Pub Date : 2026-03-01Epub Date: 2025-11-12DOI: 10.1016/j.bpsgos.2025.100654
Hassan Jubair
Dissociative disorders (DDs), including dissociative identity disorder and depersonalization disorder, are complex and often misdiagnosed psychiatric conditions due to their overlapping symptoms with other mental illnesses. Electroencephalography (EEG), a low-cost and noninvasive neuroimaging tool, is a valuable means of examining the neurophysiological signatures associated with DDs. In this review, we aim to systematically evaluate how machine learning (ML) and deep learning (DL) methods are applied to EEG data for the diagnosis and monitoring of DDs, highlighting their effectiveness, limitations, and future research directions. We reviewed and synthesized studies involving EEG-based ML and DL models applied to DD-related data. The analysis focused on EEG biomarkers, model architecture (e.g., support vector machines, convolutional neural networks [CNNs], recurrent neural networks [RNNs]), feature types (raw vs. handcrafted), performance metrics, and reported challenges. Findings indicate that DL models, especially CNN and RNN, outperform traditional ML models by learning complex spatiotemporal EEG patterns. Key EEG biomarkers identified include altered frontal EEG power, disrupted theta and alpha rhythms, and attenuated P300 components. Hybrid and raw feature–based DL approaches yielded the highest classification accuracies (up to 98.3%) in related neuropsychiatric tasks. EEG-based DL techniques offer promising advancements in diagnosing DDs. However, challenges such as data scarcity, model interpretability, and generalizability persist. Future research should focus on explainable artificial intelligence, multimodal integration, transfer learning, and personalized EEG biomarkers to bridge the gap between research and clinical application.
{"title":"Electroencephalography-Based Machine and Deep Learning Approaches for the Diagnosis of Dissociative Disorders: A Comprehensive Review","authors":"Hassan Jubair","doi":"10.1016/j.bpsgos.2025.100654","DOIUrl":"10.1016/j.bpsgos.2025.100654","url":null,"abstract":"<div><div>Dissociative disorders (DDs), including dissociative identity disorder and depersonalization disorder, are complex and often misdiagnosed psychiatric conditions due to their overlapping symptoms with other mental illnesses. Electroencephalography (EEG), a low-cost and noninvasive neuroimaging tool, is a valuable means of examining the neurophysiological signatures associated with DDs. In this review, we aim to systematically evaluate how machine learning (ML) and deep learning (DL) methods are applied to EEG data for the diagnosis and monitoring of DDs, highlighting their effectiveness, limitations, and future research directions. We reviewed and synthesized studies involving EEG-based ML and DL models applied to DD-related data. The analysis focused on EEG biomarkers, model architecture (e.g., support vector machines, convolutional neural networks [CNNs], recurrent neural networks [RNNs]), feature types (raw vs. handcrafted), performance metrics, and reported challenges. Findings indicate that DL models, especially CNN and RNN, outperform traditional ML models by learning complex spatiotemporal EEG patterns. Key EEG biomarkers identified include altered frontal EEG power, disrupted theta and alpha rhythms, and attenuated P300 components. Hybrid and raw feature–based DL approaches yielded the highest classification accuracies (up to 98.3%) in related neuropsychiatric tasks. EEG-based DL techniques offer promising advancements in diagnosing DDs. However, challenges such as data scarcity, model interpretability, and generalizability persist. Future research should focus on explainable artificial intelligence, multimodal integration, transfer learning, and personalized EEG biomarkers to bridge the gap between research and clinical application.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100654"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145798707","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}
Pub Date : 2026-03-01Epub Date: 2025-11-12DOI: 10.1016/j.bpsgos.2025.100653
Mariah DeSerisy , Huiyu Yang , Jacob W. Cohen , Juan Sanchez-Peña , David Semanek , Hajer Nakua , Gaurav H. Patel , David Pagliaccio , Amy E. Margolis
Background
Irritability is transdiagnostic and associated with considerable impairment. The behavioral presentation of irritability may vary with age, sex, and diagnosis. Although inconsistent, clinical evidence indicates that irritability may present as temper tantrums associated with neurodevelopmental disorders in young boys, whereas irritability in girls may manifest in adolescence associated with negative mood. Functional activation of subcortical regions is characteristic of irritability, but the structural correlates of irritability in these regions are underexplored. We hypothesized that age, sex, and diagnosis would modify subcortical correlates of irritability.
Methods
False discovery rate–corrected regression models tested whether associations between irritability and subcortical structures were moderated by sex, age, or diagnosis in 1792 youths from the Healthy Brain Network dataset (release 11.0), a cohort weighted for psychiatric problems. Irritability was measured via the Affective Reactivity Index. FreeSurfer 6.0.1 extracted subcortical structures.
