Molecular Psychiatry最新文献

{"title":"Epigenetic and genetic profiling of comorbidity patterns among substance dependence diagnoses","authors":"Gita A. Pathak, Robert H. Pietrzak, AnnMarie Lacobelle, Cassie Overstreet, Frank R. Wendt, Joseph D. Deak, Eleni Friligkou, Yaira Z. Nunez, Janitza L. Montalvo-Ortiz, Daniel F. Levey, Henry R. Kranzler, Joel Gelernter, Renato Polimanti","doi":"10.1038/s41380-025-03031-y","DOIUrl":"https://doi.org/10.1038/s41380-025-03031-y","url":null,"abstract":"<p>This study investigated the genetic and epigenetic mechanisms underlying the comorbidity of five substance dependence diagnoses (SDs; alcohol, AD; cannabis, CaD; cocaine, CoD; opioid, OD; tobacco, TD). A latent class analysis (LCA) was performed on 22,668 individuals from six cohorts to identify comorbid DSM-IV SD patterns. In subsets of this sample, we tested SD-latent classes with respect to polygenic overlap of psychiatric and psychosocial traits in 7659 individuals of European descent and epigenome-wide changes in 886 individuals of African, European, and Admixed-American descents. The LCA identified four latent classes related to SD comorbidities: AD + TD, CoD + TD, AD + CoD + OD + TD (i.e., polysubstance addiction, PSU), and TD. In the epigenome-wide association analysis, <i>SPATA4</i> cg02833127 was associated with CoD + TD, AD + TD, and PSU latent classes. AD + TD latent class was also associated with CpG sites located on <i>ARID1B</i>, <i>NOTCH1</i>, <i>SERTAD4</i>, and <i>SIN3B</i>, while additional epigenome-wide significant associations with CoD + TD latent class were observed in <i>ANO6</i> and <i>MOV10</i> genes. PSU-latent class was also associated with a differentially methylated region in <i>LDB1</i>. We also observed shared polygenic score (PGS) associations for PSU, AD + TD, and CoD + TD latent classes (i.e., attention-deficit hyperactivity disorder, anxiety, educational attainment, and schizophrenia PGS). In contrast, TD-latent class was exclusively associated with posttraumatic stress disorder-PGS. Other specific associations were observed for PSU-latent class (subjective wellbeing-PGS and neuroticism-PGS) and AD + TD-latent class (bipolar disorder-PGS). In conclusion, we identified shared and unique genetic and epigenetic mechanisms underlying SD comorbidity patterns. These findings highlight the importance of modeling the co-occurrence of SD diagnoses when investigating the molecular basis of addiction-related traits.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"42 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143841364","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":"Cardiovascular diseases and depression: A meta-analysis and Mendelian randomization analysis","authors":"Jun Zeng, Yuting Qiu, Chengying Yang, Xinrong Fan, Xiangyu Zhou, Chunxiang Zhang, Sui Zhu, Yang Long, Yan Wei, Kenji Hashimoto, Lijia Chang","doi":"10.1038/s41380-025-03003-2","DOIUrl":"https://doi.org/10.1038/s41380-025-03003-2","url":null,"abstract":"<p>Depression is a common psychiatric symptom among patients with cardiovascular disease (CVD), adversely affecting their health. Despite the identification of various contributing factors, the precise mechanisms linking CVD and depression remain elusive. This study conducted a meta-analysis to investigate the association between CVD and depression. Furthermore, a bidirectional Mendelian randomization (MR) analysis was undertaken to clarify the causal relationship between the two conditions. The meta-analysis included 39 studies, encompassing 63,444 patients with CVD, 12,308 of whom were diagnosed with depression. The results revealed a significant association between CVD and depression or anxiety, with an estimated overall prevalence of depression in CVD patients of 20.8%. Subgroup analyses showed that the prevalence of depression in patients with coronary artery disease and heart failure was 19.8 and 24.7%, respectively. According to a random-effects model, depressive symptoms were linked to an increase in unadjusted all-cause mortality compared with non-depressed patients. The MR analysis, employing the inverse-variance weighted method as the primary tool for causality assessment, identified significant associations between various CVD types and depression or anxiety phenotypes. These findings underscore the significant relationship between CVD and depression or anxiety, leading to an elevated risk of all-cause mortality. Moreover, the MR analysis provides the first genetically-informed evidence suggesting that depression plays a critical role in the development and progression of certain CVD subtypes. This emphasizes the need for addressing depressive symptoms in CVD patients to prevent or reduce adverse cardiovascular outcomes.