Schizophrenia Bulletin最新文献

{"title":"CYP2D6 Genotypes Do Not Affect Clozapine Levels in a Large, Multicenter Cohort: Time Has Come to Revise Food and Drug Administration's Clozapine Packet Insert.","authors":"Georgios Schoretsanitis, Nermine Laaboub, Séverine Crettol, Hasan Çağın Lenk, Line Skute Bråten, Setareh Ranjbar, Marianna Piras, Céline Dubath, Carole Grandjean, Frederik Vandenberghe, Nicolas Ansermot, Franziska Gamma, Kerstin Jessica Plessen, Armin von Gunten, Philippe Conus, Chin Bin Eap, Espen Molden","doi":"10.1093/schbul/sbaf160","DOIUrl":"https://doi.org/10.1093/schbul/sbaf160","url":null,"abstract":"<p><strong>Background and hypothesis: </strong>The US Food and Drug Administration (FDA) package insert for clozapine states that cytochrome P450 (CYP) 2D6 is important in clozapine metabolism, implying that CYP2D6 genotypes should be considered in clozapine dosing. We investigated differences for clozapine concentration-to-dose (C/D) ratios, as a pharmacokinetic measure, in relation to CYP2D6 phenotype.</p><p><strong>Study design: </strong>Linear mixed-effect regression models were applied to investigate the association between genotype-predicted CYP2D6 metabolizer phenotypes and C/D ratios including the effects of age, sex, smoking, and sampling time in a pooled sample of three cohorts, both without and with adjusting for the interaction between cohort and CYP2D6 phenotype, as well as in separate models stratified by cohort.</p><p><strong>Study results: </strong>We included 897 patients from three cohorts with a total of 10 428 clozapine and norclozapine measurements. We found no association between CYP2D6 phenotypes and clozapine or norclozapine C/D ratios or clozapine-to-norclozapine ratios in the pooled sample with or without adjustment for the interaction between cohort and CYP2D6 phenotype nor when analyzing three cohorts separately (P>.05 in all cases). Older patients and females had higher C/D ratios of clozapine and norclozapine (P<.001, P<.001, P<.001 and P=.02), whereas smokers had lower C/D ratios of clozapine and norclozapine as well as clozapine-to-norclozapine ratios (P<.001 for all three).</p><p><strong>Conclusions: </strong>We reported no association between CYP2D6 genotype-predicted phenotypes and clozapine pharmacokinetics. Dose adjustment based on CYP2D6 genotyping is unlikely to be helpful in managing clozapine-treated patients. We propose that the current FDA package insert should be updated to avoid misleading prescribers.</p>","PeriodicalId":21530,"journal":{"name":"Schizophrenia Bulletin","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145092687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Not So Hasty: The Effect of Tapering Speed on Relapse May Still Be Important.","authors":"Mark Abie Horowitz, James O'Neill, Fabrice Berna, David Taylor","doi":"10.1093/schbul/sbaf163","DOIUrl":"https://doi.org/10.1093/schbul/sbaf163","url":null,"abstract":"","PeriodicalId":21530,"journal":{"name":"Schizophrenia Bulletin","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145092675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Subcategories of the Clinical High-Risk State for Psychosis and Their Relationship to a Full First-Episode Psychosis Sample: An Exploratory Analysis of Longitudinal Outcomes.","authors":"Olivier Renaud-Charest, Vincent Paquin, Jean-Gabriel Daneault, Ashok K Malla, Ridha Joober, Srividya N Iyer, Martin Lepage, Jai L Shah","doi":"10.1093/schbul/sbaf155","DOIUrl":"https://doi.org/10.1093/schbul/sbaf155","url":null,"abstract":"<p><strong>Background and hypothesis: </strong>Subcategories of the Clinical High-Risk state for psychosis (CHR-P) have been associated with differential risk for transition to first-episode psychosis (FEP), but their relevance for longer term FEP outcomes remains unclear. We aimed to determine the prevalence of 2 CHR-P subcategories - attenuated psychotic symptoms (APS) and brief intermittent psychotic symptoms (BIPS) - in a full sample of FEP patients, along with their association with outcome trajectories following psychosis onset.</p><p><strong>Study design: </strong>Participants were recruited from an early intervention service and followed over 2 years, with repeated measures of psychotic symptoms, affective symptoms, and functioning. Pre-onset symptoms were assessed using follow-back methods to reconstruct subgroups and their prevalence within the sample. Linear mixed models were applied to examine associations between putative CHR-P subcategories and longitudinal outcomes.