Biological psychiatry global open science最新文献

{"title":"Integration of Metabolomic and Brain Imaging Data Highlights Pleiotropy Among Posttraumatic Stress Disorder, Glycoprotein Acetyls, and Pallidum Structure","authors":"Solveig Løkhammer ,&nbsp;Markos Tesfaye ,&nbsp;Brenda Cabrera-Mendoza ,&nbsp;Kristoffer Sandås ,&nbsp;Gita A. Pathak ,&nbsp;Eleni Friligkou ,&nbsp;Stéphanie Le Hellard ,&nbsp;Renato Polimanti","doi":"10.1016/j.bpsgos.2025.100482","DOIUrl":"10.1016/j.bpsgos.2025.100482","url":null,"abstract":"<div><h3>Background</h3><div>The development of posttraumatic stress disorder (PTSD) is attributable to the interplay between exposure to severe traumatic events, environmental factors, and biological characteristics. Blood and brain imaging markers have been associated with PTSD. However, to our knowledge, no study has systematically investigated the genetic relationship between PTSD, metabolic biomarkers, and brainwide imaging.</div></div><div><h3>Methods</h3><div>We integrated genome-wide data informative of PTSD, 233 metabolic biomarkers, and 3935 brain imaging-derived phenotypes (IDPs). Pleiotropy was assessed by applying global and local genetic correlation, colocalization, and genetically inferred causality.</div></div><div><h3>Results</h3><div>We observed significant genetic overlap between PTSD and glycoprotein acetyls (GlycA) (a stable inflammatory biomarker) in 2 independent cohorts (discovery <em>r</em>_g = 0.26, <em>p</em> = 1.00 × 10⁻⁴; replication <em>r</em>_g = 0.23, <em>p</em> = 5.99 × 10⁻¹⁹). Interestingly, there was no genetic correlation between anxiety and GlycA (<em>p</em> = .33). PTSD and GlycA were both genetically correlated with median T2∗ in the left pallidum (IDP-1444: <em>r</em>_g = 0.14, <em>p</em> = 1.39 × 10⁻⁵; <em>r</em>_g = −0.38, <em>p</em> = 2.50 × 10⁻³, respectively). Local genetic correlation between PTSD and GlycA was observed in 7 genetic regions (<em>p</em> &lt; 2.0 × 10⁻⁵), mapping genes related to immune and stress response, inflammation, and metabolic processes. Furthermore, we identified 1 variant, rs12048743, with evidence of horizontal pleiotropy linking GlycA and IDP-1444 (<em>z</em>_IDP-1444 = 17.14, <em>z</em>_GlycA = −6.07, theta <em>p</em> = 2.06 × 10⁻⁸). Regional colocalization was observed among GlycA, IDP-1444, and tissue-specific transcriptomic regulation for brain frontal cortex and testis (rs12048743—chr1q32.1; posterior probability &gt; 0.8). While we also tested causality between PTSD, metabolomic biomarkers, and brain IDPs, these were not consistent across different genetically informed causal inference methods.</div></div><div><h3>Conclusions</h3><div>Our findings highlight a new putative pleiotropic mechanism that links systemic inflammation and pallidum structure to PTSD.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"5 4","pages":"Article 100482"},"PeriodicalIF":4.0,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143821421","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":"Peripheral Blood Cytokines as Markers of Longitudinal Change in White Matter Microstructure Following Inpatient Treatment for Opioid Use Disorders","authors":"Eduardo R. Butelman ,&nbsp;Yuefeng Huang ,&nbsp;Sarah G. King ,&nbsp;Pierre-Olivier Gaudreault ,&nbsp;Ahmet O. Ceceli ,&nbsp;Greg Kronberg ,&nbsp;Flurin Cathomas ,&nbsp;Panos Roussos ,&nbsp;Scott J. Russo ,&nbsp;Eric L. Garland ,&nbsp;Rita Z. Goldstein ,&nbsp;Nelly Alia-Klein","doi":"10.1016/j.bpsgos.2025.100480","DOIUrl":"10.1016/j.bpsgos.2025.100480","url":null,"abstract":"<div><h3>Background</h3><div>Opioid use disorder (OUD) causes major public health morbidity and mortality. Although standard-of-care treatment with medications for OUD (MOUDs) is available, there are few biological markers of the clinical process of recovery. Neurobiological aspects of recovery can include normalization of brain white matter (WM) microstructure, which is sensitive to cytokine signaling. Here, we determined whether blood-based cytokines can be markers of change in WM microstructure following MOUD.