Biological Psychiatry最新文献

{"title":"Editorial Board Page","authors":"","doi":"10.1016/S0006-3223(25)01128-X","DOIUrl":"10.1016/S0006-3223(25)01128-X","url":null,"abstract":"","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":"97 11","pages":"Page A1"},"PeriodicalIF":9.6,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143948504","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":"Unlocking Alzheimer’s Disease Heterogeneity: The Role of Normative Modeling, Dynamic Connectivity, and Beyond","authors":"Qian Wang , Shile Qi , Rongtao Jiang , Jing Sui","doi":"10.1016/j.biopsych.2025.03.017","DOIUrl":"10.1016/j.biopsych.2025.03.017","url":null,"abstract":"","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":"97 11","pages":"Pages 1016-1017"},"PeriodicalIF":9.6,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143947791","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":"Mechanistic and Predictive Implications of Transdiagnostic Features of the Connectome","authors":"Jose M. Rubio, Elvisha Dhamala","doi":"10.1016/j.biopsych.2025.03.009","DOIUrl":"10.1016/j.biopsych.2025.03.009","url":null,"abstract":"","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":"97 11","pages":"Pages 1018-1019"},"PeriodicalIF":9.6,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143947792","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(25)01132-1","DOIUrl":"10.1016/S0006-3223(25)01132-1","url":null,"abstract":"","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":"97 11","pages":"Pages A5-A10"},"PeriodicalIF":9.6,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143947789","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(25)01129-1","DOIUrl":"10.1016/S0006-3223(25)01129-1","url":null,"abstract":"","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":"97 11","pages":"Page A2"},"PeriodicalIF":9.6,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143947787","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":"From Brain Network Dysfunction to Neuropsychiatric Symptoms in Alzheimer’s Disease","authors":"Maria Vasileiadi , Sean Michael Nestor","doi":"10.1016/j.biopsych.2025.03.014","DOIUrl":"10.1016/j.biopsych.2025.03.014","url":null,"abstract":"","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":"97 11","pages":"Pages 1020-1021"},"PeriodicalIF":9.6,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143948000","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":"Postnatal and juvenile fluoxetine treatment evokes sex-specific, opposing effects on mood-related behavior, gene expression, mitochondrial function, and dendritic architecture in the rat medial prefrontal cortex.","authors":"Utkarsha Ghai, Parul Chachra, Suchith Mendon, Balaganesh Janakiraman, Sashaina E Fanibunda, Ambalika Sarkar, Dievya Gohil, Amogh Bhaskaran Jayaprasad, Kowshik Kukkemane, Vivek Singh, Ullas Kolthur-Seetharam, Vidita A Vaidya","doi":"10.1016/j.biopsych.2025.04.026","DOIUrl":"https://doi.org/10.1016/j.biopsych.2025.04.026","url":null,"abstract":"<p><strong>Background: </strong>Serotonin shapes emotional neurocircuit development, and serotonergic neurotransmission is implicated in both the pathophysiology and treatment of neuropsychiatric disorders. The selective serotonin reuptake inhibitor, fluoxetine (Flx) is a common first-line treatment for childhood and adolescent mood disorders given a favourable risk-benefit profile. Using a rodent model we addressed specific long-term behavioral, molecular, bioenergetic and cytoarchitectural consequences of postnatal (PNFlx) and juvenile (JFlx) fluoxetine treatment.</p><p><strong>Methods: </strong>Rat pups received PNFlx (postnatal day 2: P2-P21) or JFlx (P28-48) treatment with the impact on anxiety- and despair-like behavior examined in adulthood, along with assessing global gene expression, mitochondrial function, and dendritic cytoarchitecture in the medial prefrontal cortex (mPFC).