</p><p><strong>Study results: </strong>Of 319 patients, 240 (75.24%) experienced subthreshold psychotic symptoms indicative of a CHR-P state; of these, 51 (21.25%) had potential BIPS (either alone or with APS) and 189 (78.75%) potential APS only. There were no mean differences in scores for psychotic symptoms, affective symptoms, or functioning between subgroups. However, there was a slower improvement in Global Assessment of Functioning (GAF) scores in the putative APS subgroup, which converged with the putative BIPS subgroup by year 2.</p><p><strong>Conclusions: </strong>Putative CHR-P subcategories of APS and BIPS exhibited similar outcome trajectories beyond psychosis onset, except for a possibly slower functional recovery in the putative APS subgroup. Longer term studies across stages of illness are needed to better understand the prognostic utility of these identifiers after FEP.</p>","PeriodicalId":21530,"journal":{"name":"Schizophrenia Bulletin","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145092692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Risk of Very Late-Onset Schizophrenia Following Diabetes Type 2 Onset: A Nationwide Population-Based Study of Midlife and Old-Age.","authors":"Stephen Z Levine, Arad Kodesh, Abraham Reichenberg","doi":"10.1093/schbul/sbaf159","DOIUrl":"https://doi.org/10.1093/schbul/sbaf159","url":null,"abstract":"<p><strong>Background and hypothesis: </strong>Schizophrenia is an established Type 2 Diabetes (T2D) risk factor; while the reverse hypothesis is plausible, it remains untested.</p><p><strong>Study design: </strong>This nationwide cohort study included all members (n = 99 567; Female: 52517, 52.7%) of a non-profit Israeli health maintenance organization born between 1932 and 1952. At cohort entry (aged M = 59.70, SD = 5.68) without histories of T2D or schizophrenia, the cohort was followed-up on average 14.47 (SD = 2.28) years for incident schizophrenia. Cox regression models were fit to quantify the association between T2D and schizophrenia risk with the Hazard Ratio (HR) and their 95% Confidence Intervals (CI), unadjusted and adjusted for 20 potential confounders in the primary analysis.</p><p><strong>Study results: </strong>During follow-up, schizophrenia incidence per 10 000 person-years was 0.26 (95% CI, 0.21-0.32) in individuals with T2D and 0.12 (95% CI, 0.11-0.14) in those without. In the primary analysis, T2D onset was associated with a 50% increased risk of incident schizophrenia (adjusted hazard ratio = 1.53; 95% CI, 1.11-2.10; P = .009) compared with the absence of T2D. Generally, nine complementary analyses were consistent with the primary analysis results, showing T2D was associated with an increased risk of incident schizophrenia; the association showed minimal reverse causation and antidiabetic medication was not associated with schizophrenia risk.</p><p><strong>Conclusions: </strong>In this study, the onset of T2D was associated with an increased risk of schizophrenia. This suggests that the onset of T2D may require psychosis monitoring, which is relevant to healthcare providers and clinicians in psychiatry, geriatrics, and endocrinology.</p>","PeriodicalId":21530,"journal":{"name":"Schizophrenia Bulletin","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145092621","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Restoring Synaptic Balance in Schizophrenia: Insights From a Thalamo-Cortical Conductance-Based Model.","authors":"Lioba C S Berndt, Krish D Singh, Alexander D Shaw","doi":"10.1093/schbul/sbaf149","DOIUrl":"https://doi.org/10.1093/schbul/sbaf149","url":null,"abstract":"<p><strong>Background and hypothesis: </strong>The dysconnectivity hypothesis of schizophrenia suggests that atypical neural communication underlies the disorder's diverse symptoms. Building on this framework, we propose that specific synaptic disturbances within thalamo-cortical circuits contribute to an imbalance in excitation and inhibition, leading to alteration in oscillations. Our study investigates these alterations and explores whether synaptic restoration can remediate neural activity of schizophrenia and align it with healthy patterns.