Pub Date : 2026-01-01Epub Date: 2025-09-22DOI: 10.1016/j.bpsgos.2025.100616
Dina N. Ali , Iain H. Campbell , Jonathan G. Leung , Tamahara Gonzalez Campos , Duan Liu , Mete Ercis , Matej Markota , Deniz Ceylan , Kyla Lara-Breitinger , Francisco Lopez-Jimenez , Adam S. Anderson , Aysegul Ozerdem , Stacey J. Winham , Mark A. Frye
There are substantial care gaps in optimizing treatment response for bipolar depression given, at best, a modicum of benefit from antidepressant treatment and, in contrast, a substantial cardiometabolic burden associated with regulatory-approved antipsychotic treatment. Lamotrigine (LGT) is an anticonvulsant with an evidence base in both epilepsy and bipolar disorder (BD), in particular bipolar depression "stabilizing from down under." There is a well-established bidirectional relationship between BD and epilepsy. Recognizing the complex interplay between mood, diet, and energy metabolism, lifestyle interventions have emerged as an adjunctive therapeutic approach in BD. Among these, therapeutic ketosis, with century-old evidence base in epilepsy, has regained new interest as a promising adjunctive treatment for mood and metabolic comorbidities. LGT and therapeutic ketosis both target neurobiological pathways that regulate energy metabolism and promote neuronal stability—key processes implicated in mood regulation and neuronal protection. This alignment suggests the possibility of synergistic effects in BD. In this review, we explore the overlapping mechanisms of LGT and therapeutic ketosis and provide clinical insights into their combined use in BD, offering a comprehensive perspective on this innovative treatment strategy.
{"title":"Clinical Insights Into the Mechanistic Crossroads of Lamotrigine and Therapeutic Ketosis in Bipolar Depression","authors":"Dina N. Ali , Iain H. Campbell , Jonathan G. Leung , Tamahara Gonzalez Campos , Duan Liu , Mete Ercis , Matej Markota , Deniz Ceylan , Kyla Lara-Breitinger , Francisco Lopez-Jimenez , Adam S. Anderson , Aysegul Ozerdem , Stacey J. Winham , Mark A. Frye","doi":"10.1016/j.bpsgos.2025.100616","DOIUrl":"10.1016/j.bpsgos.2025.100616","url":null,"abstract":"<div><div>There are substantial care gaps in optimizing treatment response for bipolar depression given, at best, a modicum of benefit from antidepressant treatment and, in contrast, a substantial cardiometabolic burden associated with regulatory-approved antipsychotic treatment. Lamotrigine (LGT) is an anticonvulsant with an evidence base in both epilepsy and bipolar disorder (BD), in particular bipolar depression \"stabilizing from down under.\" There is a well-established bidirectional relationship between BD and epilepsy. Recognizing the complex interplay between mood, diet, and energy metabolism, lifestyle interventions have emerged as an adjunctive therapeutic approach in BD. Among these, therapeutic ketosis, with century-old evidence base in epilepsy, has regained new interest as a promising adjunctive treatment for mood and metabolic comorbidities. LGT and therapeutic ketosis both target neurobiological pathways that regulate energy metabolism and promote neuronal stability—key processes implicated in mood regulation and neuronal protection. This alignment suggests the possibility of synergistic effects in BD. In this review, we explore the overlapping mechanisms of LGT and therapeutic ketosis and provide clinical insights into their combined use in BD, offering a comprehensive perspective on this innovative treatment strategy.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 1","pages":"Article 100616"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145520843","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 : 2026-01-01Epub Date: 2025-09-26DOI: 10.1016/j.bpsgos.2025.100619
Yuwen He , Jieting Chen , Yong Lin , Natalia Chan , Fei Gao , Lulu Liu , Xiaoqing Yin , Yao Sun , Minghui Li , Sifan Zhang , Zihan Wei , Liangxuan Yu , Xinyi Huang , Zhihai Su , Zhen Yuan
Background
Major depressive disorder (MDD) is common in adolescents, and adolescents’ brains develop intensively but are still immature, making them more vulnerable during social interaction when exposed to public psychosocial stressors. Thus, it is essential to examine how a shared psychosocial stressor, i.e., shared excluded experiences, influences social interaction in adolescents with depression.
