Clarifying the neurobiological basis of psychopathology requires characterizing the dynamic role of genetic and environmental influences and identifying biomarkers that can support neurobiologically informed models that goes beyond the strict categorical classification. In this context, we focus on the developmental period, a critical window for the emergence of mental health vulnerability, marked by heterogeneous and pleomorphic symptom expression.

Different methodological approaches were applied to distinct subsamples of participants.

In a sample of 268 twins, classical univariate twin models were used to disentangle the contributions of genetic and environmental factors to schizotypy and hypomanic personality through the use of self report scales, that well characterizes subjective experiences. The roles of stressful life events and family relationship quality was also assesed.

Preliminary findings suggest a predominant role of environmental factors in modulating these vulnerability states, with a specific role of recent exposure to stressos and family climite in modulating presence of schizotypy.

In addition, a discordant-twin design—comparing pairs concordant or discordant for psychopathological conditions (13 twin pairs and 13 healthy controls)—was employed to evaluate task performance and cortical activation patterns associated with early psychotic susceptibility, particularly those related to cognitive–emotional interference.

Overall, our findings indicate that different types of emotional interference may reveal brain activity patterns that can serve as early markers of vulnerability or resilience to psychosis, primarily affecting basic facial perception rather than emotional appraisal mechanisms.

Moreover, we examined spontaneous narrative language in a transdiagnostic sample of 318 children and adolescents to identify dimensional linguistic profiles and explore their associations with internalizing and externalizing symptoms measured by the CBCL. Using k-means clustering, we identified three distinct linguistic subtypes. One subgroup, marked by pragmatic and fluency impairments, exhibited significantly higher internalizing and externalizing symptom scores, whereas a fluent and informative subgroup showed lower levels of psychopathology.

Overall, these models were applied to both brain and clinical measures, underscoring the importance of adopting a neurodevelopmental approach that emphasizes early, non-specific manifestations alongside early alterations in subjective experience for improving the management of psychiatric disorders.

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Age at onset of depression is linked to clinical presentation and outcome, but its relevance for electroconvulsive therapy (ECT) remains unclear. We examined whether age at onset of first depressive episode requiring hospitalization predicts ECT response and remission, and whether onset age reflects distinct clinical profiles.

A nationwide register-based study, including 14,141 patients who received an index ECT series for a depressive episode in Sweden during 2008–2021, with outcome data in the Swedish Quality Register for ECT. Response was “very much/much improved” on the Clinical Global Impression – Improvement scale, and remission was a post-treatment Montgomery-Åsberg Depression Rating Scale-Self report score of 10 or less. Hierarchical logistic regression and causal mediation analyses examined associations of age at onset (early, mid, late), chronological age, baseline severity, psychotic symptoms, and somatic and psychiatric comorbidity with outcome and their mediating role.

Response and remission rates were highest in late-onset depression (84.9%, 60.2%) and lowest in early-onset depression (64.6%, 26.3%). Later onset and older age were independently associated with higher odds of both outcomes, but the onset-age association attenuated substantially after adjustment. The early-onset disadvantage operated mainly through psychiatric comorbidity and treatment complexity, and the late-onset advantage was driven by psychotic features. Associations of age, male sex, and psychotic symptoms with response differed by onset group.

Age of onset of first depressive episode requiring hospitalization was associated with clinical profiles and ECT outcomes, independent of chronological age, suggesting early- and late-onset depression are partly distinct subtypes relevant to treatment planning.

Antidepressants are essential for treating major depressive disorder, yet weight gain remains a significant side effect. It contributes to metabolic morbidity, reduced treatment adherence, and long-term cardiovascular risks.

This review provides an overview of the prevalence, pharmacological mechanisms, and clinical implications of antidepressant-associated weight gain, alongside prevention and management strategies.

A selective literature review was conducted, analyzing randomized controlled trials, meta-analyses, and large cohort studies focusing on compound-specific weight changes.

Weight gain varies significantly by substance. It is most pronounced with tricyclic antidepressants, mirtazapine, and maprotiline. Among SSRIs, paroxetine is the most weight-promoting, while fluoxetine is the most favorable. Conversely, bupropion and agomelatine are associated with weight neutrality or modest loss.