Results
Effect modification by sex indicated higher irritability associated with smaller reward-related volumes (right nucleus accumbens, bilateral caudate) in boys and with larger threat-related volumes (left amygdala) in girls. Effect modification by age or diagnosis was not significant.
Conclusions
Sex-specific subcortical correlates may explain sex-specific differences in the behavioral presentation of irritability. In models of irritability, the subcortex governs initiation of angry responses, which are dampened by prefrontal cortices. The altered volumes in reward-related regions in boys and threat-related regions in girls reported herein may be markers of early risk for irritability and/or possible targets for brain-informed interventions. Girls may benefit from irritability treatments targeting threat-based pathways, and boys may benefit from treatments targeting reward-based pathways.
{"title":"Sex-Specific Associations of Irritability With Subcortical Brain Volumes","authors":"Mariah DeSerisy , Huiyu Yang , Jacob W. Cohen , Juan Sanchez-Peña , David Semanek , Hajer Nakua , Gaurav H. Patel , David Pagliaccio , Amy E. Margolis","doi":"10.1016/j.bpsgos.2025.100653","DOIUrl":"10.1016/j.bpsgos.2025.100653","url":null,"abstract":"<div><h3>Background</h3><div>Irritability is transdiagnostic and associated with considerable impairment. The behavioral presentation of irritability may vary with age, sex, and diagnosis. Although inconsistent, clinical evidence indicates that irritability may present as temper tantrums associated with neurodevelopmental disorders in young boys, whereas irritability in girls may manifest in adolescence associated with negative mood. Functional activation of subcortical regions is characteristic of irritability, but the structural correlates of irritability in these regions are underexplored. We hypothesized that age, sex, and diagnosis would modify subcortical correlates of irritability.</div></div><div><h3>Methods</h3><div>False discovery rate–corrected regression models tested whether associations between irritability and subcortical structures were moderated by sex, age, or diagnosis in 1792 youths from the Healthy Brain Network dataset (release 11.0), a cohort weighted for psychiatric problems. Irritability was measured via the Affective Reactivity Index. FreeSurfer 6.0.1 extracted subcortical structures.</div></div><div><h3>Results</h3><div>Effect modification by sex indicated higher irritability associated with smaller reward-related volumes (right nucleus accumbens, bilateral caudate) in boys and with larger threat-related volumes (left amygdala) in girls. Effect modification by age or diagnosis was not significant.</div></div><div><h3>Conclusions</h3><div>Sex-specific subcortical correlates may explain sex-specific differences in the behavioral presentation of irritability. In models of irritability, the subcortex governs initiation of angry responses, which are dampened by prefrontal cortices. The altered volumes in reward-related regions in boys and threat-related regions in girls reported herein may be markers of early risk for irritability and/or possible targets for brain-informed interventions. Girls may benefit from irritability treatments targeting threat-based pathways, and boys may benefit from treatments targeting reward-based pathways.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100653"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145798695","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}
Pub Date : 2026-03-01Epub Date: 2025-11-10DOI: 10.1016/j.bpsgos.2025.100652
Gudmundur Einarsson , Hannes K. Arnason , Rosa S. Gisladottir , Gyda Bjornsdottir , Thorgeir E. Thorgeirsson , Astros Skuladottir , G. Bragi Walters , Saedis Saevarsdottir , Magnus K. Magnusson , Gisli H. Halldorsson , Audunn S. Snaebjarnarson , Hafsteinn Einarsson , Gardar Sveinbjornsson , Hannes Helgason , Vinicius Tragante , Gudrun A. Jonsdottir , Hildur M. Aegisdottir , Ingileif Jonsdottir , Thorarinn Gislason , Gudmar Thorleifsson , Kari Stefansson
Background
Zopiclone and zolpidem are widely prescribed hypnotic medications for insomnia, sharing similar efficacy but differing in side-effect profiles, particularly concerning taste disturbances. Identifying genetic predictors of intolerance to these medications could inform personalized treatment strategies.
Methods
We conducted a genome-wide association study to identify genetic variants associated with switching between zopiclone and zolpidem in 57,669 Icelanders, using electronic prescription data from Iceland (2003–2020), and 6590 British individuals from the UK Biobank (1990–2017). We included individuals who had received at least 3 prescriptions of either drug. We also investigated data on bitter taste perception using quinine taste test data from 2238 Icelandic individuals.
