Biological Psychiatry最新文献

{"title":"Increasing the Interpretability of Psychosis Models","authors":"Justin Buck , Guillermo Horga","doi":"10.1016/j.biopsych.2024.10.022","DOIUrl":"10.1016/j.biopsych.2024.10.022","url":null,"abstract":"","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":"97 2","pages":"Pages 99-101"},"PeriodicalIF":9.6,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142811945","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":"Decoding Early Psychoses: Unraveling Stable Microstructural Features Associated With Psychopathology Across Independent Cohorts","authors":"Haley R. Wang ,&nbsp;Zhen-Qi Liu ,&nbsp;Hajer Nakua ,&nbsp;Catherine E. Hegarty ,&nbsp;Melanie Blair Thies ,&nbsp;Pooja K. Patel ,&nbsp;Charles H. Schleifer ,&nbsp;Thomas P. Boeck ,&nbsp;Rachel A. McKinney ,&nbsp;Danielle Currin ,&nbsp;Logan Leathem ,&nbsp;Pamela DeRosse ,&nbsp;Carrie E. Bearden ,&nbsp;Bratislav Misic ,&nbsp;Katherine H. Karlsgodt","doi":"10.1016/j.biopsych.2024.06.011","DOIUrl":"10.1016/j.biopsych.2024.06.011","url":null,"abstract":"<div><h3>Background</h3><div>Patients with early psychosis (EP) (within 3 years after psychosis onset) show significant variability, which makes predicting outcomes challenging. Currently, little evidence exists for stable relationships between neural microstructural properties and symptom profiles across EP diagnoses, which limits the development of early interventions.</div></div><div><h3>Methods</h3><div>A data-driven approach, partial least squares correlation, was used across 2 independent datasets to examine multivariate relationships between white matter properties and symptomatology and to identify stable and generalizable signatures in EP. The primary cohort included patients with EP from the Human Connectome Project for Early Psychosis (<em>n</em> = 124). The replication cohort included patients with EP from the Feinstein Institute for Medical Research (<em>n</em> = 78) as part of the MEND (Multimodal Evaluation of Neural Disorders) Project. Both samples included individuals with schizophrenia, schizoaffective disorder, and psychotic mood disorders.</div></div><div><h3>Results</h3><div>In both cohorts, a significant latent component corresponded to a symptom profile that combined negative symptoms, primarily diminished expression, with specific somatic symptoms. Both latent components captured comprehensive features of white matter disruption, primarily a combination of subcortical and frontal association fibers. Strikingly, the partial least squares model trained on the primary cohort accurately predicted microstructural features and symptoms in the replication cohort. Findings were not driven by diagnosis, medication, or substance use.</div></div><div><h3>Conclusions</h3><div>This data-driven transdiagnostic approach revealed a stable and replicable neurobiological signature of microstructural white matter alterations in EP across diagnoses and datasets, showing strong covariance of these alterations with a unique profile of negative and somatic symptoms. These findings suggest the clinical utility of applying data-driven approaches to reveal symptom domains that share neurobiological underpinnings.</div></div>","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":"97 2","pages":"Pages 167-177"},"PeriodicalIF":9.6,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141440167","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":"Unique Functional Neuroimaging Signatures of Genetic Versus Clinical High Risk for Psychosis","authors":"Charles H. Schleifer ,&nbsp;Sarah E. Chang ,&nbsp;Carolyn M. Amir ,&nbsp;Kathleen P. O’Hora ,&nbsp;Hoki Fung ,&nbsp;Jee Won D. Kang ,&nbsp;Leila Kushan-Wells ,&nbsp;Eileen Daly ,&nbsp;Fabio Di Fabio ,&nbsp;Marianna Frascarelli ,&nbsp;Maria Gudbrandsen ,&nbsp;Wendy R. Kates ,&nbsp;Declan Murphy ,&nbsp;Jean Addington ,&nbsp;Alan Anticevic ,&nbsp;Kristin S. Cadenhead ,&nbsp;Tyrone D. Cannon ,&nbsp;Barbara A. Cornblatt ,&nbsp;Matcheri Keshavan ,&nbsp;Daniel H. Mathalon ,&nbsp;Carrie E. Bearden","doi":"10.1016/j.biopsych.2024.08.010","DOIUrl":"10.1016/j.biopsych.2024.08.010","url":null,"abstract":"<div><h3>Background</h3><div>22q11.2 deletion syndrome (22qDel) is a copy number variant that is associated with psychosis and other neurodevelopmental disorders. Adolescents who are at clinical high risk for psychosis (CHR) are identified based on the presence of subthreshold psychosis symptoms. Whether common neural substrates underlie these distinct high-risk populations is unknown. We compared functional brain measures in 22qDel and CHR cohorts and mapped the results to biological pathways.