Methods
We designed a 4-player Cyberball game involving 2 virtual players and 2 real players and recruited 34 dyads of healthy adolescents and 34 dyads of adolescents with depression. This allowed us to investigate the responses of adolescents with depression to shared excluded experiences and explore the underlying interpersonal neural synchronization (INS), which can indicate mutual empathy, with functional near-infrared spectroscopy.
Results
We found that shared excluded experiences enhanced adolescents’ social interaction but decreased INS between paired excluded adolescents. Such discrepancy suggested reduced mutual empathy between the excluded adolescents despite their increased interaction after shared exclusion. No significant between-group differences were observed in behavioral responses to shared excluded experiences. Subsequent analyses revealed that adolescents with MDD experienced more negative feelings compared with healthy control participants (HCs), and they demonstrated stronger INS than HCs after shared exclusion, which collectively indicate higher empathic stress in adolescents with depression. In addition, there were altered brain-behavioral association patterns in responses to shared excluded experiences in adolescents with depression.
Conclusions
Our study gives us deeper insights into how a shared psychosocial stressor impacts INS in adolescents with depression, and it suggests that INS could be more sensitive than behavioral responses at detecting social interaction deficits in adolescents with depression.
{"title":"Altered Interpersonal Neural Synchronization During Social Interaction After Shared Excluded Experiences in Adolescents With Depression","authors":"Yuwen He , Jieting Chen , Yong Lin , Natalia Chan , Fei Gao , Lulu Liu , Xiaoqing Yin , Yao Sun , Minghui Li , Sifan Zhang , Zihan Wei , Liangxuan Yu , Xinyi Huang , Zhihai Su , Zhen Yuan","doi":"10.1016/j.bpsgos.2025.100619","DOIUrl":"10.1016/j.bpsgos.2025.100619","url":null,"abstract":"<div><h3>Background</h3><div>Major depressive disorder (MDD) is common in adolescents, and adolescents’ brains develop intensively but are still immature, making them more vulnerable during social interaction when exposed to public psychosocial stressors. Thus, it is essential to examine how a shared psychosocial stressor, i.e., shared excluded experiences, influences social interaction in adolescents with depression.</div></div><div><h3>Methods</h3><div>We designed a 4-player Cyberball game involving 2 virtual players and 2 real players and recruited 34 dyads of healthy adolescents and 34 dyads of adolescents with depression. This allowed us to investigate the responses of adolescents with depression to shared excluded experiences and explore the underlying interpersonal neural synchronization (INS), which can indicate mutual empathy, with functional near-infrared spectroscopy.</div></div><div><h3>Results</h3><div>We found that shared excluded experiences enhanced adolescents’ social interaction but decreased INS between paired excluded adolescents. Such discrepancy suggested reduced mutual empathy between the excluded adolescents despite their increased interaction after shared exclusion. No significant between-group differences were observed in behavioral responses to shared excluded experiences. Subsequent analyses revealed that adolescents with MDD experienced more negative feelings compared with healthy control participants (HCs), and they demonstrated stronger INS than HCs after shared exclusion, which collectively indicate higher empathic stress in adolescents with depression. In addition, there were altered brain-behavioral association patterns in responses to shared excluded experiences in adolescents with depression.</div></div><div><h3>Conclusions</h3><div>Our study gives us deeper insights into how a shared psychosocial stressor impacts INS in adolescents with depression, and it suggests that INS could be more sensitive than behavioral responses at detecting social interaction deficits in adolescents with depression.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 1","pages":"Article 100619"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145520849","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 : 2026-01-01Epub Date: 2025-10-10DOI: 10.1016/j.bpsgos.2025.100627
Dwight L. Evans , Sergei Spitsin , Kevin G. Lynch , Chelsea D. Voytek , Menvekeh G. Daramay , Elizabeth A. Hembree , Danielle Fiore , Robert Gross , J. Cobb Scott , Steven D. Douglas , Michael E. Thase
Background
This study was a randomized controlled trial investigating the effects of a selective serotonin reuptake inhibitor (SSRI) and improvement in depressive symptoms on innate immunity and inflammation in people with HIV (PWH).
