Biological psychiatry global open science最新文献

{"title":"Bridging the Poles: What the Transcranial Magnetic Stimulation Evidence Tells Us About Bipolar Depression","authors":"Véronique Desbeaumes Jodoin","doi":"10.1016/j.bpsgos.2025.100657","DOIUrl":"10.1016/j.bpsgos.2025.100657","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100657"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145712294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Considerations for Neural Cannabis Cue-Reactivity Studies in Individuals With Cannabis Use Disorder","authors":"Erica N. Grodin , Kaitlin McManus","doi":"10.1016/j.bpsgos.2025.100669","DOIUrl":"10.1016/j.bpsgos.2025.100669","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100669"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145978094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increased Tumor Necrosis Factor Superfamily Members in Neuroinflammatory Schizophrenia and Bipolar Disorder Midbrains","authors":"Gerardo Mendez-Victoriano ,&nbsp;Yunting Zhu ,&nbsp;Layla Neuhaus ,&nbsp;Suhaana Shaik ,&nbsp;Frank Middleton ,&nbsp;Yuji Kondo ,&nbsp;Amir Fayyazuddin ,&nbsp;Daniel Hoeppner ,&nbsp;Sofía Puvogel ,&nbsp;Astrid Alsema ,&nbsp;Laura Kracht ,&nbsp;Mitsuyuki Matsumoto ,&nbsp;Bart J.L. Eggen ,&nbsp;Adam K. Walker ,&nbsp;Maree J. Webster ,&nbsp;Iris E.C. Sommer ,&nbsp;Cynthia S. Weickert","doi":"10.1016/j.bpsgos.2025.100650","DOIUrl":"10.1016/j.bpsgos.2025.100650","url":null,"abstract":"<div><h3>Background</h3><div>Neuroinflammation is a key neuropathological finding in schizophrenia and bipolar disorder, as increased cytokines are found in the midbrain of these individuals. However, the most upregulated inflammatory cytokines and most activated downstream signaling pathway(s) are unidentified.</div></div><div><h3>Methods</h3><div>We aimed to identify the most robust transcriptional change in the schizophrenia midbrain by bulk RNA sequencing (RNA-seq) and to confirm the cellular source and magnitude of change by single-nucleus RNA-seq, reverse transcriptase–polymerase chain reaction (RT-PCR), and immunohistochemistry in 61 healthy controls, 63 schizophrenia cases, and 33 bipolar disorder cases stratified into low- and high-inflammation groups.</div></div><div><h3>Results</h3><div>By RNA-seq, the TNF superfamily (TNFSF) pathway messenger RNAs (mRNAs) were among the most changed in high-inflammation schizophrenia (all <em>p</em>s ≤ .01), with TNFSF receptors (<em>TNFR1</em>, <em>TNFR2</em>, and <em>FAS</em>) being most highly expressed in astrocytes and microglia. Using RT-PCR, we confirmed that 5 TNFSF receptor mRNAs (<em>TNFR</em><em>1</em>, <em>TNFR</em><em>2</em>, <em>DR4</em>, <em>FAS</em>, and <em>TWEAKR</em>, all <em>p</em>s ≤ .01) were increased in high-inflammation schizophrenia/bipolar disorder cases compared with low-inflammation controls. Furthermore, the means for mRNA encoding cell death–related proteins acting downstream of TNF receptors (<em>P53</em>, <em>CASP1</em>, <em>CASP7</em>, <em>CASP8</em>; all <em>p</em>s ≤ .05) were increased in high-inflammation schizophrenia, as were mRNAs encoding proteins regulating cell survival (<em>BCL2</em> and <em>MCL1</em>, all <em>p</em>s ≤ .01). All 5 TNFSF receptor mRNAs positively correlated with effector protein mRNAs (all <em>p</em>s ≤ .05) and with the astrocyte-related marker <em>GFAP</em> mRNA (all <em>p</em>s ≤ .001).</div></div><div><h3>Conclusions</h3><div>Our results suggest that TNFSF transcripts represent the main activated inflammatory pathway in the midbrains of people with schizophrenia, which overlaps somewhat with bipolar disorder. These findings highlight the need for anti-inflammatory interventions targeting TNF/TNFSF receptors to test for therapeutic benefits in psychiatric patients displaying elevated inflammation.