</div></div><div><h3>Methods</h3><div>Inpatient individuals with heroin use disorder (iHUDs) (<em>n</em> = 21) with methadone or buprenorphine MOUD underwent magnetic resonance imaging (MRI) scans with diffusion tensor imaging (DTI) and provided ratings of drug cue–induced craving, arousal, and valence earlier in treatment (MRI1) and ≈14 weeks thereafter (MRI2). Healthy control participants (HCs) (<em>n</em> = 24) also underwent 2 MRI scans during a similar time interval. At MRI2, participants provided a peripheral blood sample for multiplex quantification of serum cytokines. We analyzed the correlation of a multitarget biomarker score (from a principal component analysis of 19 cytokines that differed significantly between iHUDs and HCs) with treatment-related change in DTI metrics (ΔDTI; MRI2 − MRI1).</div></div><div><h3>Results</h3><div>The cytokine biomarker score was negatively correlated with ΔDTI metrics in frontal, frontoparietal, and corticolimbic WM tracts in iHUDs but not in HCs. Also, serum levels of specific cytokines in the cytokine biomarker score, including the interleukin-related oncostatin M (OSM), similarly correlated with ΔDTI metrics in iHUDs but not in HCs. Serum levels of other specific cytokines were negatively correlated with changes in cue-induced craving and arousal in the iHUDs.</div></div><div><h3>Conclusions</h3><div>Specific serum cytokines, studied alone or as a group, may serve as accessible biomarkers of WM microstructure changes and potential recovery in iHUDs undergoing treatment with MOUD.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"5 3","pages":"Article 100480"},"PeriodicalIF":4.0,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143791630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identifying Features of Resilience to Childhood Maltreatment in Resting-State Connectivity Data From Adults With and Without a History of Mood Disorder","authors":"Mindy Westlund Schreiner ,&nbsp;Leah R. Thomas ,&nbsp;Ha D.H. Le ,&nbsp;Myah Pazdera ,&nbsp;Daniel A. Feldman ,&nbsp;Brian Farstead ,&nbsp;Katie L. Bessette ,&nbsp;Robert C. Welsh ,&nbsp;Sheila E. Crowell ,&nbsp;Erin A. Kaufman ,&nbsp;Heide Klumpp ,&nbsp;Scott A. Langenecker","doi":"10.1016/j.bpsgos.2025.100479","DOIUrl":"10.1016/j.bpsgos.2025.100479","url":null,"abstract":"<div><h3>Background</h3><div>Childhood maltreatment (CM) is associated with negative mental health outcomes. Many studies conceptualize resilience as experiencing CM without developing psychopathology (primary resilience). However, some people may develop subsequent psychopathology but recover and demonstrate higher global functioning (secondary resilience). This study investigated the role of salience and emotion network (SEN) (including the amygdala, subgenual anterior cingulate cortex, and anterior insula) and cognitive control network (CCN) (including the dorsolateral prefrontal cortex, inferior parietal lobule, and thalamus) connectivity in primary and secondary resilience.</div></div><div><h3>Methods</h3><div>We examined resting-state functional connectivity in 108 nonclinical control participants and 154 individuals with any mood disorder (AMD). We measured functioning and CM using the Global Assessment of Functioning (GAF) scale and the Childhood Trauma Questionnaire (CTQ), respectively. For primary resilience, we conducted whole-brain analyses of SEN and CCN regions to test for group × CTQ interactions. For secondary resilience, within-AMD group analyses tested for CTQ × GAF interactions.</div></div><div><h3>Results</h3><div>Group × CTQ interactions revealed that control participants with higher levels of CM showed greater within-SEN and within-CCN connectivity than participants in the AMD group. In the AMD group, participants with higher levels of CM and functioning (secondary resilience) showed greater within-CCN connectivity while participants with higher levels of CM and lower functioning showed greater within-SEN connectivity.</div></div><div><h3>Conclusions</h3><div>Greater SEN connectivity appears to play a key role in primary resilience, as observed in the control group, but only within the context of greater CCN connectivity. Future work should explore which cognitive control features are most beneficial and whether targeted interventions help foster resilience to recurrent psychopathology.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"5 3","pages":"Article 100479"},"PeriodicalIF":4.0,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143791629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationship Between Food Selectivity and Mood Problems in Youth With a Reported Diagnosis of Autism Spectrum Disorder","authors":"Elizabeth A. Li ,&nbsp;Christopher H. Legere ,&nbsp;Noah S. Philip ,&nbsp;Daniel P. Dickstein ,&nbsp;Petya D. Radoeva","doi":"10.1016/j.bpsgos.2025.100481","DOIUrl":"10.1016/j.bpsgos.2025.100481","url":null,"abstract":"<div><h3>Background</h3><div>Food selectivity and mood problems and disorders are commonly described independently in individuals with autism spectrum disorder (ASD). However, little is known about the relationship between food selectivity and mood problems and disorders in ASD.