Results
A common sequence variant, rs6488335-G, within the TAS2R∗ bitter taste receptor gene locus on chromosome 12, was associated with an increased likelihood of switching from zopiclone to zolpidem (Iceland: odds ratio [OR], 1.29; 95% CI, 1.24 to 1.35; United Kingdom: OR, 1.34; 95% CI, 1.12 to 1.59) and a decreased likelihood of switching in the reverse direction. The effect was more pronounced in women (ORfemales, 1.36; 95% CI, 1.29 to 1.44) than in men (ORmales, 1.19; 95% CI, 1.11 to 1.27). While the variant is associated with bitter taste perception of quinine, conditional analyses suggest that the pharmacogenetic association with drug switching is independent of taste perception.
Conclusions
Our findings indicate that carriers of the rs6488335-G variant, particularly homozygous women, were more likely to switch from zopiclone to zolpidem, potentially due to heightened sensitivity to taste-related side effects. Preemptive genetic testing could guide clinicians in prescribing zolpidem over zopiclone for individuals at risk, thereby reducing health care visits and improving treatment adherence.
{"title":"Variant in a Taste Receptor Locus Tied to Changes in the Use of Insomnia Medication","authors":"Gudmundur Einarsson , Hannes K. Arnason , Rosa S. Gisladottir , Gyda Bjornsdottir , Thorgeir E. Thorgeirsson , Astros Skuladottir , G. Bragi Walters , Saedis Saevarsdottir , Magnus K. Magnusson , Gisli H. Halldorsson , Audunn S. Snaebjarnarson , Hafsteinn Einarsson , Gardar Sveinbjornsson , Hannes Helgason , Vinicius Tragante , Gudrun A. Jonsdottir , Hildur M. Aegisdottir , Ingileif Jonsdottir , Thorarinn Gislason , Gudmar Thorleifsson , Kari Stefansson","doi":"10.1016/j.bpsgos.2025.100652","DOIUrl":"10.1016/j.bpsgos.2025.100652","url":null,"abstract":"<div><h3>Background</h3><div>Zopiclone and zolpidem are widely prescribed hypnotic medications for insomnia, sharing similar efficacy but differing in side-effect profiles, particularly concerning taste disturbances. Identifying genetic predictors of intolerance to these medications could inform personalized treatment strategies.</div></div><div><h3>Methods</h3><div>We conducted a genome-wide association study to identify genetic variants associated with switching between zopiclone and zolpidem in 57,669 Icelanders, using electronic prescription data from Iceland (2003–2020), and 6590 British individuals from the UK Biobank (1990–2017). We included individuals who had received at least 3 prescriptions of either drug. We also investigated data on bitter taste perception using quinine taste test data from 2238 Icelandic individuals.</div></div><div><h3>Results</h3><div>A common sequence variant, rs6488335-G, within the <em>TAS2R</em><em>∗</em> bitter taste receptor gene locus on chromosome 12, was associated with an increased likelihood of switching from zopiclone to zolpidem (Iceland: odds ratio [OR], 1.29; 95% CI, 1.24 to 1.35; United Kingdom: OR, 1.34; 95% CI, 1.12 to 1.59) and a decreased likelihood of switching in the reverse direction. The effect was more pronounced in women (OR<sub>females</sub>, 1.36; 95% CI, 1.29 to 1.44) than in men (OR<sub>males</sub>, 1.19; 95% CI, 1.11 to 1.27). While the variant is associated with bitter taste perception of quinine, conditional analyses suggest that the pharmacogenetic association with drug switching is independent of taste perception.</div></div><div><h3>Conclusions</h3><div>Our findings indicate that carriers of the rs6488335-G variant, particularly homozygous women, were more likely to switch from zopiclone to zolpidem, potentially due to heightened sensitivity to taste-related side effects. Preemptive genetic testing could guide clinicians in prescribing zolpidem over zopiclone for individuals at risk, thereby reducing health care visits and improving treatment adherence.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100652"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145746984","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}
Pub Date : 2026-03-01Epub Date: 2026-01-07DOI: 10.1016/j.bpsgos.2025.100668
Matthew L. Baum
{"title":"Global Efforts Toward Evidence-Based Laboratory Testing of Antineuronal Antibodies in Psychosis","authors":"Matthew L. Baum","doi":"10.1016/j.bpsgos.2025.100668","DOIUrl":"10.1016/j.bpsgos.2025.100668","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100668"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939219","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}
Pub Date : 2026-03-01Epub Date: 2025-11-24DOI: 10.1016/j.bpsgos.2025.100659
Vanessa A. Palzes , Brianna Costales , Stacy Sterling , Andrea Kline-Simon , Lorenzo Leggio , Mehdi Farokhnia
Background
Growing research suggests that glucagon-like peptide-1 receptor agonists (GLP-1RAs) reduce alcohol consumption, positioning them as new potential pharmacotherapies for alcohol use disorder. However, human studies examining alcohol consumption measures in generalizable samples have been limited.