Methods
The mean 17-item Hamilton Depression Rating Scale (HAMD-17) score at baseline was 19.1 for the sample (N = 108). Eligible participants were randomized to 10 weeks of double-blind therapy with either SSRI (escitalopram) or placebo. All participants concurrently received computer-assisted cognitive behavioral therapy (CCBT). Peripheral blood was obtained from each participant at baseline and at weeks 2, 4, and 10, and intracellular interferon gamma (IFN-γ) in natural killer (NK) cells, lytic units per 107 NK cells (LUNKs), interleukin 6 (IL-6), and C-reactive protein (CRP) were measured.
Results
Participants showed substantial reduction in depressive symptoms during study with final HAMD-17 score of 8.00 (average decrease of 11.0 units). However, there was no statistically significant effect of treatment, whether viewed as a group × time interaction (F1,166 = 0.00, p = .976) or as a main effect for group (F1,667 = 0.50, p = .479). There were no statistically significant differences between the groups on the immune parameters over time. There was little evidence that the magnitude of symptom improvement was associated with changes in immune measures.
Conclusions
Our study did not demonstrate superiority of treatment with SSRI+CCBT versus placebo+CCBT. Patients in both arms showed improvement of depression symptoms, which did not correlate with changes in immune markers. We found no evidence of decreased inflammation (IL-6, CRP) or immune restoration (LUNKs or intracellular IFN-γ) following treatment with CCBT with or without active escitalopram. While antidepressant treatment is indicated for PWH with depression, we observed no evidence of direct immunologic benefits.
本研究是一项随机对照试验，旨在研究选择性血清素再摄取抑制剂（SSRI）和抑郁症状的改善对HIV （PWH）患者先天免疫和炎症的影响。方法样本（108例）17项汉密尔顿抑郁评定量表（HAMD-17）基线平均得分为19.1分。符合条件的参与者被随机分配到SSRI（艾司西酞普兰）或安慰剂的10周双盲治疗。所有参与者同时接受计算机辅助认知行为治疗（CCBT）。在基线和第2周、第4周和第10周采集每位参与者的外周血，并测量自然杀伤（NK）细胞中的细胞内干扰素γ (IFN-γ)、每107个NK细胞（LUNKs）的溶解单位、白细胞介素6 （IL-6）和c反应蛋白（CRP）。结果受试者抑郁症状明显减轻，最终HAMD-17评分为8.00分（平均下降11.0分）。然而，无论是作为组间交互作用（f1166 = 0.00, p = .976）还是作为组内主要作用（f1667 = 0.50, p = .479），治疗均无统计学显著影响。各组间免疫参数随时间变化无统计学差异。几乎没有证据表明症状改善的程度与免疫措施的改变有关。结论我们的研究并未证明SSRI+CCBT治疗优于安慰剂+CCBT治疗。两组患者均表现出抑郁症状的改善，这与免疫标记物的变化无关。我们没有发现在CCBT治疗后炎症（IL-6， CRP）或免疫恢复（lunk或细胞内IFN-γ）减少的证据。虽然抗抑郁治疗适用于伴有抑郁症的PWH，但我们没有观察到直接免疫益处的证据。
{"title":"A Placebo-Controlled Randomized Trial of the Effects of Escitalopram on Depressive Symptoms and Immune Function in People With HIV","authors":"Dwight L. Evans , Sergei Spitsin , Kevin G. Lynch , Chelsea D. Voytek , Menvekeh G. Daramay , Elizabeth A. Hembree , Danielle Fiore , Robert Gross , J. Cobb Scott , Steven D. Douglas , Michael E. Thase","doi":"10.1016/j.bpsgos.2025.100627","DOIUrl":"10.1016/j.bpsgos.2025.100627","url":null,"abstract":"<div><h3>Background</h3><div>This study was a randomized controlled trial investigating the effects of a selective serotonin reuptake inhibitor (SSRI) and improvement in depressive symptoms on innate immunity and inflammation in people with HIV (PWH).</div></div><div><h3>Methods</h3><div>The mean 17-item Hamilton Depression Rating Scale (HAMD-17) score at baseline was 19.1 for the sample (<em>N</em> = 108). Eligible participants were randomized to 10 weeks of double-blind therapy with either SSRI (escitalopram) or placebo. All participants concurrently received computer-assisted cognitive behavioral therapy (CCBT). Peripheral blood was obtained from each participant at baseline and at weeks 2, 4, and 10, and intracellular interferon gamma (IFN-γ) in natural killer (NK) cells, lytic units per 10<sup>7</sup> NK cells (LUNKs), interleukin 6 (IL-6), and C-reactive protein (CRP) were measured.