</p><p><strong>Results: </strong>PNFlx and JFlx evoked long-lasting, opposing changes in anxiety- and despair-like behavior in male, but not female, rats. The PNFlx- and JFlx-evoked increase and decrease in anxiety- and despair-like behavior respectively, were accompanied by distinctive, minimally overlapping, transcriptional changes in the mPFC in adulthood. Furthermore, we noted starkly differing outcomes of PNFlx and JFlx on mitochondrial function and dendritic cytoarchitecture in the mPFC. The PNFlx evoked despair-like behavior was reversed by adult-onset treatment with nicotinamide, a NAD⁺precursor that enhances mitochondrial bioenergetics.</p><p><strong>Conclusions: </strong>Collectively, our findings highlight distinct developmental epochs wherein fluoxetine exposure can program long-term, sex-specific, opposing outcomes on mood-related behavior, accompanied by persistent changes in gene expression, mitochondrial function and neuronal cytoarchitecture in the mPFC in adulthood. This motivates future studies to examine a potential role for altered bioenergetics in shaping the differential impact of early fluoxetine treatment on emotionality.</p>","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":" ","pages":""},"PeriodicalIF":9.6,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143964183","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":"Parsing clinical and neurobiological sources of heterogeneity in depression.","authors":"Kayla Hannon, Ty Easley, Wei Zhang, Daphne Lew, Aristeidis Sotiras, Yvette I Sheline, Andre Marquand, Deanna M Barch, Janine D Bijsterbosch","doi":"10.1016/j.biopsych.2025.04.025","DOIUrl":"https://doi.org/10.1016/j.biopsych.2025.04.025","url":null,"abstract":"<p><strong>Background: </strong>Patients with depression vary from one-another in their clinical and neuroimaging presentation, yet the relationship between clinical and neuroimaging sources of variation is poorly understood. Determining sources of heterogeneity in depression is important to gain insights into its diverse and complex neural etiology. This study aims to test if depression heterogeneity is characterized by subgroups that differ both clinically and neurobiologically and/or whether multiple neuroimaging profiles give rise to the same clinical presentation.</p><p><strong>Methods: </strong>This study utilizes population-based data from the UK Biobank over multiple imaging sites. Clinically dissociated groups were selected to isolate clinical characteristics of depression (symptoms of anhedonia, depressed mood, and somatic disturbance; severity indices of lifetime chronicity and acute impairment; and late onset). Residual neuroimaging heterogeneity within each group was assessed using neuroimaging driven clustering.</p><p><strong>Results: </strong>The clinically dissociated subgroups had significantly larger neuroimaging normative deviations than a comparison heterogeneous group and had distinct neuroimaging profiles from each other. Imaging driven clustering within each clinically dissociated group identified two stable subtypes within the acute impairment group that differed significantly in cognitive ability, despite identical clinical profiles.</p><p><strong>Conclusions: </strong>The study identified distinct neuroimaging profiles related to particular clinical depression features that may explain inconsistencies in the literature and sub-clusters within the acute impairment group with cognitive differences that were only differentiable by neuroimaging. Our results provide evidence that multiple neuroimaging profiles may give rise to the same clinical presentation, emphasizing the presence of complex interactions between clinical and neuroimaging sources of heterogeneity.