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100650"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute Estradiol Bridges Gut Microbiome Composition With Cognition","authors":"Georgia E. Hodes,&nbsp;Dawson R. Kropp","doi":"10.1016/j.bpsgos.2025.100662","DOIUrl":"10.1016/j.bpsgos.2025.100662","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100662"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145885179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mineralocorticoid Receptor in Glutamatergic Neurons Modulates Anxiety Exclusively in Male Mice Via Regulation of the Actin-Bundling Factor Fam107a","authors":"Huanqing Yang ,&nbsp;Sowmya Narayan ,&nbsp;Joeri Bordes ,&nbsp;Lotte van Doeselaar ,&nbsp;Carlo De Donno ,&nbsp;Matthias Eder ,&nbsp;Danusa Menegaz ,&nbsp;Rosa-Eva Huettl ,&nbsp;Lea-Maria Brix ,&nbsp;Shiladitya Mitra ,&nbsp;Margherita Springer ,&nbsp;Marianne B. Müller ,&nbsp;Alon Chen ,&nbsp;Jan M. Deussing ,&nbsp;Juan Pablo Lopez ,&nbsp;Mathias V. Schmidt","doi":"10.1016/j.bpsgos.2025.100651","DOIUrl":"10.1016/j.bpsgos.2025.100651","url":null,"abstract":"<div><h3>Background</h3><div>Exposure to stressful life events is a major risk factor for many psychiatric disorders. The mineralocorticoid receptor (MR) is a key regulator of the hypothalamic-pituitary-adrenal axis, a central stress response component. Stress-related mental disorders, such as anxiety and depression, are associated with MR dysfunction in the brain, but its cell type–specific contributions to emotional behavior and cognitive function remain unclear.</div></div><div><h3>Methods</h3><div>Using a mouse model with a specific deletion of MR in forebrain glutamatergic neurons, we tested the behavioral, structural, and functional impact of MR in this neuronal population (<em>n</em> = 9–14 for behavioral and <em>n</em> = 3–4 for structural and functional analyses).</div></div><div><h3>Results</h3><div>We revealed a specific function of MR in regulating baseline anxiety in male but not female mice. This distinct behavioral phenotype was associated with hippocampal structural and functional alterations. Furthermore, we identified a previously unrecognized downstream target of MR, the actin-bundling factor Fam107a, whose expression is tightly regulated by MR. Overexpression of Fam107a in the hippocampus was sufficient to rescue the increased anxiety phenotype of glutamatergic MR knockout mice.</div></div><div><h3>Conclusions</h3><div>Together, our results underline the central role of MR as a potential target in understanding the intricate interplay between stress, resilience, and mental health.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100651"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145885178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Socioeconomic Status Is Associated With Reward Processing, Interleukin 1β, Striatal Connectivity, and Antidepressant Outcomes in Individuals With Major Depressive Disorder: A CAN-BIND-1 Report","authors":"Sara Jani ,&nbsp;Stefanie Hassel ,&nbsp;Jane A. Foster ,&nbsp;Gustavo Turecki ,&nbsp;Nicholas Bock ,&nbsp;Nathan Churchill ,&nbsp;Daniel J. Mueller ,&nbsp;Raymond W. Lam ,&nbsp;Valerie H. Taylor ,&nbsp;Roumen Milev ,&nbsp;Claudio Soares ,&nbsp;Susan Rotzinger ,&nbsp;Sakina J. Rizvi ,&nbsp;Sidney H. Kennedy ,&nbsp;Benicio N. Frey ,&nbsp;Katharine Dunlop","doi":"10.1016/j.bpsgos.2025.100649","DOIUrl":"10.1016/j.bpsgos.2025.100649","url":null,"abstract":"<div><h3>Background</h3><div>Major depressive disorder (MDD) is a common condition with heterogeneous risk factors. Socioeconomic status (SES) is one such risk factor, which is negatively linked to MDD treatment outcomes and symptom severity. SES is associated with altered resting-state functional connectivity (RSFC) in reward-processing circuitry and elevated proinflammatory cytokine levels in individuals without depression. However, how the negative consequences of low SES exacerbate MDD psychopathology is poorly understood.</div></div><div><h3>Methods</h3><div>Data on SES (household income and education), depression severity, self-reported reward processing, serum proinflammatory cytokine levels, and neuroimaging for 323 adult participants (211 patients with MDD receiving open-label escitalopram, 112 control participants without depression; 63.4% female) were obtained from the CAN-BIND-1 (Canadian Biomarker Integration in Depression Study-1) dataset. General linear models assessed the effects of MDD diagnosis and SES on self-reported reward processing and proinflammatory cytokine levels. Whole-brain seed-to-voxel RSFC analyses were performed for the dorsal and ventral striatum leveraging 249 participants (150 patients with MDD, 99 control participants; 62.2% female). We also assessed the impact of SES on response to open-label escitalopram.