Methods
In this cohort study, we analyzed electronic health records from a large, integrated health care system (Kaiser Permanente Northern California) to examine the association between new prescriptions of GLP-1RAs and change in alcohol use among adults. Propensity score matching was utilized to account for differences in baseline characteristics between GLP-1RA–treated (n = 1214) and untreated (n = 1063) individuals. Changes in average drinks consumed per week (drinks/week) from baseline to follow-up (up to 1 year) were compared between groups using difference-in-differences (D-I-D) analysis. Stratified analyses examined treatment effect variation by sex, obesity, and baseline alcohol use risk level.
Results
Both GLP1-RA–treated and untreated groups reduced their drinks/week from baseline to follow-up (mean change [95% CI] = −1.81 [−2.11 to −1.51] and −1.38 [−1.70 to −1.06], respectively); the group difference did not reach statistical significance (D-I-D [95% CI] = −0.43 [−0.87 to 0.01]). Among individuals with low-risk baseline alcohol use, including 1126 (92.8%) GLP-1RA–treated and 996 (93.7%) untreated individuals, receipt of GLP-1RAs was associated with significantly greater reductions in drinks/week (D-I-D [95% CI] = −0.32 [−0.64 to −0.01]). Treatment effects did not vary by sex or obesity.
Conclusions
GLP-1RAs may be effective in reducing average weekly alcohol consumption, even in individuals with low-risk use. The small subsample of individuals with high-risk use limited our ability to estimate associations in this group.
{"title":"Glucagon-Like Peptide-1 Receptor Agonists and Alcohol Use: A Real-Word Observational Study in a Large, Integrated Health Care System","authors":"Vanessa A. Palzes , Brianna Costales , Stacy Sterling , Andrea Kline-Simon , Lorenzo Leggio , Mehdi Farokhnia","doi":"10.1016/j.bpsgos.2025.100659","DOIUrl":"10.1016/j.bpsgos.2025.100659","url":null,"abstract":"<div><h3>Background</h3><div>Growing research suggests that glucagon-like peptide-1 receptor agonists (GLP-1RAs) reduce alcohol consumption, positioning them as new potential pharmacotherapies for alcohol use disorder. However, human studies examining alcohol consumption measures in generalizable samples have been limited.</div></div><div><h3>Methods</h3><div>In this cohort study, we analyzed electronic health records from a large, integrated health care system (Kaiser Permanente Northern California) to examine the association between new prescriptions of GLP-1RAs and change in alcohol use among adults. Propensity score matching was utilized to account for differences in baseline characteristics between GLP-1RA–treated (<em>n</em> = 1214) and untreated (<em>n</em> = 1063) individuals. Changes in average drinks consumed per week (drinks/week) from baseline to follow-up (up to 1 year) were compared between groups using difference-in-differences (D-I-D) analysis. Stratified analyses examined treatment effect variation by sex, obesity, and baseline alcohol use risk level.</div></div><div><h3>Results</h3><div>Both GLP1-RA–treated and untreated groups reduced their drinks/week from baseline to follow-up (mean change [95% CI] = −1.81 [−2.11 to −1.51] and −1.38 [−1.70 to −1.06], respectively); the group difference did not reach statistical significance (D-I-D [95% CI] = −0.43 [−0.87 to 0.01]). Among individuals with low-risk baseline alcohol use, including 1126 (92.8%) GLP-1RA–treated and 996 (93.7%) untreated individuals, receipt of GLP-1RAs was associated with significantly greater reductions in drinks/week (D-I-D [95% CI] = −0.32 [−0.64 to −0.01]). Treatment effects did not vary by sex or obesity.</div></div><div><h3>Conclusions</h3><div>GLP-1RAs may be effective in reducing average weekly alcohol consumption, even in individuals with low-risk use. The small subsample of individuals with high-risk use limited our ability to estimate associations in this group.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100659"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145885177","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}
Pub Date : 2026-03-01Epub Date: 2025-10-30DOI: 10.1016/j.bpsgos.2025.100643
Rafael Navarro-González , Pedro Luque-Laguna , Rodrigo de Luis-García , Derek K. Jones , Kate Merritt , Anthony S. David
Background
Psychotic experiences (hallucinations and delusions: PEs) are linked to structural brain variation, but their relationship to magnetic resonance imaging (MRI)–derived brain age is unclear. We hypothesized that young adults reporting PEs would show an increased brain-age gap (predicted − chronological age) and that this gap would diverge over 10 years.