</p>","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":" ","pages":""},"PeriodicalIF":9.6,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143960624","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":"Generative Artificial Intelligence Models for Developing Neuroimaging Markers of Psychiatric Disorders.","authors":"Chadi G Abdallah, David van Dijk","doi":"10.1016/j.biopsych.2025.05.002","DOIUrl":"10.1016/j.biopsych.2025.05.002","url":null,"abstract":"","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":" ","pages":""},"PeriodicalIF":9.6,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143960896","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":"Thalamo-cortical structural co-variation networks are related to familial risk for schizophrenia in the context of lower nuclei volume estimates in patients: an ENIGMA study.","authors":"Annalisa Lella, Linda A Antonucci, Roberta Passiatore, Loredana Bellantuono, Pierluigi Selvaggi, Teresa Popolizio, Guido Di Sciascio, Alessandro Saponaro, Patrizia Ricci, Mario Altamura, Giuseppe Blasi, Antonio Rampino, Chris Vriend, Vince D Calhoun, Kelly Rootes-Murdy, Aaron L Goldman, Inmaculada Baeza, Josefina Castro-Fornieles, Gisela Sugranyes, Elena De la Serna, Edith Pomarol-Clotet, Mar Fatjó-Vilas, Raymond Salvador, Andriana Karuk, Paola Fuentes-Claramonte, David C Glahn, Amanda L Rodrigue, John Blangero, Lei Wang, Taeyoung Lee, Karolin E Einenkel, Saskia Hamers, Oliver Gruber, Adrian Preda, Young-Chul Chung, Soyolsaikhan Odkhuu, Corentin Vallée, Paola Dazzan, Machteld Marcelis, Stijn Michielse, Katharina Brosch, Frederike Stein, Igor Nenadić, Benjamin Straube, Florian Thomas-Odenthal, Tilo Kircher, Sean Carruthers, Susan L Rossell, Phillip J Sumner, Tamsyn E Van Rheenen, Caroline Demro, Ian S Ramsay, Scott R Sponheim, Rebekka Lencer, Susanne Meinert, Tim Hahn, Udo Dannlowski, Dominik Grotegerd, Mariateresa Ciccarelli, Felice Iasevoli, Giuseppe Pontillo, Godfrey D Pearlson, Derin Cobia, Fabrizio Piras, Nerisa Banaj, Daniela Vecchio, Marjolein E A Barendse, Neeltje E M van Haren, Hang Joon Jo, Kang Sim, Yann Quidé, Melissa J Green, Rachael Slate, Giacomo Cecere, Wolfgang Omlor, Stephanie Homan, Philipp Homan, Sophia I Thomopoulos, Jessica A Turner, Theo G M van Erp, Paul M Thompson, Alessandro Bertolino, Giulio Pergola","doi":"10.1016/j.biopsych.2025.03.027","DOIUrl":"https://doi.org/10.1016/j.biopsych.2025.03.027","url":null,"abstract":"<p><strong>Background: </strong>Structural brain differences in the thalamus and the cortex have been widely reported in schizophrenia (SCZ) relative to neurotypical controls (NC). Most prior studies examined the thalamus as a whole, single region-of-interest. Additionally, findings in individuals at familial high-risk for schizophrenia (FHR) remain inconclusive. Here, we investigated whether local and network-wide thalamic-related structural alterations vary as a function of familial risk for schizophrenia.</p><p><strong>Methods: </strong>Structural MRI scans were obtained from 5,197 participants (3,409 NC, 257 FHR, 1,531 SCZ) across 32 cross-sectional samples within the ENIGMA Consortium. Random-effects meta-analyses, and network analyses were conducted on (i) local thalamic alterations (volume estimates of seven thalamic subdivisions), and (ii) network-wide thalamic alterations (thickness and surface-related thalamo-cortical/cortico-cortical co-variation patterns) across groups (NC, FHR, SCZ).</p><p><strong>Results: </strong>Individuals with SCZ showed significantly lower gray matter volume estimates in the anterior, pulvinar, medial, posterior, and ventral thalamic subdivisions compared to NC (q_FDR<0.05). FHR did not differ from NC. At the network-wide level, thalamo-cortical co-variations discriminated FHR from NC (q_FDR<0.05), with FHR showing intermediate co-variation between SCZ and NC. Cortico-cortical co-variation patterns revealed that SCZ and FHR shared similarly disconnected clustering configurations, distinct from NC (q_FDR<0.05).</p><p><strong>Conclusions: </strong>Results revealed lower thalamic volume estimates in SCZ but not in FHR, hence yielding no evidence of a familial risk trait, whereas thalamo-cortical and cortico-cortical co-variation estimates were associated with familial risk for SCZ These findings suggest that, once the thalamus is parsed into subdivisions, network-wide thalamo-cortical features may identify trait-dependent, neurobiological correlates of genetic risk for SCZ.</p>","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":" ","pages":""},"PeriodicalIF":9.6,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143958189","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}