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"88 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143847134","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":"Retraction Note: mGluR5 hypofunction is integral to glutamatergic dysregulation in schizophrenia.","authors":"Hoau-Yan Wang, Mathew L MacDonald, Karin E Borgmann-Winter, Anamika Banerjee, Patrick Sleiman, Andrew Tom, Amber Khan, Kuo-Chieh Lee, Panos Roussos, Steven J Siegel, Scott E Hemby, Warren B Bilker, Raquel E Gur, Chang-Gyu Hahn","doi":"10.1038/s41380-025-02986-2","DOIUrl":"https://doi.org/10.1038/s41380-025-02986-2","url":null,"abstract":"","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":" ","pages":""},"PeriodicalIF":9.6,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144020456","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":"Animal studies reveal downregulation of the Beclin-1 autophagy pathway as shared mechanism in Autism Spectrum Disorder: a systematic review and meta-analysis","authors":"A Abromeit, CR Hooijmans, C LeMaoult, CM Drion, MJH Kas","doi":"10.1038/s41380-025-03028-7","DOIUrl":"https://doi.org/10.1038/s41380-025-03028-7","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Background</h3><p>Autism Spectrum Disorder (ASD) is a heterogeneous neurodevelopmental condition with complex etiology, involving genetic and environmental influences on brain development and behavior. Dysregulation of mammalian target of rapamycin (mTOR) signaling alters neuronal growth and synaptic plasticity, and has emerged as a potential underlying pathway in ASD.</p><h3 data-test=\"abstract-sub-heading\">Goal and methods</h3><p>To investigate mTOR dysregulation as a common mechanism in ASD, we performed a systematic review, and a meta-analysis of 192 studies examining mTOR signaling in diverse genetic and environmental animal models.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>Our random-effects model identified significant alterations in mTOR pathway-related proteins. For several proteins (p-AKT, PTEN, p-mTOR, p-EIF4e, LC3-II, p-S6K and p-S6), subgroup analyses revealed clear species-, sex-, age-, or brain region-specific effects. Interestingly, Beclin-1 was consistently downregulated across all subgroups.</p><h3 data-test=\"abstract-sub-heading\">Conclusion</h3><p>Our findings support mTOR-pathway dysregulation in ASD. The observed consistent downregulation of Beclin-1 highlights autophagy as a common mechanism, and provides new leads for novel ASD biomarker and treatment development.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"14 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143841361","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 moderation of genetic risk for ten major psychiatric and substance use disorders by the genetic aptitude for educational attainment","authors":"Kenneth S. Kendler, Henrik Ohlsson, Jan Sundquist, Kristina Sundquist","doi":"10.1038/s41380-025-03022-z","DOIUrl":"https://doi.org/10.1038/s41380-025-03022-z","url":null,"abstract":"<p>We seek to clarify the impact of the Genetic Aptitude for Educational Attainment (GAEA) on risk for 10 psychiatric disorders divided into 4 groups: Internalizing, Externalizing, Eating/Compulsive and Psychotic. Educational attainment and psychiatric and substance use disorder information were obtained from national Swedish registries. GAEA and disorder-specific family genetic risk score (FGRS) were calculated from extended pedigrees. In males, information on IQ and resilience was obtained from the Swedish conscript registry. Affected individuals were born in Sweden from 1973–1995 to Swedish born parents. Controlling for disorder specific FGRS, GAEA were negatively and substantially associated with risk for externalizing and internalizing disorders, minimally associated with psychotic disorder risk and positively and modestly associated with risk for eating/compulsive disorders. While the majority of GAEA effect on risk for externalizing disorders was mediated through impact on IQ, for internalizing disorders, mediation was largely through resilience. For externalizing and internalizing disorders, interactions between GAEA and disorder specific FGRS were robust and negative – the slope of disorder risk with increasing genetic liability was steepest in those with low GAEA. For eating disorders, interactions were modest and positive –the slope of risk with increasing genetic liability being steepest in individuals with high GAEA. We found that the impact of GAEA on risk for psychiatric and substance can be substantial and varies widely across disorders in magnitude, direction, and mediation. GAEA also often interacts, sometimes robustly, with disorder specific genetic risk factors. Comprehensive risk models for psychiatric disorders should consider the inclusion of GAEA.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"64 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143847138","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":"A single-cell genomic atlas for the effects of chronic ethanol exposure in the mouse dorsal striatum","authors":"Erin Wildermuth, Michael S. Patton, Marcia Cortes-Gutierrez, Zeal Jinwala, Benjamin H. Grissom, Rianne R. Campbell, Henry R. Kranzler, Mary Kay Lobo, Seth A. Ament, Brian N. Mathur","doi":"10.1038/s41380-025-03014-z","DOIUrl":"https://doi.org/10.1038/s41380-025-03014-z","url":null,"abstract":"<p>Alcohol use disorder (AUD) is characterized by compulsive drinking, which is thought to be mediated by effects of chronic intermittent ethanol exposure on the dorsal striatum, the input nucleus of the basal ganglia. Despite significant efforts to understand the impact of ethanol on the dorsal striatum, the rich diversity of striatal cell types and multitude of ethanol targets expressed by them necessitates an unbiased, discovery-based approach. In this study, we used single-nuclei RNA-sequencing (snRNA-seq; <i>n</i> = 86,715 