Methods
A multilayer perceptron (2628 training scans; age 6–50 years; mean absolute error = 4.3 years, R2 = 0.72) estimated brain age from T1-weighted MRIs in the ALSPAC (Avon Longitudinal Study of Parents and Children). Participants were scanned at around age 20 years (N = 245; 124 with PEs) and again at around 30 years (N = 279; 69 with PEs); 113 participants contributed both scans. Linear mixed-effects models tested case-control, severity, and time-by-group effects.
Results
At the initial time point, individuals with PEs showed a larger brain-age gap than control individuals (d [95% CI] = 0.70 [0.14 to 1.27]; q = .029). The brain-age gap showed a trend-level association with PE severity (d [95% CI] = 1.32 [0.00 to 2.64]; q = .098). At the follow-up, the group difference was nonsignificant (d [95% CI] = 0.22 [−0.08 to 0.51]; q = .153). No longitudinal case-control divergence reached significance, likely reflecting limited power.
Conclusions
Young adults who report PEs display an older-looking brain in early adulthood, consistent with atypical brain maturation. However, the gap does not clearly widen or contract by age 30. Multimodal, longitudinal cohorts spanning adolescence to midadulthood are needed to map psychosis-related atypical brain maturation.
{"title":"Increased Brain-Age Gap in Young Adults With Psychotic Experiences","authors":"Rafael Navarro-González , Pedro Luque-Laguna , Rodrigo de Luis-García , Derek K. Jones , Kate Merritt , Anthony S. David","doi":"10.1016/j.bpsgos.2025.100643","DOIUrl":"10.1016/j.bpsgos.2025.100643","url":null,"abstract":"<div><h3>Background</h3><div>Psychotic experiences (hallucinations and delusions: PEs) are linked to structural brain variation, but their relationship to magnetic resonance imaging (MRI)–derived brain age is unclear. We hypothesized that young adults reporting PEs would show an increased brain-age gap (predicted − chronological age) and that this gap would diverge over 10 years.</div></div><div><h3>Methods</h3><div>A multilayer perceptron (2628 training scans; age 6–50 years; mean absolute error = 4.3 years, <em>R</em><sup>2</sup> = 0.72) estimated brain age from T1-weighted MRIs in the ALSPAC (Avon Longitudinal Study of Parents and Children). Participants were scanned at around age 20 years (<em>N</em> = 245; 124 with PEs) and again at around 30 years (<em>N</em> = 279; 69 with PEs); 113 participants contributed both scans. Linear mixed-effects models tested case-control, severity, and time-by-group effects.</div></div><div><h3>Results</h3><div>At the initial time point, individuals with PEs showed a larger brain-age gap than control individuals (<em>d</em> [95% CI] = 0.70 [0.14 to 1.27]; <em>q</em> = .029). The brain-age gap showed a trend-level association with PE severity (<em>d</em> [95% CI] = 1.32 [0.00 to 2.64]; <em>q</em> = .098). At the follow-up, the group difference was nonsignificant (<em>d</em> [95% CI] = 0.22 [−0.08 to 0.51]; <em>q</em> = .153). No longitudinal case-control divergence reached significance, likely reflecting limited power.</div></div><div><h3>Conclusions</h3><div>Young adults who report PEs display an older-looking brain in early adulthood, consistent with atypical brain maturation. However, the gap does not clearly widen or contract by age 30. Multimodal, longitudinal cohorts spanning adolescence to midadulthood are needed to map psychosis-related atypical brain maturation.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100643"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145798696","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}
Pub Date : 2026-03-01Epub Date: 2025-11-29DOI: 10.1016/j.bpsgos.2025.100661
Bernd Feige , Katharina von Zedtwitz , Isabelle Matteit , Andrea Schlump , Volker A. Coenen , Kathrin Nickel , Kimon Runge , Harald Prüss , Alexander Rau , Marco Reisert , Swantje Matthies , Katharina Domschke , Simon J. Maier , Ludger Tebartz van Elst , Dominique Endres
Background
Intermittent rhythmic delta/theta activity (IRDA/IRTA) detected via electroencephalography (EEG) has been implicated in the pathophysiology of neuropsychiatric illnesses. Therefore, a combined EEG and functional magnetic resonance imaging (fMRI) approach was applied in a transdiagnostic group of patients with different causalities, i.e., autoimmune-mediated (in suspected autoimmune psychiatric syndromes [APS]) and primary psychiatric (borderline personality disorder [BPD]) causalities, as well as in healthy control (HC) participants, to characterize the brain regions functionally correlated with IRDA/IRTA.