</div></div><div><h3>Results</h3><div>Participants showed substantial reduction in depressive symptoms during study with final HAMD-17 score of 8.00 (average decrease of 11.0 units). However, there was no statistically significant effect of treatment, whether viewed as a group × time interaction (<em>F</em><sub>1,166</sub> = 0.00, <em>p</em> = .976) or as a main effect for group (<em>F</em><sub>1,667</sub> = 0.50, <em>p</em> = .479). There were no statistically significant differences between the groups on the immune parameters over time. There was little evidence that the magnitude of symptom improvement was associated with changes in immune measures.</div></div><div><h3>Conclusions</h3><div>Our study did not demonstrate superiority of treatment with SSRI+CCBT versus placebo+CCBT. Patients in both arms showed improvement of depression symptoms, which did not correlate with changes in immune markers. We found no evidence of decreased inflammation (IL-6, CRP) or immune restoration (LUNKs or intracellular IFN-γ) following treatment with CCBT with or without active escitalopram. While antidepressant treatment is indicated for PWH with depression, we observed no evidence of direct immunologic benefits.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 1","pages":"Article 100627"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145684513","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 : 2026-01-01Epub Date: 2026-01-15DOI: 10.1016/S2667-1743(25)00226-5
{"title":"Subscribers Page","authors":"","doi":"10.1016/S2667-1743(25)00226-5","DOIUrl":"10.1016/S2667-1743(25)00226-5","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 1","pages":"Article 100672"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145976263","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 : 2026-01-01Epub Date: 2025-09-30DOI: 10.1016/j.bpsgos.2025.100624
Priscila Dib Gonçalves , James O. Woodruff , Maria Olivia Pozzolo Pedro , Milenna T. van Dijk , Emilie Bruzelius , Silvia S. Martins , Gretchen Bandoli , Alexandra Potter , Leigh-Anne Cioffredi , Ardesheer Talati , Matthew D. Albaugh
Understanding the impact of prenatal cannabis exposure (PCE) on brain development is increasingly important given rising cannabis use during pregnancy. Many existing reviews on this topic are more than 5 years old and may not reflect recent social shifts that could impact cannabis use during pregnancy; they also have not utilized the recently available large longitudinal datasets for more robust and population-representative investigations. In this narrative review, we aim to provide an updated and expanded examination of the associations between PCE and magnetic resonance imaging (MRI)–based brain outcomes from in utero development to adolescence. We included studies published after 2019 that used at least one of the following measures: structural MRI, diffusion-weighted imaging, resting-state fMRI, and/or task-based fMRI. Across 9 studies that met criteria, 1 study focused on MRI outcomes in utero, 2 in infancy, and 6 in early adolescence, and only 3 studies included MRI and behavior outcomes. PCE was linked to differences in frontal, parietal, and temporal areas, spanning from in utero to adolescence across multiple MRI modalities. However, in the current state of the literature, detecting a consistent trend on PCE’s impact on MRI findings was not possible. Furthermore, we found several divergences in study design: varying approaches to assessment (e.g., self-report vs. urine toxicology); difficulties in accounting for prenatal exposure to multiple substances; limited information on timing, frequency, potency, or mode of consumption; and the influence of parental or postnatal factors. Future research should implement designs that can rigorously capture the abovementioned elements to permit replication and eventual meta-analyses on this critical topic.