While short-term treatment may cause initial weight loss, long-term use often results in gradual gain. Mechanisms include H1, M1, and 5-HT2C receptor antagonism and modulation of appetite-regulating neuropeptides (leptin, ghrelin). Notably, a 5% weight increase within the first month correlates with a 5.5-fold increased risk of metabolic syndrome (MetS) by the sixth month. Newer agents like vortioxetine and vilazodone show promise in minimizing these metabolic burdens.

Weight gain is a critical adverse effect that requires proactive management. Treatment should integrate careful drug selection, early monitoring, and emerging therapies such as GLP-1 receptor agonists. Balancing psychiatric efficacy with metabolic safety is essential to improve adherence and restore the “whole person.”

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The relationship among food insecurity, financial strain, and depression and anxiety is complex and likely bidirectional, yet most studies have examined this relationship unidirectionally and cross-sectionally. Our study investigates the longitudinal bidirectional relationship among depression and/or anxiety and food insecurity and financial strain.

Food insecurity and financial strain were measured at four waves across 13 years in the NESDA cohort. Clinical diagnoses of depression and anxiety were determined using the CIDI. Symptom severity was assessed using the IDS-SR and BAI. Lagged multilevel models examined whether food insecurity and financial strain predicted changes in depression and/or anxiety and vice versa. All models adjusted for age, sex, education, household income contributors, and prior outcome levels.

Among 2,567 individuals (mean age 42.4 years (SD 13.2), 34.6% women), higher food insecurity and financial strain significantly predicted increased odds of onset of depressive disorders (OR = 2.12, 95% CI: 1.43–3.15 and OR = 1.92, 95% CI: 1.51–2.45, respectively), and greater depressive symptom severity at the next wave (p’s for trend < .001 and p = .001, respectively). Associations with anxiety disorders and symptom severity were weaker. Conversely, depressive disorders and symptoms predicted higher subsequent food insecurity and financial strain, whereas anxiety symptoms did not.

Our findings support a bidirectional temporal association among food insecurity, financial strain and depression, with weaker evidence for anxiety. Approaches that address financial hardship and mental health may be beneficial. Further long-term studies in diverse populations are needed to clarify mechanisms linking financial insecurity with mental health and to guide effective intervention development.

The role of loneliness and social isolation in the progression from incident type 2 diabetes mellitus (T2DM) to subsequent depression remains underexplored. Further investigation is essential to better understand how these factors influence disease progression.

This study enrolled 427,594 participants without T2DM and depression at baseline. Multistate models were employed to assess the impact of loneliness and social isolation on transitions from a healthy state to incident T2DM, then to subsequent depression, and finally to death. These associations were further examined across individuals with varying glycemic statuses, including normal glucose tolerance and prediabetes.

Over a median follow-up period of 13.66 years, 14,141 incident cases of T2DM, 1,149 subsequent cases of depression, and 33,024 death events were recorded. Loneliness and social isolation were associated with elevated risks of disease progression across most transitions. For the transition from incident T2DM to subsequent depression, the loneliness group exhibited a significantly higher risk (HR = 1.802, 95% CI: 1.521–2.135) compared to the no-loneliness group. Similarly, the most isolated group had an HR of 1.390 (95% CI: 1.185–1.632) compared to the least isolated group. Additionally, participants with prediabetes faced a higher risk of developing depression following T2DM compared to those with normal glucose tolerance. Interaction analyses revealed that employment status and history of cancer modified the association between loneliness and the transition from baseline to death.

These findings underscore the importance of targeted interventions to address loneliness and social isolation, potentially reducing the risk of disease progression and mortality in individuals with T2DM.

Premenstrual dysphoric disorder, included for the first time in DSM-5 and ICD-11, is defined by the timing of affective symptoms in relation to the menstrual cycle. Gold-standard diagnosis involves prospective charting of symptoms, which must be confined to the premenstrual phase and minimal/absent at other times. Using this diagnostic method, the pooled prevalence of premenstrual dysphoric disorder is 3.2%, a much smaller proportion than experience broadly define premenstrual syndromes. Correct diagnosis is important as evidence-based treatments, including both selective serotonin reuptake inhibitors and hormonal therapies, are available. Additionally, a range of mental and physical disorders demonstrate menstrual exacerbation, deterioration of symptoms linked with the menstrual cycle. Depression, bipolar disorder and schizophrenia all have evidence of menstrual worsening. I will discuss diagnosis and treatment implications for these menstrual-related disorders.

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Electroconvulsive therapy (ECT) is a safe and effective medical treatment, yet provision varies internationally. We provide an up-to-date review of ECT practice in Nordic and western European countries.

