suicidal ideation is taken seriously. Moreover, professionals reported a significant increase in the use of specific brief interventions, namely safety planning and referring youth to additional care. Brief interventions that did not demonstrate significant change post-training included lethal means safety counseling and collaboration with caregivers. This is one of the first studies to evaluate the impact of AMSR training, a widely disseminated suicide prevention training, on self-reported clinical practices. Findings have important implications for efforts aimed at training a competent and confident professional workforce.

Ocular diseases and mental disorders represent major global public health challenges. Although prior studies have explored associations between ophthalmic conditions and psychiatric disorders, systematic investigations into their underlying mechanistic connections remain limited. This review synthesizes evidence from high-quality literature to delineate the bidirectional links between ophthalmic and psychiatric health. We first provide an epidemiological overview of their comorbidity, followed by an analysis of the mechanisms through which ocular diseases may induce or exacerbate mental disorders and, conversely, how psychiatric conditions may promote the onset and progression of ocular pathology. Furthermore, we discuss medication safety in the context of monotherapy for either condition, emphasizing cross-system adverse effects and their clinical implications. By systematically elucidating the bidirectional mechanisms linking ocular and psychiatric diseases, this review aims to improve the recognition and evaluation of their interactions in clinical practice and to provide a theoretical foundation for patient-centered, integrated management of ophthalmic-psychiatric comorbidities.

Landmark descriptions of autism in the 1940s were based on clinical work with children. Research over the subsequent 80 years has largely focused on the experiences and needs of autistic children, with recent neuroimaging and genetic studies contributing significant insights into the developmentally driven neurobiological underpinnings of this condition. However, autism is a lifelong neurodevelopmental condition and adolescence and adulthood introduces new developmental transitions and life experiences that require specific consideration. Together, the articles in this Collection-Autism in Adolescence and Adulthood-highlight the need to understand autistic experiences and neurobiology in adolescence and adulthood through a context-sensitive lens that considers developmentally relevant experiences. Across diverse methodologies, including behavioural, physiological, qualitative, and computational (machine learning), a particular focus is on understanding and supporting emotion regulation, wellbeing and mental health. Collectively, the papers highlight that adolescence and adulthood are periods of autistic development that warrant focussed scientific attention. They also underscore that autistic flourishing in adolescence and adulthood depends on a society that embraces neurodiversity and is committed to meaningful change.

ObjectiveNarcissism is commonly described through grandiosity, entitlement, admiration seeking, exploitation and impaired empathy. This perspective article proposes that these features can be clinically organised around a common function: the regulation of felt superiority.ConclusionsThe superiority-motive framework is offered as an integrative formulation, not as a replacement for existing theories. Freud, Adler, Kohut, Kernberg and Rosenfeld each described aspects of narcissistic self-investment, inferiority, mirroring failure, pathological grandiosity, aggression, envy and destructive superiority. Contemporary work similarly locates entitlement, antagonism and status pursuit near the core of narcissism. A superiority formulation helps explain grandiose fantasy, grandiose and vulnerable presentations, status sensitivity, differential diagnosis and collaborative formulation. Clinically, the model encourages assessment of the patient's preferred "ladder" of superiority, the developmental meanings attached to that ladder, the triggers that threaten rank, and the defensive tactics used to restore it.

w?>Bipolar disorder (BD) is associated with reduced life expectancy, but it is unknown if this extends into later life or if older-age bipolar disorder (OABD) represents a survival cohort.

In this prospective cohort study, 227 adults aged ≥50 years with BD from the Dutch Older Bipolars (DOBi) study were compared with 681 matched (on age and sex) controls (CG) from the Longitudinal Aging Study Amsterdam (LASA). All-cause mortality was assessed over 8 years. Kaplan-Meier survival, restricted mean survival time, and Cox proportional hazards models were applied.

In total, 37 (16.3%) OABD and 138 (20.3%) CG participants died during the 8-year follow-up. Kaplan-Meier curves indicated earlier mortality in OABD. Restricted mean survival time over 7.5 years was 2500.7 days (95% confidence interval [CI] 2419.9-2581.5) in OABD and 2607.2 days (95% CI 2572.3-2642.0) in CG, corresponding to an average survival difference of 106.4 days (3.5 months; 95% CI 18.4-194.5; p = 0.018). In Cox models, OABD was associated with higher mortality risk compared with CG (hazard ratio (HR) = 1.72; 95% CI 1.17-2.54; p = 0.006).

In this longitudinal cohort study, OABD had significantly higher all-cause mortality than age- and sex-matched population controls, with a shorter restricted mean survival time and an increased hazard of death over 8 years. Thus, excess mortality persists into later life, and OABD is not solely a survivor cohort. Targeted strategies addressing modifiable physical health and lifestyle risk factors are warranted to reduce premature mortality in this vulnerable population.

Psychiatric disorders are highly prevalent among individuals living with obesity and contribute to treatment resistance, poor adherence, and adverse health outcomes. Yet, obesity management often remains fragmented, with limited integration between endocrinology, psychiatry, and behavioral health. This Perspective advocates for a mental health framework for obesity care. We emphasize the need for future investigations to test the clinical relevance of behavioral phenotyping as a complementary approach to pharmacotherapy, including GLP-1 receptor agonists, to enhance treatment personalization. By reframing obesity as a disease deeply intertwined with mental health, we emphasize the need for multidisciplinary care models that incorporate psychological assessment, stigma reduction, and patient-centered nutrition counseling. Advancing this framework will require closer collaboration between medical and mental health disciplines and greater investment in neurobehavioral research to improve long-term outcomes in obesity care.