{"title":"Investigating Links Between Prenatal Cannabis Exposure and Brain Development Using Magnetic Resonance Imaging Techniques: A Narrative Review","authors":"Priscila Dib Gonçalves , James O. Woodruff , Maria Olivia Pozzolo Pedro , Milenna T. van Dijk , Emilie Bruzelius , Silvia S. Martins , Gretchen Bandoli , Alexandra Potter , Leigh-Anne Cioffredi , Ardesheer Talati , Matthew D. Albaugh","doi":"10.1016/j.bpsgos.2025.100624","DOIUrl":"10.1016/j.bpsgos.2025.100624","url":null,"abstract":"<div><div>Understanding the impact of prenatal cannabis exposure (PCE) on brain development is increasingly important given rising cannabis use during pregnancy. Many existing reviews on this topic are more than 5 years old and may not reflect recent social shifts that could impact cannabis use during pregnancy; they also have not utilized the recently available large longitudinal datasets for more robust and population-representative investigations. In this narrative review, we aim to provide an updated and expanded examination of the associations between PCE and magnetic resonance imaging (MRI)–based brain outcomes from in utero development to adolescence. We included studies published after 2019 that used at least one of the following measures: structural MRI, diffusion-weighted imaging, resting-state fMRI, and/or task-based fMRI. Across 9 studies that met criteria, 1 study focused on MRI outcomes in utero, 2 in infancy, and 6 in early adolescence, and only 3 studies included MRI and behavior outcomes. PCE was linked to differences in frontal, parietal, and temporal areas, spanning from in utero to adolescence across multiple MRI modalities. However, in the current state of the literature, detecting a consistent trend on PCE’s impact on MRI findings was not possible. Furthermore, we found several divergences in study design: varying approaches to assessment (e.g., self-report vs. urine toxicology); difficulties in accounting for prenatal exposure to multiple substances; limited information on timing, frequency, potency, or mode of consumption; and the influence of parental or postnatal factors. Future research should implement designs that can rigorously capture the abovementioned elements to permit replication and eventual meta-analyses on this critical topic.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 1","pages":"Article 100624"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145520842","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 : 2026-01-01Epub Date: 2025-11-12DOI: 10.1016/j.bpsgos.2025.100628
Christal N. Davis
{"title":"Using Genetics to Shed Light on the Scientific Gray Zone of Functional Seizures","authors":"Christal N. Davis","doi":"10.1016/j.bpsgos.2025.100628","DOIUrl":"10.1016/j.bpsgos.2025.100628","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 1","pages":"Article 100628"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145520847","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}
Various cognitive and emotional factors shape our perception of time. Notably, individuals experiencing depressive symptoms often report changes in their time perception, characterized by a phenomenon termed depressive time dilation, or a subjective slowing of temporal flow. However, research on this topic has yielded conflicting and inconclusive findings, leaving the mechanisms behind altered time perception in depression largely unknown. In this study, we aim to explore the neural dynamics underlying the influence of emotional experiences on time perception in relation to depressive symptomatology.
Methods
A total of 120 university students participated in a retrospective time estimation task after watching either sad or neutral emotion-eliciting videos. Moreover, participants’ electroencephalographic (EEG) activity was recorded for the whole duration of the experiment by means of a high-density EEG cap. The severity of depressive symptoms was assessed using the Patient Health Questionnaire-9.
Results
Our findings revealed notable differences between individuals with depressive symptoms and healthy control individuals. Specifically, emotional modulation influenced time estimations exclusively in healthy control individuals. Moreover, individuals with depressive symptoms exhibited a significant relationship between beta band power and retrospective time estimations, specifically after watching the neutral video.