European experts contributed data from peer-reviewed literature, governmental publications, unpublished administrative datasets, and hitherto unpublished surveys. The primary outcome was the number of individuals treated with ECT in each country per year. Primary analysis compared the annual treated person rate per million population in the most recent year since 2015 for which data were available. Secondary analysis compared trends in rates over 25 years, in countries for which a reliable outcome was available at two or more time points.

Across 15 countries, 12 had data meeting primary analysis criteria. Of these, all Nordic countries had annual treated patient rates per million population over 200, Italy 2.7, and other western European countries between 30 and 100. German-, Dutch-, and French-speaking countries saw increases in ECT use over 25 years, while English-speaking countries exhibited declines. Unilateral placement varied from 16% of treatments in the United Kingdom to 79% in Norway. Everywhere, most ECT was given for depressive episodes.

Although the optimal rate of use is unknown, widely differing rates across European nations suggest ECT is underused in some high-income countries, depriving patients of vital medical care. The European ECT community must support the development of reliable data collection on usage across the continent and service improvement where provision is underdeveloped, to ensure appropriate treatment is offered to all patients for whom it is indicated.

The menstrual cycle represents a unique opportunity to study the effects of ovarian hormones on the brain given the distinct peaks of estradiol and progesterone in the ovulatory and luteal cycle phase. Evidence of neuroplastic effects of estradiol at the cellular level is reflected in hippocampal volume changes during the ovulatory phase, while progesterone increases during the luteal phase relate to changes in basal ganglia volumes. Likewise fronto-striatal activity increases with progesterone during the luteal phase across a variety of tasks and imaging modalities. Nevertheless these changes in brain structure and activity remain very modest in effect size. More impressive however are changes in brain connectivity, which have been replicated across a variety of methods and modalities. While cognitive performance remains relatively stable along the menstrual cycle, neural networks adapt to changing hormonal milieaus, shaping new pathways for information through the brain. These changes may even be strong enough to predict a woman’s cycle phase from her brain connectivity patterns. However, mental health trajectories along the menstrual cycle are highly individualized reflected in premenstrual symptomatologies. The talk will characterize the female brain across different menstrual cycle phases and summarize behavioral evidence related to premenstrual symptom trajectories along the menstrual cycle. Finally it will discuss a road forward to linking the two phenomena.

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In a world where digital connection is constant, many young people are quietly withdrawing from real-life engagement. Hikikomori, a condition first described in Japan, refers to severe social withdrawal and prolonged home confinement. However, once considered culture-specific, similar patterns are now seen globally, including among university students facing intense academic and social demands. In a recent cross-sectional study conducted across Turkey, 183 medical students were assessed using the Adaptive Behaviors Scale for Hikikomori Self-Report (ABS-H-SR), the Symptom Checklist-90-Revised (SCL-90-R), the Beck Depression Inventory, and a detailed sociodemographic form. Results indicated reduced class attendance, increased digital dependency, social isolation, and impaired interpersonal functioning, patterns that became more pronounced in the aftermath of the COVID-19 pandemic. These behaviours often stem from cognitive and emotional factors such as fear of failure, perfectionism, and avoidance. Digital environments may offer temporary relief, but they can also reinforce withdrawal. Integrating cognitive-behavioural, psychodynamic, and neurocognitive perspectives, this presentation conceptualises Hikikomori as a transdiagnostic expression of social dysfunction shaped by cultural and technological forces. Culturally sensitive therapeutic approaches (including stepped-care models and digital-era adaptations) will be discussed as ways to support reconnection and recovery in vulnerable student populations.

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Real-world data for intranasal esketamine in treatment-resistant depression (TRD) are needed to characterize effectiveness, suicidality, and tolerability in routine care. We evaluated induction phase outcomes in outpatients with TRD treated at the University Hospital Vienna.

This retrospective single-center registry study included adults with TRD initiating supervised intranasal esketamine. The primary endpoint was the change in clinician-rated depressive symptom severity (MADRS) from the pre-treatment (PV) to the end of induction (EOI) visit. MADRS scores across baseline (BL), PV, and EOI were analyzed using a mixed model for repeated measures. Secondary outcomes included MADRS three-factor change, self-rated depression score trajectories (PHQ-9), response/remission rates, suicidal ideation, and tolerability.