</div></div><div><h3>Methods</h3><div>To study the relationship between food selectivity and mood problems and disorders, we analyzed data from youth (ages 10–13 years) with a parent-reported diagnosis of ASD from the Adolescent Brain Cognitive Development Study (ABCD Study), with available data for the Block Kids Food Screener (parental report) and the Child Behavior Checklist (CBCL) (<em>N</em> = 173, male:female participant ratio = 6.5:1).</div></div><div><h3>Results</h3><div>We did not find a statistically significant association between food selectivity and mood problems or disorders. Food selectivity for protein foods (i.e., consumption of a decreased variety of protein foods) was associated with more severe aggressive behavior/irritability (CBCL Aggressive Behavior T-score) (<em>N</em> = 173, ρ = 0.196, <em>p</em> = .010) in youth with ASD, although the relationship was no longer statistically significant after multiple comparison correction (<em>p</em> = .086).</div></div><div><h3>Conclusions</h3><div>While our results are negative overall for an association between food selectivity and mood problems and disorders in children with ASD, our findings should be interpreted with caution in the context of limitations of the presented analysis. Accordingly, future studies and analyses could incorporate objective measures and prospective tracking of food intake and food selectivity, deeper phenotyping of mood problems (including irritability), and detailed information about factors that could affect the relationship between food selectivity and mood in youth with ASD (such as the use of supplements and medications).</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"5 4","pages":"Article 100481"},"PeriodicalIF":4.0,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143834630","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":"α-Ketoglutarate Is a Circulatory Exercise Factor That Promotes Learning and Memory Recall and Has Antidepressant Properties","authors":"Fady Eid ,&nbsp;Perla El Ahmad ,&nbsp;Reine Khoury ,&nbsp;Diala El Masri ,&nbsp;Yara El Zoghby ,&nbsp;Yasmin Sahlloul ,&nbsp;Joanna Fadel ,&nbsp;Zena Haddad ,&nbsp;Amar Mezher ,&nbsp;Litsa Maria Ghayad ,&nbsp;Yorgo El Sabbagh ,&nbsp;Lea Gerges ,&nbsp;Mahmoud Lakis ,&nbsp;Christopher Sahyoun ,&nbsp;Ghinwa El Khoury ,&nbsp;Joseph S. Stephan ,&nbsp;Sama F. Sleiman","doi":"10.1016/j.bpsgos.2025.100477","DOIUrl":"10.1016/j.bpsgos.2025.100477","url":null,"abstract":"<div><h3>Background</h3><div>Depression poses a significant societal burden, necessitating effective treatment options. Conventional approaches often fall short, highlighting the need for alternatives. Exercise has emerged as a promising nonpharmacological strategy for improving mental health outcomes. Exercise promotes memory recall and alleviates depression by modulating BDNF (brain-derived neurotrophic factor) expression. The effects of exercise on BDNF are influenced by circulatory metabolites known as exercise factors.</div></div><div><h3>Methods</h3><div>Associative and spatial memory were evaluated in mice receiving α-ketoglutarate (aKG) and in exercise mice given a glutaminase inhibitor. To prevent and treat depression-like behaviors, male mice underwent daily defeat sessions by a CD1 aggressor for 10 days. Behavior was assessed on day 11 using social interaction and open-field tests. Mice received aKG for 5 days prior to the stress paradigm or as treatment for 14 days following the stress paradigm, after which social behavior was reassessed. BDNF signaling was examined via Western blots.</div></div><div><h3>Results</h3><div>aKG was identified as a metabolite released into the bloodstream following exercise in male mice. aKG was shown to mediate the positive effects of exercise on spatial learning and memory formation. aKG was also shown to have prophylactic and antidepressant effects in a chronic social defeat stress model of depression.