</div></div><div><h3>Methods</h3><div>We analyzed 2 large multisite cohorts with resting-state functional magnetic resonance imaging data: 1) a 22qDel cohort (<em>n</em> = 164, 47% female) and typically developing (TD) control participants (<em>n</em> = 134, 56% female); and 2) a cohort of CHR individuals (<em>n</em> = 240, 41% female) and TD control participants (<em>n</em> = 149, 46% female) from the NAPLS-2 (North American Prodrome Longitudinal Study-2). We computed global brain connectivity (GBC), local connectivity (LC), and brain signal variability (BSV) across cortical regions and tested case-control differences for 22qDel and CHR separately. Group difference maps were related to published brain maps using autocorrelation-preserving permutation.</div></div><div><h3>Results</h3><div>BSV, LC, and GBC were significantly disrupted in individuals with 22qDel compared with TD control participants (false discovery rate–corrected <em>q</em> &lt; .05). Spatial maps of BSV and LC differences were highly correlated with each other, unlike GBC. In the CHR group, only LC was significantly altered versus the control group, with a different spatial pattern than the 22qDel group. Group differences mapped onto biological gradients, with 22qDel effects being strongest in regions with high predicted blood flow and metabolism.</div></div><div><h3>Conclusions</h3><div>22qDel carriers and CHR individuals exhibited different effects on functional magnetic resonance imaging temporal variability and multiscale functional connectivity. In 22qDel carriers, strong and convergent disruptions in BSV and LC that were not seen in CHR individuals suggest distinct functional brain alterations.</div></div>","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":"97 2","pages":"Pages 178-187"},"PeriodicalIF":9.6,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142054847","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 Computational Account of the Development and Evolution of Psychotic Symptoms","authors":"Albert Powers ,&nbsp;Phillip A. Angelos ,&nbsp;Alexandria Bond ,&nbsp;Emily Farina ,&nbsp;Carolyn Fredericks ,&nbsp;Jay Gandhi ,&nbsp;Maximillian Greenwald ,&nbsp;Gabriela Hernandez-Busot ,&nbsp;Gabriel Hosein ,&nbsp;Megan Kelley ,&nbsp;Catalina Mourgues ,&nbsp;William Palmer ,&nbsp;Julia Rodriguez-Sanchez ,&nbsp;Rashina Seabury ,&nbsp;Silmilly Toribio ,&nbsp;Raina Vin ,&nbsp;Jeremy Weleff ,&nbsp;Scott Woods ,&nbsp;David Benrimoh","doi":"10.1016/j.biopsych.2024.08.026","DOIUrl":"10.1016/j.biopsych.2024.08.026","url":null,"abstract":"<div><div>The mechanisms of psychotic symptoms such as hallucinations and delusions are often investigated in fully formed illness, well after symptoms emerge. These investigations have yielded key insights but are not well positioned to reveal the dynamic forces underlying symptom formation itself. Understanding symptom development over time would allow us to identify steps in the pathophysiological process leading to psychosis, shifting the focus of psychiatric intervention from symptom alleviation to prevention. We propose a model for understanding the emergence of psychotic symptoms within the context of an adaptive, developing neural system. We make the case for a pathophysiological process that begins with cortical hyperexcitability and bottom-up noise transmission, which engenders inappropriate belief formation via aberrant prediction error signaling. We argue that this bottom-up noise drives learning about the (im)precision of new incoming sensory information because of diminished signal-to-noise ratio, causing a compensatory relative overreliance on prior beliefs. This overreliance on priors predisposes to hallucinations and covaries with hallucination severity. An overreliance on priors may also lead to increased conviction in the beliefs generated by bottom-up noise and drive movement toward conversion to psychosis. We identify predictions of our model at each stage, examine evidence to support or refute those predictions, and propose experiments that could falsify or help select between alternative elements of the overall model. Nesting computational abnormalities within longitudinal development allows us to account for hidden dynamics among the mechanisms driving symptom formation and to view established symptoms as a point of equilibrium among competing biological forces.