Of 229 screened patients, 176 initiated esketamine and 156 completed induction. MADRS at BL was 31.5 (SD 6.4), PHQ-9 was 18.5 (SD 4.7). In the primary model, adjusted mean MADRS was 30.3 at PV and 17.7 at EOI, yielding a change of −12.5 points (95%CI −14.1 to −11.0; p < 0.001; Hedges’ g = 1.8). All MADRS factors improved, with the largest reduction in the affective–anhedonic domain. PHQ-9 decreased steadily across treatments. Remission was 27.2% and response 57.4% at EOI. Suicidal ideation decreased significantly; no suicide or serious self-harm occurred during induction. Adverse events (AEs) were recorded in 34.7%, with AE-related discontinuation in 3.4%.

Esketamine induction was associated with marked improvement in depressive symptoms and suicidality, with acceptable tolerability under supervised administration. Longer-term registry follow-up and controlled comparative studies are needed to further define the benefit–risk profile beyond induction phase.

Cognitive deficits are one of the core features of older-age bipolar disorder (OABD). Psychotropic medications may influence cognition, especially in older populations, where anticholinergic effects are relevant. This cross-sectional study aimed to investigate the potential impact of anticholinergic load on cognitive performance in individuals with OABD.

One hundred and twenty-one euthymic or partially remitted OABD patients were included. Cognitive performance was assessed using a neuropsychological battery and summarized into attention, processing speed, working memory, visual and verbal memory, and executive functions. Anticholinergic load was assessed using the CRIDECO Anticholinergic Load Scale (CALS), and pharmacological burden was quantified using the defined daily dose (DDD). Associations were examined using hierarchical multivariable linear regression models, considering also relevant clinical covariates.

The interaction between CALS and DDD was associated with lower visual and verbal memory scores (p = 0.04). Age was inversely associated with cognitive performance across all domains (all p < 0.01). A higher number of manic episodes was associated with poorer attention, visual and verbal memory, and processing speed (all p < 0.01). Lifetime psychotic symptoms were associated with worse working memory (p = 0.02), and higher diazepam-equivalent doses were associated with worse visual and verbal memory performance (p = 0.02).

Although anticholinergic medications may contribute to cognitive burden, their impact appears dose-related and limited compared with the broader influence of illness-related factors. In OABD patients, prioritizing the management of illness-related characteristics alongside careful pharmacological management may therefore be crucial for preserving cognitive functioning.

Social Isolation (SI) in youth is an increasingly prevalent condition that can evolve into severe forms of withdrawal, such as Hikikomori syndrome. SI often acts as a precursor or a core symptom of various psychiatric conditions, including depression, social anxiety, and psychosis. Traditional in-person interventions often struggle to engage these individuals due to the inherent social barriers associated with the condition. Consequently, there is an urgent need for flexible, digital-based therapeutic approaches.

The SOLITAIRE project aims to evaluate the feasibility and preliminary efficacy of a multimodal digital intervention for adolescents and young adults experiencing moderate to severe SI. The study specifically investigates the impact of remote Cognitive Behavioural Therapy (CBT), both alone and in combination with online Cognitive Remediation (CR), on social isolation, associated clinical symptoms, and neurocognitive functioning.

This multicentric clinical trial involves adolescents and young adults (aged 11-45) recruited across two Italian clinical sites. Inclusion is based on a moderate-to-severe SI profile, assessed via the 25-item Hikikomori Questionnaire (HQ-25). Participants are randomised to receive either tele-CBT alone or a synergistic CBT+CR intervention over approximately eight weeks. Clinical outcomes (e.g., SI, depression, social anxiety, alexithymia, and impulsivity) and cognitive performance (attention, memory, and social cognition) are assessed at baseline (T0) and post-treatment (T1).

Recruitment for the SOLITAIRE project began in June 2023 and is scheduled for completion in May 2026. To date, 51 participants completed the study, and further participants are currently undergoing assessment and intervention. Preliminary baseline data (T0) indicate that participants exhibit high levels of social isolation (HQ-25), often accompanied by varying degrees of depressive symptoms, alexithymia, and social anxiety. Longitudinal analyses to compare pre- and post-treatment outcomes (T0 vs. T1) and to evaluate the specific added value of CR are currently underway. Updated statistical findings, including the latest available data on treatment efficacy and dropout rates, will be presented at the conference.

While the project is still ongoing, the SOLITAIRE study represents a significant effort to address the unmet needs of socially isolated youth through accessible digital tools. Based on the preliminary results of this study, it will be possible to implement larger randomised controlled trials to further validate and refine this approach, ultimately contributing to the development of more effective, personalised remote interventions to promote real-world social reintegration and improve the quality of life for this vulnerable population.

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Brain-structural and language abnormalities in people with psychotic symptoms (PSx) have long been reported. A key question is whether language alterations are a potential behavioral readout of brain cortical gray matter changes. Adding to previous evidence for this in the cases of cortical thinning and gyrification, we here used structural MRI (sMRI) to relate a complexity-theoretical metric, the Largest Lyapunov Exponent (lambda [λ]), to computational linguistic complexity metrics extracted from spontaneous speech. This study aimed to identify psychosis-related regional changes in structural complexity using λ and an explainable AI (XAI) approach. We hypothesized that altered structural complexity will relate to computational language features that have previously been shown to track brain dysconnectivity in schizophrenia in fMRI.

MRI data were acquired from 92 patients with PSx and 38 healthy controls (HCs) from the TOPSY study. Nonlinear analysis of gray matter distribution was performed by extracting the λ for gray matter voxels. XAI was employed to identify the voxels contributing significantly to classifying PSx against HCs. Finally, the brain voxels’ contribution was tested for associations with word perplexity and syntactic and semantic complexity metrics, from spontaneous speech as obtained from picture descriptions, and with clinical symptom severity (SOFAS and PANSS scores).

The classification framework resulted in a balanced accuracy of 75.9%. The voxels contributing most to the classification decision were located in the temporal lobe, cingulum, angular, lingual, calcarine, occipital, fusiform, and parietal cortices, and parts of the cerebellum and vermis. Structural complexity in these regions was significantly associated with clinical variables (SOFAS and PANSS), word perplexity, and lexical diversity.

We present a new analytical framework using spatial series extracted from sMRI, demonstrating that alterations in structural complexity are an identifiable feature of psychosis, which co-vary with probabilistic and structural changes in speech as a behavioral readout.

This talk will introduce the idea of using personalized approaches to brain stimulation by making using of neuroimaging and will describe a study that used fMRI-guided, neuronavigated sham-controlled TMS to modulate social cognition in adults with and without autism. Results of this study, indeed, demonstrate that fMRI-guided excitatory TMS of right temporo-parietal cortex differentially improves social information processing in the verum-patient group as assessed by a computational probabilistic learning task.

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The management of patients with schizophrenia co-occurring with substance use disorders (dual diagnosis) represents one of the most complex challenges in contemporary psychiatry and requires an integrated therapeutic approach addressing both psychotic symptoms and addictive behaviors simultaneously. Sequential treatment models, in which substance use is managed prior to the psychiatric disorder, are increasingly considered insufficient and are associated with a higher risk of relapse, rehospitalization, and deterioration of social functioning.

Patients with dual diagnosis are characterized by greater variability in the course of psychosis, increased vulnerability to symptom exacerbation following substance exposure, poorer response to treatment, higher clinical instability, and an elevated risk of extrapyramidal symptoms and adverse effects related to polypharmacy. Current clinical recommendations emphasize the preferential use of antipsychotics with a low metabolic and neurological burden, avoidance of sedating agents and combinations that potentiate central nervous system depression, careful assessment of pharmacokinetic interactions (particularly involving CYP3A4 and CYP2D6 pathways), and consideration of long-acting injectable formulations in patients with low adherence.

Despite the high prevalence of dual diagnosis, most clinical guidelines remain disorder-specific and provide limited practical guidance on antipsychotic selection in this population. In this clinical gap, therapeutic decisions should be guided by pharmacodynamic profiles, impact on reward circuitry, and real-world clinical evidence. Emerging expert literature increasingly supports the use of D2/D3 partial agonists, particularly agents with high D3 affinity, as a mechanistically coherent strategy aligned with the neurobiology of both psychosis and addiction.

Importantly, effective management must also include systematic identification and treatment of somatic complications related to substance use and antipsychotic therapy, as untreated physical comorbidities significantly worsen prognosis, adherence, and overall clinical outcomes.

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Pharmacotherapies have shown limited efficacy in cannabis use disorder (CUD). This exploratory study examined the real-world effectiveness of commonly used psychiatric medications in reducing the risk of substance use and psychiatric hospitalisations among individuals with CUD.

We conducted a nationwide prospective cohort study using Swedish health and administrative registers. The cohort included 51,947 individuals aged 16–64 years with a first CUD diagnosis (ICD-10 F12) between 2006 and 2021. Medication use was modelled as time-dependent with the PRE2DUP method. Within-individual Cox regression was used to compare hospitalisation risk during medication use versus non-use. The primary outcome was hospitalisation for substance use disorder (SUD).

ADHD (aHR: 0.85; 95% CI: 0.81–0.88) and SUD medications (aHR: 0.97; 0.93–0.99) were associated with reduced SUD hospitalisation risk. In contrast, antipsychotics (aHR: 1.12; 1.09–1.15), antidepressants (aHR: 1.09; 1.06–1.11), and benzodiazepines (aHR: 1.14; 1.11–1.17) were associated with increased risk, while mood stabilisers showed no significant effect. Specific agents, including clozapine (aHR: 0.47; 0.31–0.73), naltrexone (aHR: 0.79; 0.71–0.88), buprenorphine (aHR: 0.92; 0.88–0.96), lisdexamfetamine (aHR: 0.74; 0.69–0.79), methylphenidate (aHR: 0.90; 0.86–0.94), and ADHD polytherapy (aHR: 0.85; 0.75–0.96), were associated with reduced risk.

Most psychiatric medications were not associated with a reduced risk of SUD in individuals diagnosed with CUD. However, pharmacotherapies for ADHD, opioid or alcohol use disorder, and treatment-resistant schizophrenia were linked to better outcomes, likely reflecting the underlying clinical trajectories of other comorbid psychiatric disorders rather than direct therapeutic effects on CUD.

Environmental risk factors play a central role in the development of psychosis; however, psychiatric research has traditionally examined these exposures in isolation. This has limited our ability to capture the complex, cumulative, and intercorrelated nature of environmental experiences across the life course.

In this talk, we will outline the shift from single-exposure models toward a poly-environmental perspective grounded in the exposome concept. We will first review how environmental liability has historically been investigated in psychiatry, and then introduce contemporary strategies to quantify environmental risk, ranging from simple cumulative indices to scores weighted by meta-analytic effect sizes. Particular emphasis will be placed on the Exposome Score for Schizophrenia (ES-SCZ), which integrates multiple environmental exposures while explicitly accounting for their intercorrelations. We will describe how the ES-SCZ is constructed, what distinguishes it from previous environmental risk scores, and why modeling exposure dependency is critical for understanding psychosis risk.

We will then review recent empirical findings applying the ES-SCZ across the psychosis spectrum, including subclinical psychotic experiences and clinical outcomes. Finally, we will discuss agnostic, data-driven approaches such as exposome-wide association studies (ExWAS) as complementary tools to hypothesis-driven research.

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Suicide is a serious public health issue and the leading non-accidental cause of death among adolescents in Spain. Although a previous suicide attempt is the strongest risk factor for a new attempt, studies focused specifically on adolescent reattempters remain scarce. This study aims to identify modulating factors for suicide reattempts in a clinical adolescent population following an index attempt, using network analysis.

We recruited a total of 287 adolescents aged 12 to 17, treated in emergency services after a recent suicide attempt. Data collection involved structured clinical interviews and validated self-report questionnaires assessing sociodemographic, psychopathological, and behavioral variables. Our network analysis explored significant correlations (r ≥ 0.2) between variables and their relative influence on suicidal behavior, with a particular focus on reattempts (1-year follow-up).

Variables related to emotional and behavioral difficulties, childhood trauma, and depressive symptoms were the most central and influential within the network. In contrast, suicide reattempts and their frequency appeared as peripheral nodes with no significant direct associations. Emotional abuse was associated with a higher total number of suicide attempts, and the Self-Awareness of Mental Health intervention was linked to a longer time before reattempt.

This study highlights the complexity of suicide reattempt risk factors in adolescents, emphasizing the importance of indirect interactions rather than isolated predictors. Incorporating standardized self-report tools may enhance clinical assessment and prevention strategies. Through network analysis, this research offers an innovative perspective to understand the multivariate nature of suicide risk in adolescent populations.

Psychotic experiences (PEs) are subclinical psychotic symptoms observed in the general population, particularly during childhood and adolescence, where they are typically transient. However, persistent PEs associated with functional impairment confer an increased risk of transition to clinical psychosis. This presentation will examine genomic and environmental risk factors for persistent and distressing PEs in a large longitudinal adolescent cohort.

None Declared