</div></div><div><h3>Results</h3><div>Participants with MDD from households with lower incomes displayed lower goal pursuit behaviors, decreased interleukin 1β levels, and slower improvement to escitalopram relative to those from households with higher incomes. Using a lenient <em>z</em> &gt; 2.3 threshold, MDD household income correlated with striatal RSFC with the dorsolateral prefrontal and posterior cingulate cortices.</div></div><div><h3>Conclusions</h3><div>Our results elucidate the role of SES and its negative consequences in altering reward processing and antidepressant treatment efficacy in MDD, corroborating previous literature suggesting that SES significantly impacts health outcomes. Better characterizing the relationship between SES and MDD psychopathology may inform future treatment approaches and intervention development.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100649"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145798708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early Pubertal Development Is a Risk Factor for Psychotic-Like Experiences in Boys and Girls","authors":"Eric R. Larson ,&nbsp;Natasha Chaku ,&nbsp;Alexandra Moussa-Tooks","doi":"10.1016/j.bpsgos.2025.100647","DOIUrl":"10.1016/j.bpsgos.2025.100647","url":null,"abstract":"<div><h3>Background</h3><div>Puberty has long been identified as a risk factor for psychosis, although retrospective, cross-sectional, and single-sex indicators of puberty have limited our ability to pinpoint biopsychosocial mechanisms contributing to risk. The current study determined whether individual differences in the timing (onset) and tempo (pace) of pubertal development conferred risk for psychotic-like experiences (PLEs) in youth across biological sex.</div></div><div><h3>Methods</h3><div>Data included 11,758 youths (6134 boys and 5624 girls) from the ABCD (Adolescent Brain Cognitive Development) Study (average age = 9.9 years at baseline, 12.9 years at 3-year follow-up). Pubertal timing and tempo (overall, adrenarche, gonadarche) were derived from sex-specific linear mixed-effects models using the Pubertal Development Scale. Sex-specific negative binomial multilevel models estimated effects of categorical and continuously measured pubertal timing and tempo and their interaction on year-3 PLEs per the Prodromal Questionnaire-Brief Child.</div></div><div><h3>Results</h3><div>In both sexes, earlier pubertal timing was associated with elevated PLEs (βs = 0.23 to 0.31), and later pubertal timing was associated with fewer PLEs (βs = −0.22 to −0.52) relative to on-time peers. In boys only, faster pubertal tempo was associated with fewer PLEs relative to on-track peers (βs = −0.21 to −0.30). Analyses with continuous pubertal timing and tempo demonstrated an association between earlier adrenarchal timing and more PLEs in girls only (β = −0.21) and an interaction between adrenarchal timing and tempo in boys only (β = −0.80).</div></div><div><h3>Conclusions</h3><div>Early pubertal timing in both sexes and faster pubertal tempo in males increases PLEs. Understanding the unique experiences associated with a youth’s pubertal maturation, particularly adrenarche, can advance identification and prevention efforts for children and adolescents at greatest clinical risk.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100647"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145841259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the Genetic Overlap Between Metabolic Traits and Anorexia Nervosa","authors":"Danielle M. Adams ,&nbsp;Murray J. Cairns","doi":"10.1016/j.bpsgos.2025.100678","DOIUrl":"10.1016/j.bpsgos.2025.100678","url":null,"abstract":"<div><h3>Background</h3><div>Anorexia nervosa (AN) is an eating disorder with complex biology that remains largely uncharacterized. Recent genome-wide association studies have identified genetic associations between metabolic traits and AN that may relate to the underlying pathophysiology of the condition. Moreover, observational studies have identified evidence of dysregulated metabolic traits in AN, with emerging evidence suggesting that some of these findings are also observed in weight-restored individuals. While there is evidence for putative shared genetic factors linking metabolic traits and AN, the biology underpinning these genetic relationships has not been thoroughly investigated.