</div></div><div><h3>Conclusions</h3><div>aKG acts as a prophylactic and antidepressant to effectively counteract social avoidance behaviors by modulating BDNF levels in the hippocampus and nucleus accumbens.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"5 3","pages":"Article 100477"},"PeriodicalIF":4.0,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143791549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Contrasting Individual-Specific Resilience and Compensation Personalization Frameworks: The Case of Rumination","authors":"Sigal Zilcha-Mano","doi":"10.1016/j.bpsgos.2025.100478","DOIUrl":"10.1016/j.bpsgos.2025.100478","url":null,"abstract":"<div><h3>Background</h3><div>Rumination has been identified as a potential mechanism of therapeutic change, particularly in directive and focused psychotherapies for depression. Previous research has predominantly focused on either trait-like individual differences or state-like changes in rumination without integrating these aspects. In the current study, we propose a computational approach to investigating whether rumination serves as a compensatory or a resilience mechanism by integrating trait-like and state-like effects.</div></div><div><h3>Methods</h3><div>Rumination and depressive symptoms were assessed (in <em>N</em> = 100) pretreatment and repeatedly throughout treatment. Mixed-level models were used to examine whether pretreatment trait-like rumination interacted with a time-variant variable of in-treatment state-like changes in rumination to predict subsequent changes in treatment outcomes. These models were used to determine whether individuals with higher or lower pretreatment trait-like levels of rumination benefited more from state-like reductions in rumination, thus contrasting the compensatory and resilience theoretical frameworks.</div></div><div><h3>Results</h3><div>As hypothesized, the findings supported the compensatory framework; individuals with higher pretreatment trait-like levels of rumination benefited most from greater state-like reductions in rumination during treatment, as evidenced by greater subsequent symptom reduction (<em>p</em> = .04).</div></div><div><h3>Conclusions</h3><div>The findings refine our understanding of rumination as an individual-specific mechanism of therapeutic change, dependent on an individual’s trait-like levels of rumination. The proposed computational approach enabled an empirical comparison of the 2 main theoretical frameworks of treatment personalization, compensatory and resilience, offering new insights into mechanisms that drive therapeutic change. Future studies could leverage the paradigm proposed here to examine for which patients and in what contexts mechanisms of change function as compensatory versus resilience mechanisms.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"5 3","pages":"Article 100478"},"PeriodicalIF":4.0,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143807597","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":"Guide for Authors","authors":"","doi":"10.1016/S2667-1743(25)00021-7","DOIUrl":"10.1016/S2667-1743(25)00021-7","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"5 2","pages":"Article 100467"},"PeriodicalIF":4.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143619778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Neural Circuit Basis for the Sex-Specific Modulation of Binge Alcohol Drinking","authors":"Larry S. Zweifel","doi":"10.1016/j.bpsgos.2024.100444","DOIUrl":"10.1016/j.bpsgos.2024.100444","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"5 2","pages":"Article 100444"},"PeriodicalIF":4.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143619780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Can Small Nucleolar RNAs Contribute to Neuropsychiatric Disorders? Insights and Future Perspectives","authors":"Yogesh Dwivedi","doi":"10.1016/j.bpsgos.2025.100447","DOIUrl":"10.1016/j.bpsgos.2025.100447","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"5 2","pages":"Article 100447"},"PeriodicalIF":4.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143619781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial Board Page","authors":"","doi":"10.1016/S2667-1743(25)00018-7","DOIUrl":"10.1016/S2667-1743(25)00018-7","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"5 2","pages":"Article 100464"},"PeriodicalIF":4.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143619775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}