</p><p><strong>Study design: </strong>We analyzed magnetoencephalography data from schizophrenia patients and healthy controls using dynamic causal modeling to identify synaptic differences in thalamo-cortical circuits. The analysis focused on N-methyl-D-aspartate (NMDA), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), gamma-aminobutyric acid type A (GABA-A), and gamma-aminobutyric acid type B (GABA-B) receptor-mediated connections. In silico synaptic restoration analysis simulated the effects of targeted adjustments to these receptor-mediated connections to assess whether altered neural activity in schizophrenia could be restored to match control patterns.</p><p><strong>Study results: </strong>Schizophrenia patients showed statistically significant differences in increased NMDA receptor excitation in superficial pyramidal neurons and reduced GABA-B receptor inhibition between interneurons and pyramidal cells. Parameter recovery analysis revealed limitations for these specific parameters, suggesting that receptor-level interpretations should be made with caution. The in silico synaptic restoration analysis indicated that coordinated modifications across multiple synaptic pathways could potentially remediate neural activity to resemble healthy controls.</p><p><strong>Conclusions: </strong>This restoration approach suggests the complex nature of synaptic dysfunction in schizophrenia may involve coordinated changes across multiple synaptic parameters rather than isolated alterations. While our findings provide preliminary evidence extending the dysconnectivity theory of schizophrenia, the parameter recovery limitations suggest that specific receptor claims should be interpreted with caution.</p>","PeriodicalId":21530,"journal":{"name":"Schizophrenia Bulletin","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145034138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TRPV1 Suppresses Microglial Inflammatory Activation to Ameliorate Schizophrenia-Associated Behaviors in Maternal Separation Rats.","authors":"Fashuai Chen, Keke Hao, Chang Shu, Ying Xiong, Rui Xu, Huan Huang, Biwen Peng, Zhongchun Liu, Gavin P Reynolds, Gaohua Wang, Huiling Wang","doi":"10.1093/schbul/sbaf153","DOIUrl":"https://doi.org/10.1093/schbul/sbaf153","url":null,"abstract":"<p><strong>Background and hypothesis: </strong>Schizophrenia is linked to hippocampal dysfunction and microglial inflammatory activation. Our prior clinical findings revealed significantly reduced transient receptor potential vanilloid 1 (TRPV1) expression in both first-episode and recurrent schizophrenia patients, with levels inversely correlating with symptom severity, implicating TRPV1 dysfunction in disease progression. Preclinical maternal separation (MS) models recapitulate schizophrenia-like behavioral and synaptic deficits, paralleled by hippocampal microglial TRPV1 downregulation. We hypothesize that early-life stress-induced TRPV1 deficiency in microglia disrupts the calmodulin-dependent protein kinase II (CaMKII)/nuclear factor-erythroid 2-related factor 2 (NRF2)/Sirtuin 3 (SIRT3) signaling axis, thereby amplifying microglial inflammatory responses and synaptic dysfunction underlying cognitive and behavioral impairments.</p><p><strong>Study design: </strong>Using a 24-h acute MS model in postnatal day 9 rats, we assessed hippocampal microglial TRPV1 expression, synaptic plasticity, and schizophrenia-like behaviors. Pharmacological (capsaicin, CAP) and genetic (adeno-associated virus (AAV)-mediated overexpression/knockdown (KD)) TRPV1 manipulations were applied. Co-cultures of TRPV1-knockout (KO) microglia and neurons were used to dissect cell-specific effects.</p><p><strong>Study results: </strong>MS reduced microglial TRPV1, increased pro-inflammatory cytokines, and induced hyperlocomotion, cognitive deficits, and impaired sensory gating. CAP or microglial TRPV1 overexpression restored synaptic plasticity and reversed behavioral deficits. Conversely, TRPV1 KD worsened neuronal dysfunction. TRPV1-KO microglia, but not neurons, promoted inflammation and neuronal damage via CaMKII/NRF2/SIRT3 downregulation.</p><p><strong>Conclusions: </strong>These findings provided novel insights into the role of microglial TRPV1 in schizophrenia pathogenesis, establishing it as an upstream regulator of the CaMKII/NRF2/SIRT3 signaling axis-a pathway not previously linked to TRPV1 in neuroinflammation. Our work identifies microglia-specific TRPV1 modulation as a new therapeutic strategy for schizophrenia, highlighting its therapeutic potential for cognitive and negative symptoms in schizophrenia.