</div></div><div><h3>Methods</h3><div>To further explore shared genetic architecture between metabolic traits and AN with regional specificity, we investigated spatially localized genetic correlation and Bayesian colocalization between 6 metabolic traits (body mass index, high-density lipoprotein, leptin, fasting insulin, insulin resistance, and type 2 diabetes) (<em>n</em> = 30,931–659,316) and AN (<em>n</em> = 72,517).</div></div><div><h3>Results</h3><div>Significant local genetic correlation was identified across 60 regions, between genetic liability to AN and one of the 6 metabolic traits, after Benjamini-Hochberg correction. Three of these regions showed strong evidence of colocalization with a shared variant (posterior probability &gt; 0.8), indicating potential functional mechanisms related to the trait associations for high-density lipoprotein and body mass index.</div></div><div><h3>Conclusions</h3><div>Using evidence of local genetic correlation and colocalization, we found independent regions of the genome that may determine the genome-wide genetic correlation between metabolic traits and AN and identified specific shared genes which may assist with our mechanistic understanding of the inherent biological link between AN and metabolites.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100678"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146168070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Model-Based Electroencephalography Phenotyping Uncovers Distinct Neurocomputational Mechanisms Underlying Learning Impairments Across Psychopathologies","authors":"Nadja R. Ging-Jehli ,&nbsp;Rachel Rac-Lubashevsky ,&nbsp;Krishn Bera ,&nbsp;Megan A. Boudewyn ,&nbsp;Cameron S. Carter ,&nbsp;Molly A. Erickson ,&nbsp;James M. Gold ,&nbsp;Steven J. Luck ,&nbsp;J. Daniel Ragland ,&nbsp;Andrew P. Yonelinas ,&nbsp;Angus W. MacDonald III ,&nbsp;Deanna M. Barch ,&nbsp;Michael J. Frank","doi":"10.1016/j.bpsgos.2025.100660","DOIUrl":"10.1016/j.bpsgos.2025.100660","url":null,"abstract":"<div><h3>Background</h3><div>Major depressive disorder (MDD), bipolar disorder (BP), and schizophrenia (SCZ) involve learning impairments with poorly understood mechanisms. Understanding both the similarities and differences in these mechanisms is important to guide the development of new, targeted interventions.</div></div><div><h3>Methods</h3><div>A total of 255 participants diagnosed with MDD (<em>n</em> = 54), BP (<em>n</em> = 47), or SCZ (<em>n</em> = 67) or without any clinical diagnoses (control [CTRL]) (<em>n</em> = 87) performed an associative learning task. Computational modeling quantified the mechanistic interplay between working memory (WM) and reinforcement learning (RL). The latent RL and WM signatures in the electroencephalography (EEG) dynamics showed shared and distinct neurocognitive mechanisms underlying learning.</div></div><div><h3>Results</h3><div>All clinical groups showed learning impairments at the behavioral level. Model-based EEG analyses linked these impairments to distinct patterns in the dynamic interplay between latent RL and WM mechanisms, contrasting with the typical patterns observed in the CTRL group. SCZ was characterized by reduced neural markers of WM, weakening the cooperative influence of WM onto RL (reduced WM recruitment), and reduced integration of negative feedback. Conversely, MDD was characterized by reduced reciprocal influence of RL onto WM, reducing the tendency to upregulate WM contribution with reward history (impaired WM management). Finally, BP was characterized by deficits in both WM and RL recruitment, along with higher WM decay.</div></div><div><h3>Conclusions</h3><div>Behavioral learning impairments that seem similar across clinical groups can be linked to distinct neurocognitive mechanisms via integrative neurocomputational modeling. Our approach provides insights into the interplay of underlying learning mechanisms and how they manifest differently across psychopathologies.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100660"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146078099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Harnessing Analysis of Individual Differences in Behavior to Identify Novel Mechanisms Relevant to Neuropsychiatric Disorders","authors":"Mary M. Torregrossa","doi":"10.1016/j.bpsgos.2025.100639","DOIUrl":"10.1016/j.bpsgos.2025.100639","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 1","pages":"Article 100639"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145520846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}