</div></div>","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":"97 2","pages":"Pages 117-127"},"PeriodicalIF":9.6,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142280063","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 Contribution of Mosaic Chromosomal Alterations to Schizophrenia","authors":"Kaihui Chang ,&nbsp;Xuemin Jian ,&nbsp;Chuanhong Wu ,&nbsp;Chengwen Gao ,&nbsp;Yafang Li ,&nbsp;Jianhua Chen ,&nbsp;Baiqiang Xue ,&nbsp;Yonghe Ding ,&nbsp;Lixia Peng ,&nbsp;Baokun Wang ,&nbsp;Lin He ,&nbsp;Yifeng Xu ,&nbsp;Changgui Li ,&nbsp;Xingwang Li ,&nbsp;Zhuo Wang ,&nbsp;Xiangzhong Zhao ,&nbsp;Dun Pan ,&nbsp;Qiangzhen Yang ,&nbsp;Juan Zhou ,&nbsp;Zijia Zhu ,&nbsp;Zhiqiang Li","doi":"10.1016/j.biopsych.2024.06.015","DOIUrl":"10.1016/j.biopsych.2024.06.015","url":null,"abstract":"<div><h3>Background</h3><div>Mosaic chromosomal alterations are implicated in neuropsychiatric disorders, but the contribution to schizophrenia (SCZ) risk for somatic copy number variations (sCNVs) emerging in early developmental stages has not been fully established.</div></div><div><h3>Methods</h3><div>We analyzed blood-derived genotype arrays from 9715 patients with SCZ and 28,822 control participants of Chinese descent using a computational tool (MoChA) based on long-range chromosomal information to detect mosaic chromosomal alterations. We focused on probable early developmental sCNVs through stringent filtering. We assessed the burden of sCNVs across varying cell fraction cutoffs, as well as the frequency with which genes were involved in sCNVs. We integrated this data with the PGC (Psychiatric Genomics Consortium) dataset, which comprises 12,834 SCZ cases and 11,648 controls of European descent, and complemented it with genotyping data from postmortem brain tissue of 936 participants (449 cases and 487 controls).</div></div><div><h3>Results</h3><div>Patients with SCZ had a significantly higher somatic losses detection rate than control participants (1.00% vs. 0.52%; odds ratio = 1.91; 95% CI, 1.47–2.49; two-sided Fisher’s exact test, <em>p</em> = 1.49 × 10⁻⁶). Further analysis indicated that the odds ratios escalated proportionately (from 1.91 to 2.78) with the increment in cell fraction cutoffs. Recurrent sCNVs associated with SCZ (odds ratio &gt; 8; Fisher’s exact test, <em>p</em> &lt; .05) were identified, including notable regions at 10q21.1 (<em>ZWINT</em>), 3q26.1 (<em>SLITRK3</em>), 1q31.1 (<em>BRINP3</em>) and 12q21.31-21.32 (<em>MGAT4C</em> and <em>NTS</em>) in the Chinese cohort, and some regions were validated with PGC data. Cross-tissue validation pinpointed somatic losses at loci like 1p35.3-35.2 and 19p13.3-13.2.</div></div><div><h3>Conclusions</h3><div>The study highlights the significant impact of mosaic chromosomal alterations on SCZ, suggesting their pivotal role in the disorder’s genetic etiology.</div></div>","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":"97 2","pages":"Pages 198-207"},"PeriodicalIF":9.6,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141465944","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":"Guide for Authors","authors":"","doi":"10.1016/S0006-3223(24)01802-X","DOIUrl":"10.1016/S0006-3223(24)01802-X","url":null,"abstract":"","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":"97 4","pages":"Pages A5-A10"},"PeriodicalIF":9.6,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143137531","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":"Clinical Phenotypes Associated With White Matter Microstructural Abnormalities Across Early Psychoses","authors":"Godfrey D. Pearlson","doi":"10.1016/j.biopsych.2024.11.001","DOIUrl":"10.1016/j.biopsych.2024.11.001","url":null,"abstract":"","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":"97 2","pages":"Pages 102-103"},"PeriodicalIF":9.6,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142811942","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 Future of Schizophrenia Care: A Lived Experience–Based Call for Innovation","authors":"Brandon Staglin","doi":"10.1016/j.biopsych.2024.09.013","DOIUrl":"10.1016/j.biopsych.2024.09.013","url":null,"abstract":"","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":"97 2","pages":"Pages 107-108"},"PeriodicalIF":9.6,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142340639","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":"Mosaic Chromosomal Alterations/Somatic Copy Number Variations: A New Frontier in Genetic Association Studies of Complex Diseases","authors":"Dawei Li","doi":"10.1016/j.biopsych.2024.10.023","DOIUrl":"10.1016/j.biopsych.2024.10.023","url":null,"abstract":"","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":"97 2","pages":"Pages 104-106"},"PeriodicalIF":9.6,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142811896","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":"Subscribers Page","authors":"","doi":"10.1016/S0006-3223(24)01799-2","DOIUrl":"10.1016/S0006-3223(24)01799-2","url":null,"abstract":"","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":"97 4","pages":"Page A2"},"PeriodicalIF":9.6,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143137533","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}