Methods
Overall, 135 EEG-fMRI datasets met the quality criteria, including 33 patients with suspected APS, 59 cases with BPD, and 43 HC participants. fMRI data were obtained using ultrafast MR encephalography and analyzed using AFNI. IRDA/IRTA events were separated from artifacts using independent component analysis and detected algorithmically. Brain regions (clusters) significantly correlated with IRDA/IRTA were first determined in all participants. Clusters occurring across all groups were classified as consensus areas. The groups were also analyzed individually, adding disease- or disorder-specific clusters not overlapping with the consensus areas.
Results
Eleven consensus areas were identified across the 3 groups: 5 of them showed increased activity (Brodmann area [BA] 43-right [r], BA 2-left [l], BA 4-r, BA 18-r, BA 26/29/30-r), and 6 had reduced activity (BA 39-l, BA 10-l, BA 23-l, BA 19-l, BA 10-r, BA 18-l). The APS group showed 5 additional clusters, all with reduced activity (BAs 39-r, 1/3-r, 8-r, 4-l, 21-r). The BPD group showed one further cluster with increased activity (BA 17-l).
Conclusions
In this study, IRDA/IRTA-related brain activity changes across the groups were identified, with excitatory brain activity especially in fronto-centro-temporal brain areas with similarities to the salience network. Additional disease- or disorder-specific changes were discovered in APS and BPD.
{"title":"Functional Brain Activity Associated With Intermittent Rhythmic Delta/Theta Activity: A Transdiagnostic Electroencephalography–Functional Magnetic Resonance Imaging Resting-State Study","authors":"Bernd Feige , Katharina von Zedtwitz , Isabelle Matteit , Andrea Schlump , Volker A. Coenen , Kathrin Nickel , Kimon Runge , Harald Prüss , Alexander Rau , Marco Reisert , Swantje Matthies , Katharina Domschke , Simon J. Maier , Ludger Tebartz van Elst , Dominique Endres","doi":"10.1016/j.bpsgos.2025.100661","DOIUrl":"10.1016/j.bpsgos.2025.100661","url":null,"abstract":"<div><h3>Background</h3><div>Intermittent rhythmic delta/theta activity (IRDA/IRTA) detected via electroencephalography (EEG) has been implicated in the pathophysiology of neuropsychiatric illnesses. Therefore, a combined EEG and functional magnetic resonance imaging (fMRI) approach was applied in a transdiagnostic group of patients with different causalities, i.e., autoimmune-mediated (in suspected autoimmune psychiatric syndromes [APS]) and primary psychiatric (borderline personality disorder [BPD]) causalities, as well as in healthy control (HC) participants, to characterize the brain regions functionally correlated with IRDA/IRTA.</div></div><div><h3>Methods</h3><div>Overall, 135 EEG-fMRI datasets met the quality criteria, including 33 patients with suspected APS, 59 cases with BPD, and 43 HC participants. fMRI data were obtained using ultrafast MR encephalography and analyzed using AFNI. IRDA/IRTA events were separated from artifacts using independent component analysis and detected algorithmically. Brain regions (clusters) significantly correlated with IRDA/IRTA were first determined in all participants. Clusters occurring across all groups were classified as consensus areas. The groups were also analyzed individually, adding disease- or disorder-specific clusters not overlapping with the consensus areas.</div></div><div><h3>Results</h3><div>Eleven consensus areas were identified across the 3 groups: 5 of them showed increased activity (Brodmann area [BA] 43-right [r], BA 2-left [l], BA 4-r, BA 18-r, BA 26/29/30-r), and 6 had reduced activity (BA 39-l, BA 10-l, BA 23-l, BA 19-l, BA 10-r, BA 18-l). The APS group showed 5 additional clusters, all with reduced activity (BAs 39-r, 1/3-r, 8-r, 4-l, 21-r). The BPD group showed one further cluster with increased activity (BA 17-l).</div></div><div><h3>Conclusions</h3><div>In this study, IRDA/IRTA-related brain activity changes across the groups were identified, with excitatory brain activity especially in fronto-centro-temporal brain areas with similarities to the salience network. Additional disease- or disorder-specific changes were discovered in APS and BPD.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100661"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146038036","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}
Pub Date : 2026-03-01Epub Date: 2026-01-30DOI: 10.1016/j.bpsgos.2025.100684
Argel Aguilar-Valles
{"title":"DCC and the Architecture of Stress Vulnerability: A Guidance Cue for Depression","authors":"Argel Aguilar-Valles","doi":"10.1016/j.bpsgos.2025.100684","DOIUrl":"10.1016/j.bpsgos.2025.100684","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100684"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146078097","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}
Pub Date : 2026-03-01Epub Date: 2025-12-18DOI: 10.1016/j.bpsgos.2025.100680
Wangjingyi Liao , Engin Keser , Andrea Allegrini , Kaili Rimfeld , Robert Plomin , Margherita Malanchini
Background
Cognitive functioning is a critical dimension of psychopathology that remains underinvestigated. Because cognitive deficits often transcend diagnostic boundaries, it has been challenging to delineate specific relationships between psychiatric disorders and cognitive functioning. Genetic research offers novel, powerful tools to disentangle shared (transdiagnostic) from disorder-specific effects, thereby opening new avenues for understanding how psychopathology relates to cognition.