</p>","PeriodicalId":21530,"journal":{"name":"Schizophrenia Bulletin","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145034146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identity and Psychosis Risk in Sexual Minority Youth: Temporal Dynamics of Identity and Suspiciousness Through Experience Sampling Methodology.","authors":"Margaux Sageot, Inez Myin-Germeys, Robin Achterhof, Anu P Hiekkaranta, Kristof Vansteeland, Ruud van Winkel","doi":"10.1093/schbul/sbaf157","DOIUrl":"https://doi.org/10.1093/schbul/sbaf157","url":null,"abstract":"<p><strong>Background and hypotheses: </strong>Sexual minority youth are at increased risk for psychotic experiences, potentially due to identity-related difficulties. We hypothesized that sexual minority youth would report greater identity difficulties, and that these difficulties would be associated with heightened suspiciousness in daily life. Finally, we examined whether these associations differ between sexual minority and heterosexual adolescents.</p><p><strong>Study design: </strong>Experience Sampling Method (ESM) and questionnaire data were collected from 1913 Flemish adolescents (aged 11-20). Identity functioning was assessed using a validated questionnaire (Erikson Psychosocial Stage Inventory, EPSI) and momentary assessments via ESM. Suspiciousness was also measured through ESM. Multilevel linear regression models tested within- and between-person associations between identity functioning and suspiciousness, and explored moderation by sexual minority status.</p><p><strong>Study results: </strong>Sexual minority participants reported significantly lower identity synthesis, higher identity confusion, and greater momentary identity difficulties. At the within-person level, lower momentary identity functioning predicted higher suspiciousness both concurrently and at subsequent time points. Suspiciousness also predicted later identity difficulties, indicating a bidirectional relationship. Sexual minority status moderated these effects: Identity confusion was more strongly associated with suspiciousness in sexual minority youth, while identity synthesis appeared protective only in heterosexual youth.</p><p><strong>Conclusions: </strong>Identity difficulties are closely linked to suspiciousness in adolescents, particularly among sexual minority youth. The bidirectional relationship suggests a reinforcing cycle that may increase vulnerability to psychotic experiences. These findings stress the need for preventive interventions that address identity integration during adolescence, especially for sexual minority adolescents navigating identity development in a heteronormative context.</p>","PeriodicalId":21530,"journal":{"name":"Schizophrenia Bulletin","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145034199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Health, Disability, and Economic Inactivity Following a Diagnosis of a Severe Mental Illness: Cohort Study of Electronic Health Records Linked at the Individual-Level, to Census from England.","authors":"L Cybulski, M E Dewey, R Hildersley, C Morgan, R Stewart, M Wuerth, J Das-Munshi","doi":"10.1093/schbul/sbae195","DOIUrl":"10.1093/schbul/sbae195","url":null,"abstract":"<p><strong>Background: </strong>The association of social and clinical indicators with employment, disability, and health outcomes among individuals with severe mental illnesses (SMI) remains unclear. Existing evidence primarily comes from smaller cohort studies limited by shorter follow-up and high attrition, or registry-based research, which lacks information on important social determinants.</p><p><strong>Study design: </strong>We utilized a novel data linkage consisting of clinical records of individuals diagnosed with schizophrenia-spectrum or bipolar disorders from the South London and Maudsley Mental Health Trust, linked at the individual-level to the 2011 UK Census, a rich source for sociodemographic information. Using logistic regression, we estimated adjusted odds ratios (aORs) and 95% confidence intervals to determine associations between socioeconomic and clinical indicators and economic inactivity, self-rated health, and disability outcomes.