cells) to examine the impact of chronic intermittent ethanol exposure on the dorsal striatum in C57BL/6 male and female mice. We detected 462 differentially expressed genes at FDR &lt; 0.05, the majority of which were mapped to spiny projection neurons (SPNs), the most prominent cell type in the striatum. Gene co-expression network analysis and functional annotation of differentially expressed genes revealed down-regulation of postsynaptic intracellular signaling cascades in SPNs. Inflammation-related genes were down-regulated across many neuronal and non-neuronal cell types. Gene set enrichment analyses also pointed to altered states of rare cell types, including the induction of angiogenesis-related genes in vascular cells. A gene module down-regulated specifically in canonical SPNs was enriched for calcium-signaling genes and components of glutamatergic synapses, as well as for genes associated with genetic risk for AUD. Genetic perturbations of six of this module’s hub genes – <i>Foxp1</i>, <i>Bcl11b</i>, <i>Pde10a</i>, <i>Rarb, Rgs9</i>, and <i>Itgr1</i> – had causal effects on its expression in the mouse striatum and/or on the broader set of differentially expressed genes in alcohol-exposed mice. These data provide important clues as to the impact of ethanol on striatal biology and provide a key resource for future investigation.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"30 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143841362","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":"Neocortical tau propagation is a mediator of clinical heterogeneity in Alzheimer’s disease","authors":"Anjalika Chongtham, Aarthi Ramakrishnan, Marissa Farinas, Diede W. M. Broekaart, Joon Ho Seo, Carolyn W. Zhu, Mary Sano, Li Shen, Ana C. Pereira","doi":"10.1038/s41380-025-02998-y","DOIUrl":"https://doi.org/10.1038/s41380-025-02998-y","url":null,"abstract":"<p>Heterogeneity in progression of clinical dementia obstructs the general therapeutic potential of current treatments for Alzheimer’s disease (AD). Though the mechanisms of this heterogeneity remain unclear, the characterization of bioactive tau species and factors that regulate their seeding behavior might give valuable insight as pathological tau is well correlated with cognitive impairment. Here, we conducted an innovative investigation into the molecular basis of widespread, connectivity-based tau propagation that begins in the inferior temporal gyrus (ITG) and spreads to neocortical areas such as the prefrontal cortex (PFC). Biochemical analysis of human postmortem ITG and PFC tissues revealed individual variability in tau seeding, which correlated with cognitive decline, particularly in the ITG, a region known for promoting accelerated tau propagation. Notably, this study presents the first evidence that site-specific phosphorylation and isoform composition of both aggregation-prone high-molecular-weight (HMW) tau and the relatively unexplored, yet potentially crucial in AD progression low-molecular-weight (LMW) tau significantly contribute to tau propagation and cognitive decline. Our findings underscore the importance of comprehensively considering diverse tau forms including both HMW and LMW tau species in understanding AD progression. Additionally, these results are the first to identify distinct morphological strains within the AD brain associated with differing seeding propensity, potentially enabling patient stratification based on their tau profile. Furthermore, RNA-seq analyses of gene expression patterns in the ITG revealed molecular heterogeneity associated with tau seeding potential. Patients with higher levels of seed-competent tau displayed greater impairments in synaptic and neural plasticity, and increased neuroinflammation. This multidisciplinary study offers novel insights into various molecular mechanisms driving AD progression, suggesting potential molecular targets for early intervention and improved patient subtyping, which is critical for developing precision medicine approaches.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"6 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143836920","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":"Harnessing neuroimaging-guided transcranial magnetic stimulation for precision therapy in substance use disorders","authors":"Smita Sahay, Madhu Vishnu Sankar Reddy Rami Reddy, Charlotte Lennox, Emma Wolinsky, Robert E. McCullumsmith, Tanvir Singh","doi":"10.1038/s41380-025-03024-x","DOIUrl":"https://doi.org/10.1038/s41380-025-03024-x","url":null,"abstract":"<p>Substance use disorders (SUDs) are a critical public health challenge characterized by high relapse rates, with existing treatments often proving inadequate. The focus of this review is to provide an update on the current state of transcranial magnetic stimulation (TMS) as a therapeutic intervention for SUDs and discuss neuroimaging-guided TMS practices. This review explores the neurobiology underlying SUDs, emphasizing the roles of the prefrontal cortex, striatal circuits, and dopaminergic pathways, and examines the theory that TMS modulates neurocircuitry to impact addiction-related behaviors. We discuss TMS procedural aspects and provide a comparative analysis of TMS protocols, focusing on repetitive, deep, single-pulse, paired-pulse, and a more recent approach, theta burst