Methods
We used genomic structural equation modeling to identify transdiagnostic and disorder-specific genetic risk. We derived polygenic scores in a longitudinal twin sample (N = 7764) to examine associations between genetic risk for psychopathology and domains of cognitive functioning across development.
Results
The results showed that relationships between psychopathology and cognition are primarily driven by disorder-specific genetic risk rather than by transdiagnostic factors. Associations differed across disorders and cognitive domains. Within-family analyses indicated that associations between genetic risk for psychopathology and cognition operated through distinct pathways. While for some disorders (e.g., attention-deficit/hyperactivity disorder), the effects could be attributed to confounding by environmental differences between nuclear families, for others (e.g., autism spectrum disorder), effects were robust to environmental confounding.
Conclusions
In contrast to psychiatric symptoms, which are most effectively predicted by transdiagnostic genetic risk, our findings highlight the need to consider disorder-specific genetic effects when examining associations between psychopathology and cognition. Focusing solely on transdiagnostic risk is unlikely to capture the full complexity of these relationships or enhance our understanding of the distinct cognitive profiles associated with psychopathology.
{"title":"Disorder-Specific Genetic Effects Drive the Associations Between Psychopathology and Cognitive Functioning","authors":"Wangjingyi Liao , Engin Keser , Andrea Allegrini , Kaili Rimfeld , Robert Plomin , Margherita Malanchini","doi":"10.1016/j.bpsgos.2025.100680","DOIUrl":"10.1016/j.bpsgos.2025.100680","url":null,"abstract":"<div><h3>Background</h3><div>Cognitive functioning is a critical dimension of psychopathology that remains underinvestigated. Because cognitive deficits often transcend diagnostic boundaries, it has been challenging to delineate specific relationships between psychiatric disorders and cognitive functioning. Genetic research offers novel, powerful tools to disentangle shared (transdiagnostic) from disorder-specific effects, thereby opening new avenues for understanding how psychopathology relates to cognition.</div></div><div><h3>Methods</h3><div>We used genomic structural equation modeling to identify transdiagnostic and disorder-specific genetic risk. We derived polygenic scores in a longitudinal twin sample (<em>N</em> = 7764) to examine associations between genetic risk for psychopathology and domains of cognitive functioning across development.</div></div><div><h3>Results</h3><div>The results showed that relationships between psychopathology and cognition are primarily driven by disorder-specific genetic risk rather than by transdiagnostic factors. Associations differed across disorders and cognitive domains. Within-family analyses indicated that associations between genetic risk for psychopathology and cognition operated through distinct pathways. While for some disorders (e.g., attention-deficit/hyperactivity disorder), the effects could be attributed to confounding by environmental differences between nuclear families, for others (e.g., autism spectrum disorder), effects were robust to environmental confounding.</div></div><div><h3>Conclusions</h3><div>In contrast to psychiatric symptoms, which are most effectively predicted by transdiagnostic genetic risk, our findings highlight the need to consider disorder-specific genetic effects when examining associations between psychopathology and cognition. Focusing solely on transdiagnostic risk is unlikely to capture the full complexity of these relationships or enhance our understanding of the distinct cognitive profiles associated with psychopathology.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100680"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146078096","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}
Pub Date : 2026-03-01Epub Date: 2025-12-13DOI: 10.1016/j.bpsgos.2025.100664
Jessica P.Y. Hua , Brian J. Roach , Holly K. Hamilton , Peter M. Bachman , Aysenil Belger , Ricardo E. Carrión , Erica Duncan , Jason K. Johannesen , Gregory A. Light , Margaret Niznikiewicz , Jean Addington , Carrie E. Bearden , Kristin S. Cadenhead , Diana O. Perkins , William S. Stone , Elaine F. Walker , Scott W. Woods , Tyrone D. Cannon , Daniel H. Mathalon
Background
Reduced mismatch negativity (MMN) is a widely replicated schizophrenia biomarker. Time-frequency analyses suggest that deficient phase synchrony and/or power of electroencephalography (EEG) event-related oscillations, especially theta, contribute to MMN deficits in schizophrenia. Whether theta oscillations assessed from a passive auditory oddball paradigm are abnormal in clinical high-risk for psychosis (CHR-P) individuals and whether these oscillations predict CHR-P clinical outcomes remain unclear. These questions were addressed using data from NAPLS2 (North American Prodrome Longitudinal Study 2).