</p><p><strong>Results: </strong>The sample comprised 8249 people with SMI diagnoses. Economic inactivity (77.3%), disability (68.3%) and poor health (61.1%) were highly prevalent. Longer duration of illness and comorbid substance misuse were associated with economic inactivity, poorer self-rated health, and disability, with associations noted between living alone and all outcomes (aORs and 95% CI: Economic inactivity: 1.72, 1.45-2.03; disability: 1.48, 1.31-1.68; poor health: 1.32, 1.18-1.49). Relative to the White British group, Black African, South Asian, and Other Black groups were more likely to be economically inactive. Black Caribbean and other groups were less likely to report poorer self-rated health or disability.</p><p><strong>Conclusions: </strong>Our findings highlight considerable disability, poorer health, and economic inactivity experienced by people with SMI. Addressing comorbid substance misuse and social isolation could play a role in improving outcomes.</p>","PeriodicalId":21530,"journal":{"name":"Schizophrenia Bulletin","volume":" ","pages":"1367-1379"},"PeriodicalIF":4.8,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12414549/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142751512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Relapse in BDNF Receptors Expression in Patients With a First Episode of Schizophrenia.","authors":"Miquel Bioque, Vicent Llorca-Bofí, Karina S MacDowell, Sílvia Amoretti, Gisela Mezquida, Manuel J Cuesta, Covadonga M Diaz-Caneja, Ángela Ibáñez, Rafael Segarra, Ana González-Pinto, Alexandra Roldán, Pilar A Sáiz, Anna Mané, Antonio Lobo, Albert Martínez-Pinteño, Guillermo Cano-Escalera, Esther Berrocoso, Miquel Bernardo","doi":"10.1093/schbul/sbaf012","DOIUrl":"10.1093/schbul/sbaf012","url":null,"abstract":"<p><strong>Background and hypothesis: </strong>Relapsing after a first episode of schizophrenia (FES) is a main predictor of clinical and functional prognosis. Brain-derived neurotrophic factor (BDNF) plays a critical role in neuronal development and plasticity, and its signaling may be altered by successive relapses.</p><p><strong>Design: </strong>We assessed the impact of first relapse in the expression of the 2 isoforms of the BDNF tropomyosin-related kinase B (TrkB) receptor (active full-length TrkB-F and inactive truncated TrkB-T) in peripheral blood mononuclear cells from 53 FES patients in clinical remission followed up for 3 years.</p><p><strong>Results: </strong>The group of participants that relapsed (n = 24) during the follow-up presented a significant decrease in the expression of the active TrkB-F receptor compared to baseline (M = 100 ± 28.13 vs. M = 83.42 ± 33.84, t = 2.5, P = .02), with no changes in the inactive TrkB-T receptor expression nor in BDNF plasma levels. This decrease also led to a significant decline in the F/T ratio (M = 1.13 ± 0.38 vs. 0.94 ± 0.36, t = 2.17, P = .041). No significant differences were found in the receptors' expression nor in plasma levels in the group of cases that remained in remission (n = 29). These results were not associated with baseline differences between the groups in terms of the BDNF signaling pathway biomarkers, clinical or treatment variables.</p><p><strong>Conclusions: </strong>These findings highlight the biological impact that a relapse produces over the systemic BDNF-TrkB signaling pathway, potentially undermining crucial neuronal functions. Identifying the actors involved can help design specific interventions for relapse prevention and improve the functional prognosis of people in the early stages of schizophrenia.</p>","PeriodicalId":21530,"journal":{"name":"Schizophrenia Bulletin","volume":" ","pages":"1339-1350"},"PeriodicalIF":4.8,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12414558/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143469004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prevention of Antipsychotic-Induced Weight Gain: Beyond Metformin.","authors":"Paula Iruzubieta, Javier Crespo","doi":"10.1093/schbul/sbaf123","DOIUrl":"10.1093/schbul/sbaf123","url":null,"abstract":"","PeriodicalId":21530,"journal":{"name":"Schizophrenia Bulletin","volume":" ","pages":"1180-1181"},"PeriodicalIF":4.8,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12414546/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144848572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}