Conclusions
These results suggest that cognitive processes related to depression may disrupt the link between emotions and time perception. Overall, our study contributes to a deeper understanding of the interplay between emotional experience, cognitive processes, and time perception in individuals with depressive symptoms.
{"title":"Emotional Blunting and Time Estimation in Depression","authors":"Francesca Mura , Vincenzo Catrambone , Gaetano Valenza , Virginie Van Wassenhove , Giovanna Mioni , Claudio Gentili","doi":"10.1016/j.bpsgos.2025.100626","DOIUrl":"10.1016/j.bpsgos.2025.100626","url":null,"abstract":"<div><h3>Background</h3><div>Various cognitive and emotional factors shape our perception of time. Notably, individuals experiencing depressive symptoms often report changes in their time perception, characterized by a phenomenon termed depressive time dilation, or a subjective slowing of temporal flow. However, research on this topic has yielded conflicting and inconclusive findings, leaving the mechanisms behind altered time perception in depression largely unknown. In this study, we aim to explore the neural dynamics underlying the influence of emotional experiences on time perception in relation to depressive symptomatology.</div></div><div><h3>Methods</h3><div>A total of 120 university students participated in a retrospective time estimation task after watching either sad or neutral emotion-eliciting videos. Moreover, participants’ electroencephalographic (EEG) activity was recorded for the whole duration of the experiment by means of a high-density EEG cap. The severity of depressive symptoms was assessed using the Patient Health Questionnaire-9.</div></div><div><h3>Results</h3><div>Our findings revealed notable differences between individuals with depressive symptoms and healthy control individuals. Specifically, emotional modulation influenced time estimations exclusively in healthy control individuals. Moreover, individuals with depressive symptoms exhibited a significant relationship between beta band power and retrospective time estimations, specifically after watching the neutral video.</div></div><div><h3>Conclusions</h3><div>These results suggest that cognitive processes related to depression may disrupt the link between emotions and time perception. Overall, our study contributes to a deeper understanding of the interplay between emotional experience, cognitive processes, and time perception in individuals with depressive symptoms.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 1","pages":"Article 100626"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145684593","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 : 2026-01-01Epub Date: 2026-01-15DOI: 10.1016/S2667-1743(25)00228-9
{"title":"Guide for Authors","authors":"","doi":"10.1016/S2667-1743(25)00228-9","DOIUrl":"10.1016/S2667-1743(25)00228-9","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 1","pages":"Article 100674"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145976265","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 : 2026-01-01Epub Date: 2026-01-15DOI: 10.1016/S2667-1743(25)00225-3
{"title":"Editorial Board Page","authors":"","doi":"10.1016/S2667-1743(25)00225-3","DOIUrl":"10.1016/S2667-1743(25)00225-3","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 1","pages":"Article 100671"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145976262","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 : 2026-01-01Epub Date: 2025-09-06DOI: 10.1016/j.bpsgos.2025.100608
Per-Olof Nylander , Erik Lexne , Christer Lehman , Lars Brudin , Finn Bengtsson
Background
Family history (FH) of affective disorders (ADs) is important for the course of bipolar disorder (BD).
Methods
In a long-term study (mean 25 years), 192 patients with BD diagnosed by DSM-IV criteria were recruited from lithium dispensaries. Differences between patients with and without an FH of ADs were studied.
Results
Patients with an FH of AD had poorer lithium response (p = .027), earlier age of onset (AOO) (p < .001), were younger (p = .009), made suicide attempts (SAs) earlier after onset (p = .012), and had more episodes/year (p = .017) and depressive episodes/year (p = .010) before SA. SAs were more common (p = .028) in patients with an FH of AD. SAs were more common (p = .001) before lithium treatment, and SAs (p < .001) were only present in patients with an FH of AD within the first 5 years after AOO. Patients with an FH of AD had more episodes (p = .009), episodes/year (p = .002), depressive episodes (p < .001), and depressive episodes/year (p < .001) during their lifetime. