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We aimed to explore temporal patterns of mental healthcare expenditure over the period 2015−2020 by age and type of mental healthcare, as well as by sex. A records-based cohort study using comprehensive data from health insurers in the Netherlands at the 4-number postal code level was performed. We used cluster-weighted linear regressions to examine temporal patterns of mental healthcare expenditure by age group (young: 18−34 vs old: 35−65), sex, and type of care. We examined the interaction of age with sex by adding the interaction between age, year, and sex to the model. The predicted costs were higher for ages 18−34 compared to older adults aged 35−64 for all mental healthcare costs except general practitioner mental healthcare (GP-MHC). The baseline regression coefficient for the young age group was 0.23 (95%-CI = 0.21;0.24) for all mental healthcare costs combined, 0.22 (95%-CI = 0.21;0.24) for specialized mental healthcare (SPECIALIST-MHC), 0.08 (95%-CI = 0.07;0.09) for basic mental health care (BASIC-MHC) and −0.02 (95%-CI = −0.03;-0.01) for GP-MHC. There was evidence for an interaction between age and year (p < 0.0001). Women had higher mental healthcare costs than men at all time points. We found an interaction between age, sex and year (p < 0.0001), with a stronger increase in the age-cost association SPECIALIST-MHC in women, while men showed a lower but more strongly increasing age-cost association for BASIC-MHC and GP-MHC. Our study found that while young women represent an increasing share of SPECIALIST-MHC, BASIC-MHC, and GP-MHC show a stronger rise in costs for young men. Future research should address whether this is due to an overlooked need for care among young men.

Age is the main risk factor of neurodegenerative diseases, but environmental exposure and lifestyle are important candidates for understanding their etiology. Accumulating evidence suggests that “exposome”, described as the totality of human environmental exposures from conception onwards, represents major modifiable risk factors for most neurodegenerative diseases and dementia. In this commentary, we discuss and provide our opinion about the urgent need for a constructive dialog between political stakeholders, researchers, and physicians to implement specific strategies to counteract and reduce the onset of neurodegenerative diseases.

The aim of this review was to discuss early intervention options for clinical high-risk states of psychosis, the limitations of the high-risk concept, and the importance of population-based approaches in preventing psychosis. Interventions for individuals at high risk of psychosis can be classified into two main categories: pharmacological and non-pharmacological. When selecting any of these intervention options, it should be taken into account that only a small proportion of individuals in the high-risk group will have a transition to clinical psychosis. Therefore, it is necessary to avoid aggressive interventions. Pharmacotherapies, particularly antipsychotics, are generally not considered as a treatment of choice for individuals at high risk of psychosis due to their potential side-effect profiles, whereas cognitive behavioral therapies and family-oriented therapies are the leading alternatives with virtually no side effects. However, meta-analyses have shown that none of the interventions are specifically more effective than needs-based treatment (including placebo) in preventing transition to psychosis. These interventions might not be effective in preventing transition to psychosis; however, they may improve the outcomes of psychosis. Accumulating evidence suggests that the targeted prevention approaches focusing on the clinical high risk of psychosis concept have major limitations in terms of the impact on reducing psychosis incidence in the general population compared to the population-based approaches. Recently, psychosis-focused prevention approaches have been replaced by easily accessible youth mental health centers that provide services for transdiagnostic conditions. Future studies on the efficacy of these community-based youth mental health services may provide guidance on how to prevent psychosis.

Background The experience sampling method (ESM) builds an intensive time series of experiences and contexts in the flow of daily life, typically consisting of around 70 reports, collected at 8–10 random time points per day over a period of up to 10 days. Methods With the advent of widespread smartphone use, ESM can be used in routine clinical practice. Multiple examples of ESM data collections across different patient groups and settings are shown and discussed, varying from an ESM evaluation of a 6‐week randomized trial of mindfulness, to a twin study on emotion dynamics in daily life. Results Research shows that ESM‐based self‐monitoring and feedback can enhance resilience by strengthening the capacity to use natural rewards. Personalized trajectories of starting or stopping medication can be more easily initiated and predicted if sensitive feedback data are available in real time. In addition, personalized trajectories of symptoms, cognitive abilities, symptoms impacting on other symptoms, the capacity of the dynamic system of mental health to “bounce back” from disturbance, and patterns of environmental reactivity yield uniquely personal data to support shared decision making and prediction in clinical practice. Finally, ESM makes it possible to develop insight into previous implicit patterns of thought, experience, and behavior, particularly if rapid personalized feedback is available. Conclusions ESM enhances clinical practice and research. It is empowering, providing co‐ownership of the process of diagnosis, treatment evaluation, and routine outcome measurement. Blended care, based on a mix of face‐to‐face and ESM‐based outside‐the‐office treatment, may reduce costs and improve outcomes.

Antipsychotics are associated with bodyweight gain and metabolic disturbance. Previous meta-analyses were limited to mainly antipsychotic switch studies in patients with a diagnosis of schizophrenia or psychosis with short follow-up periods. The present meta-analysis aimed to analyse the impact of weight change in antipsychotic-naive and antipsychotics switch patients and whether body weight change depended on diagnosis. We performed a meta-analysis of clinical trials of antipsychotics that reported weight change, irrespective of psychiatric diagnosis. Outcome measure was body weight change. Studies were classified into antipsychotic-naive and antipsychotic-switch. Forest plots stratified by antipsychotic and the duration of antipsychotic use were generated and results were summarised in figures. In total, 404 articles were included for the quantitative synthesis. 58 articles were on antipsychotic naive patients. In the antipsychotic naive group, all antipsychotics resulted in body weight gain. In the antipsychotic switch group, most antipsychotics likewise resulted in bodyweight gain, with exception of amisulpride, aripiprazole and ziprasidone that showed no body weight gain or even some weight loss after switching antipsychotics. Diagnosis was not a discriminating factor of antipsychotic induced weight change. Antipsychotic use resulted in substantial increase in body weight in antipsychotic-naive patients. In antipsychotic-switch patients the weight gain was mild and not present in amisulpride, aripiprazole and ziprasidone. In both groups, weight gain was irrespective of the psychiatric diagnosis.

Individuals with a psychiatric inpatient admission in adolescence have a high risk of schizophrenia-spectrum disorders (SSDs) when followed to adulthood. Whether psychotic symptoms predict subsequent SSDs in inpatient cohorts, however, is an important unanswered question. The sample consisted of adolescents (aged 13-17) admitted to psychiatric inpatient care (Oulu, Finland) from April 2001 to March 2006. Psychotic symptoms were assessed with the Schedule for Affective Disorders and Schizophrenia. Specialized health care use and diagnoses were followed up in national health care registers until June 2023. Cox regression was used to predict SSDs by the presence of baseline psychotic symptoms. Of 404 adolescent inpatients admitted with non-psychotic mental disorders, 28% (  = 113) reported psychotic symptoms: 17% (  = 68) subthreshold and 11% (  = 45) full threshold. By the end of follow-up, 23% of the total cohort went on to be diagnosed with an SSD. Subthreshold psychotic symptoms did not differentiate patients who would subsequently develop SSDs (cumulative incidence 24%; HR = 1.42, 95%CI = 0.81-2.50). Full-threshold psychotic symptoms, on the other hand, were associated with an increased risk of subsequent SSDs (cumulative incidence 33%; HR = 2.00, 95%CI = 1.12-3.56). Most subsequent SSDs (83%), however, occurred in individuals who had not reported threshold psychotic symptoms during inpatient admission. There was a high risk of subsequent SSDs among adolescent psychiatry inpatients when followed over time. SSDs were not predicted by subthreshold psychotic symptoms. Full-threshold psychotic symptoms were associated with an increased risk of subsequent SSDs, though with low sensitivity.

AimTo investigate whether circulating T cells including regulatory T cells (Treg) and derived cytokines contribute to the immune imbalance observed in schizophrenia.MethodsForty patients with schizophrenia and 40 age, sex, body mass index, education, and smoking status–matched healthy controls (HC) are included in the study. We stained cells with anti-CD14, anti-CD3, anti-CD4, anti-CD8, anti-CD19, anti-CD20, and anti-CD16/56. Peripheral blood mononuclear cells (PBMCs) were isolated and stained with the human FoxP3 kit containing anti-CD4/anti-CD25 and intracellular anti-Foxp3. PBMCs were cultured for 72 h and stimulated with anti-CD3/anti-CD28. Cytokines (IL-2, IL-4, IL-6, IL-10, IFN-γ, TNF-α, and IL-17A) were measured from the culture supernatant and plasma using the Th1/Th2/Th17 cytokine bead array kit.ResultsIn comparison with HC, Treg percentages in schizophrenia were higher (1.17 ± 0.63 vs 0.81 ± 0.53, P = 0.005) in unstimulated but lower in the stimulated condition (0.73 ± 0.69 vs 0.97 ± 0.55, P = 0.011). Activated T cell percentages were higher in schizophrenia than HC in unstimulated (2.22 ± 0.78 vs 1.64 ± 0.89, P = 0.001) and stimulated (2.25 ± 1.01 vs 1.72 ± 1.00, P = 0.010) conditions. The culture supernatant levels of IL-6 (7505.17 ± 5170.07 vs 1787.81 ± 1363.32, P < 0.001), IL-17A (191.73 ± 212.49 vs 46.43 ± 23.99, P < 0.001), TNF-α (1557 ± 1059.69 vs 426.57 ± 174.62, P = 0.023), and IFN-γ (3204.13 ± 1397.06 vs 447.79 ± 270.13, P < 0.001); and plasma levels of IL-6 (3.83 ± 3.41vs 1.89 ± 1.14, P = 0.003) and IL-17A (1.20 ± 0.84 vs 0.83 ± 0.53, P = 0.033) were higher in patients with schizophrenia than HC.ConclusionOur explorative study shows reduced level of Foxp3 expressing Treg in a stimulated condition with induced levels of proinflammatory cytokines in patients with schizophrenia.

Background and Hypothesis Although studies have identified social fragmentation as an important risk factor for schizophrenia and other psychotic disorders, it is unknown whether it may impact social functioning. This study investigates whether social fragmentation during childhood predicts maladaptation to school as well as social functioning during childhood and adulthood. Study Design Data were collected from the North American Prodrome Longitudinal Study. Participants included adults at clinical high risk for psychosis (CHR-P) and healthy comparisons (HC). Maladaptation to school and social functioning during childhood were assessed retrospectively and social functioning in adulthood was assessed at baseline. Study Results Greater social fragmentation during childhood was associated with greater maladaptation to school (adjusted β = 0.21; 95% CI: 0.02 to 0.40). Social fragmentation was not associated with social functioning during childhood (unadjusted β = −0.08; 95% CI: −0.31 to 0.15). However, greater social fragmentation during childhood predicted poorer social functioning in adulthood (adjusted β = −0.43; 95% CI: −0.79 to −0.07). Maladaptation to school mediated 15.7% of the association between social fragmentation and social functioning. The association between social fragmentation and social functioning was stronger among adults at CHR-P compared to HC (adjusted β = −0.42; 95% CI: −0.82 to −0.02). Conclusions This study finds that social fragmentation during childhood is associated with greater maladaptation to school during childhood, which in turn predicts poorer social functioning in adulthood. Further research is needed to disentangle aspects of social fragmentation that may contribute to social deficits, which would have implications for the development of effective interventions at the individual and community levels.

Cognitive deficits may be characteristic for only a subgroup of first-episode psychosis (FEP) and the link with clinical and functional outcomes is less profound than previously thought. This study aimed to identify cognitive subgroups in a large sample of FEP using a clustering approach with healthy controls as a reference group, subsequently linking cognitive subgroups to clinical and functional outcomes. 204 FEP patients were included. Hierarchical cluster analysis was performed using baseline brief assessment of cognition in schizophrenia (BACS). Cognitive subgroups were compared to 40 controls and linked to longitudinal clinical and functional outcomes (PANSS, GAF, self-reported WHODAS 2.0) up to 12-month follow-up. Three distinct cognitive clusters emerged: relative to controls, we found one cluster with preserved cognition ( = 76), one moderately impaired cluster ( = 74) and one severely impaired cluster ( = 54). Patients with severely impaired cognition had more severe clinical symptoms at baseline, 6- and 12-month follow-up as compared to patients with preserved cognition. General functioning (GAF) in the severely impaired cluster was significantly lower than in those with preserved cognition at baseline and showed trend-level effects at 6- and 12-month follow-up. No significant differences in self-reported functional outcome (WHODAS 2.0) were present. Current results demonstrate the existence of three distinct cognitive subgroups, corresponding with clinical outcome at baseline, 6- and 12-month follow-up. Importantly, the cognitively preserved subgroup was larger than the severely impaired group. Early identification of discrete cognitive profiles can offer valuable information about the clinical outcome but may not be relevant in predicting self-reported functional outcomes.

Potentially neurotoxic systems involved in traumatic and degenerative diseases of the brain were assessed in acute psychosis. Astrocyte-derived exosomes (ADEs) and neuron-derived exosomes (NDEs) were immunoprecipitated from plasma of ten untreated first-episode psychotics (FPs) and ten matched normal controls (Cs). Neural mitochondrial electron transport and complement proteins were extracted, quantified by ELISAs and normalized with levels of CD81 exosome marker. Levels of subunits 1 and 6 of NADH-ubiquinone oxidoreductase (complex I) and subunit 10 of cytochrome b-c1 oxidase (complex III), but not of subunit 1 of cytochrome C oxidase (complex IV) or superoxide dismutase 1 (SOD1) were significantly lower in ADEs and NDEs of FPs than Cs. This dysregulated pattern of electron transport proteins is associated with increased generation of reactive oxygen species. ADE glial fibrillary acidic protein levels were significantly higher in FPs than Cs, indicating a higher percentage of inflammatory astrocytes in FPs. ADE levels of C3b opsonin were significantly higher and those of C5b-9 attack complex was marginally higher in FPs than Cs. A significantly lower ADE level of the C3 convertase inhibitor CD55 may explain the higher levels of C3 convertase-generated C3b. ADE levels of the neuroprotective protein leukemia inhibitory factor (LIF) were significantly lower in FPs than Cs, whereas levels of IL-6 were no different. Plasma neural exosome levels of electron transport and complement proteins may be useful in predicting FP and guiding therapy. SOD mimetics, C3 convertase inhibitors and LIF receptor agonists also may have therapeutic benefits in FP.