stimulation. We review recent randomized clinical trials (RCTs) to demonstrate reductions in cravings and use across SUDs as well as highlight the need for standardized protocols. We emphasize the power of combining neuroimaging techniques to show functional connectivity changes in the brain and identify potential biomarkers predictive of SUD treatment response, an unexplored area of discussion. With these topics, this review highlights the potential of TMS as a versatile and effective therapeutic modality for SUDs, especially when combined with neuroimaging. Key findings emphasize the necessity for future research to address methodological challenges, such as standardizing protocols and optimizing stimulation parameters. The integration of neuroimaging provides insights into functional connectivity changes, enabling enhanced precision and individualized treatment strategies. By validating TMS approaches and incorporating multimodal techniques, this field can advance toward a more robust clinical utility in addressing the complex neurocircuitry of addiction-related behaviors underlying SUDs.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"24 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143841363","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":"Targeted splicing approach for alleviation of a neurexin 1 haploinsufficiency model","authors":"Hong Lu, Kyle M. Roddick, Yuan Ge, Long Zuo, Peng Zhang, Olivia Lam, Klara Marsh, Rachel O. L. Wong, Richard E. Brown, Ann Marie Craig","doi":"10.1038/s41380-025-03017-w","DOIUrl":"https://doi.org/10.1038/s41380-025-03017-w","url":null,"abstract":"<p><i>NRXN1</i> encoding the synaptic organizing protein neurexin 1 (Nrxn1) is among the strongest risk genes for autism spectrum disorders as well as other neuropsychiatric disorders. The most common contributing mutation is a deletion in one allele. While mice lacking one form of the protein, Nrxn1α, have been characterized, information is lacking on animal models with heterozygous deletion of all isoforms, as well as on therapeutic approaches directly targeting Nrxn1. We report that <i>Nrxn1</i>^<i>+/−</i> mice with a deletion affecting all isoforms, α, β and γ, show deficits in excitatory synaptic transmission affecting presynaptic and postsynaptic properties at hippocampal CA3-CA1 synapses, and show increased repetitive behaviors. Based on previous studies indicating that exclusion of the insert at Nrxn1 splice site 5 (S5) boosts synaptic transmission, we tested S5 exclusion as a therapeutic approach. Genetic exclusion of S5 in the remaining <i>Nrxn1</i> allele alleviated the deficits, restoring miniature excitatory postsynaptic current frequency, paired pulse ratio, AMPA/NMDA ratio, and repetitive behaviors to wild type levels and partially restoring Nrxn1 protein level in <i>Nrxn1</i>^{<i>ΔS5/-</i>} compared to <i>Nrxn1</i>^<i>+/−</i> mice. These data suggest that S5 exclusion may be a beneficial therapeutic direction in cases of neuropsychiatric disorders involving <i>NRXN1</i>.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"24 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143832131","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":"Population-level individualized prospective prediction of opioid overdose using machine learning","authors":"Yang S. Liu, Derek V. Pierce, Dan Metes, Yipeng Song, Lawrence Kiyang, Mengzhe Wang, Kathryn Dong, Dean T. Eurich, Scott Patten, Russell Greiner, Yanbo Zhang, Jake Hayward, Andrew Greenshaw, Bo Cao","doi":"10.1038/s41380-025-02992-4","DOIUrl":"https://doi.org/10.1038/s41380-025-02992-4","url":null,"abstract":"<p>The opioid overdose epidemic has rapidly expanded in North America, with rates accelerating during the COVID-19 pandemic. No existing study has demonstrated prospective opioid overdose at a population level. This study aimed to develop and validate a population-level individualized prospective prediction model of opioid overdose (OpOD) using machine learning (ML) and de-identified provincial administrative health data. The OpOD prediction model was based on a cohort of approximately 4 million people in 2017 to predict OpOD cases in 2018 and was subsequently tested on cohort data from 2018, 2019, and 2020 to predict OpOD cases in 2019, 2020, and 2021, respectively. The model’s predictive performance, including balanced accuracy, sensitivity, specificity, and area under the Receiver Operating Characteristics Curve (AUC), was evaluated, achieving a balanced accuracy of 83.7, 81.6, and 85.0% in each respective year. The leading predictors for OpOD, which were derived from health care utilization variables documented by the Canadian Institute for Health Information (CIHI) and physician billing claims, were treatment encounters for drug or alcohol use, depression, neurotic/anxiety/obsessive-compulsive disorder, and superficial skin injury. The main contribution of our study is to demonstrate that ML-based individualized OpOD prediction using existing population-level data can provide accurate prediction of future OpOD cases in the whole population and may have the potential to inform targeted interventions and policy planning.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"24 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143832439","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}