Methods
EEG was recorded from 77 CHR-P individuals who converted to psychosis (CHR-Cs), 238 CHR-P nonconverters (CHR-NCs) who completed a 24-month follow-up, and 241 healthy control (HC) individuals. Theta oscillations elicited by standard and deviant tones were calculated. Theta (4–6 Hz) intertrial phase coherence (ITC) and total power were compared between groups and evaluated as predictors of time to psychosis conversion in the full CHR-P sample. Furthermore, analyses of covariance were used to assess whether theta deficits persisted while covarying for MMN.
Results
The CHR-C group, relative to the HC and CHR-NC groups, had reduced theta ITC for standards and deviants (ps < .029) and reduced total power for standards and deviants relative to the HC group (p = .021). Reduced theta ITC for standards and deviants predicted earlier psychosis conversion. The previously reported deficit in MMN amplitude in the CHR-C group was no longer significant after accounting for theta ITC or total power averaged across stimuli (ps > .187), but this was not true for theta ITC or total power deviant-standard difference scores (ps < .039).
Conclusions
These results implicate abnormalities in microcircuit generators of theta oscillations in CHR-P individuals at highest risk.
{"title":"Theta Oscillations Assessed From a Passive Auditory Oddball Paradigm in Individuals at Clinical High-Risk for Psychosis and Healthy Control Individuals: Associations with Clinical Outcomes and Mismatch Negativity","authors":"Jessica P.Y. Hua , Brian J. Roach , Holly K. Hamilton , Peter M. Bachman , Aysenil Belger , Ricardo E. Carrión , Erica Duncan , Jason K. Johannesen , Gregory A. Light , Margaret Niznikiewicz , Jean Addington , Carrie E. Bearden , Kristin S. Cadenhead , Diana O. Perkins , William S. Stone , Elaine F. Walker , Scott W. Woods , Tyrone D. Cannon , Daniel H. Mathalon","doi":"10.1016/j.bpsgos.2025.100664","DOIUrl":"10.1016/j.bpsgos.2025.100664","url":null,"abstract":"<div><h3>Background</h3><div>Reduced mismatch negativity (MMN) is a widely replicated schizophrenia biomarker. Time-frequency analyses suggest that deficient phase synchrony and/or power of electroencephalography (EEG) event-related oscillations, especially theta, contribute to MMN deficits in schizophrenia. Whether theta oscillations assessed from a passive auditory oddball paradigm are abnormal in clinical high-risk for psychosis (CHR-P) individuals and whether these oscillations predict CHR-P clinical outcomes remain unclear. These questions were addressed using data from NAPLS2 (North American Prodrome Longitudinal Study 2).</div></div><div><h3>Methods</h3><div>EEG was recorded from 77 CHR-P individuals who converted to psychosis (CHR-Cs), 238 CHR-P nonconverters (CHR-NCs) who completed a 24-month follow-up, and 241 healthy control (HC) individuals. Theta oscillations elicited by standard and deviant tones were calculated. Theta (4–6 Hz) intertrial phase coherence (ITC) and total power were compared between groups and evaluated as predictors of time to psychosis conversion in the full CHR-P sample. Furthermore, analyses of covariance were used to assess whether theta deficits persisted while covarying for MMN.</div></div><div><h3>Results</h3><div>The CHR-C group, relative to the HC and CHR-NC groups, had reduced theta ITC for standards and deviants (<em>p</em>s < .029) and reduced total power for standards and deviants relative to the HC group (<em>p</em> = .021). Reduced theta ITC for standards and deviants predicted earlier psychosis conversion. The previously reported deficit in MMN amplitude in the CHR-C group was no longer significant after accounting for theta ITC or total power averaged across stimuli (<em>p</em>s > .187), but this was not true for theta ITC or total power deviant-standard difference scores (<em>p</em>s < .039).</div></div><div><h3>Conclusions</h3><div>These results implicate abnormalities in microcircuit generators of theta oscillations in CHR-P individuals at highest risk.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100664"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146078098","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}
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