Functional magnetic resonance imaging (fMRI) is the most commonly used technique for non-invasive exploration of human cognition and neuroscience. Conventional T2*-weighted single-echo resting-state fMRI (SE-rfMRI) is limited by signal loss in regions prone to susceptibility artifacts and inseparable confounding from non-neuronal baseline (i.e., initial signal intensity S0) fluctuations. While multi-echo optimally combined rfMRI (ME-OC) effectively mitigates signal loss, confounding from S0 fluctuations remains unaddressed. Here, we leverage quantitative T2* fluctuation from ME-rfMRI to derive intrinsic functional metrics that are biophysically cleaner and more robust. Across both cortical and subcortical brain regions, we systematically evaluated the test-retest reliability and functional validity of two key local metrics, amplitude of low-frequency fluctuation (ALFF) and regional homogeneity (ReHo), derived from our proposed method against those from conventional SE-rfMRI and ME-OC. In subcortical regions, T2*-derived metrics showed the highest mean ICCs among the three signal representations for both ALFF (ICC = 0.67, 0.66, and 0.54) and ReHo (ICC = 0.73, 0.67, and 0.63) for T2* fluctuation, ME-OC, and SE-rfMRI, respectively. A similar regionally selective pattern was observed in cortical areas susceptible to magnetic field inhomogeneities, including the orbitofrontal cortex (ALFF ICC = 0.87, 0.75, and 0.82), insula (0.83, 0.61, and 0.71), and temporal pole (0.80, 0.73, and 0.79) for T2* fluctuation, ME-OC, and SE-rfMRI, respectively. In terms of functional validity, ALFF from T2* fluctuation uniquely revealed significant condition-related differences in the right putamen, inferior frontal gyrus, and suborbital sulcus, which both ME-OC and SE-rfMRI failed to detect. Together, our findings suggest that quantitative T2*-derived metrics may provide a reliable and more biophysically specific characterization of intrinsic fMRI signal fluctuations, particularly in subcortical and susceptibility-prone cortical regions, and may complement conventional approaches in future research applications.

The development of the brain involves extensive structuring of neural circuit architecture. Exposure to addictive substances during this period may disrupt brain maturation, increasing vulnerability to psychopathology. Synaptic pruning (i.e. a key process refining neural circuits) is particularly sensitive to environmental factors, including substance exposure. Although substance-related changes in synapse organization are well documented in adults, effects during early development remain poorly characterized. The aim of this review is to determine whether exposure to addictive substances during key developmental stages altersalter markers of synaptic organization in animal models.

A scoping review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR) guidelines. Preclinical studies investigating changes to dendritic spines or synaptic protein markers in animals before postnatal day 50 were included. Comprehensive searches were performed in MEDLINE®, Embase, CINAHL, PsycINFO®, and Scopus from database inception to February 2024.

From 8256 publications, only 34 studies met inclusion criteria. Limited findings suggest that stimulant exposure in juvenile rodents may increase dendritic spine measures in striatal regions. Our results also suggest that alcohol increases presynaptic markers and immature spines, but may decrease post-synaptic markers and mature spines. Finally, neonatal alcohol, and juvenile to adolescent stimulant and THC exposure are moderately associated with reductions in dendritic spine density in the frontal cortex.

Substance exposure during early brain development may alter synaptic structure and proteins important for brain function. Further investigation of pre- and post-synaptic elements is required to better understand synaptic alterations in the developing brain.

Psychotic-like experiences (PLEs) and autistic traits across development are associated with poor mental health outcomes. However, the relationship between PLEs and autistic traits, and their links with clinical and biological predictors of longitudinal outcomes, remain poorly understood.

PLEs and autistic traits were measured across a three year period using the Prodromal Questionnaire Brief and Child Behavior Checklist in 9,963 adolescents from the Adolescent Brain Cognitive Development Study®. Separate Growth Mixture Models identified trajectories for PLEs and autistic traits. Associations between trajectories with longitudinal internalizing and externalizing symptoms, cognition, environmental adversity, and harmonized diffusion measures of baseline fractional anisotropy (FA), were examined.

Four trajectories were found for both PLEs and autistic traits: persistently low, persistently elevated, increasing, and decreasing. Persistently low trajectories were associated with favorable profiles across measures. Increasing or persistently elevated PLEs were associated with lower baseline FA, cognition, and socioeconomic disadvantage and linked to worsening internalizing symptoms and environmental adversity. Persistently elevated autistic traits were associated with lower cognition, more environmental adversity, and reduced FA. Overlapping trajectories of co-elevated or increasing PLEs and autistic traits conferred the highest risk, with impairments across measures. Compared to only-elevated autistic traits, only-elevated PLEs were associated with lower psychopathology, higher family conflict and life events, lower cognition, and specific white matter alterations.

Adolescents with distinct longitudinal PLEs and autistic traits trajectories differed on psychopathology, cognitive performance, environmental adversity, and white matter microstructure. Examining trajectory-specific differences highlights heterogeneity in early adolescent neurodevelopment and may support the advancement of early-detection strategies for at-risk youth.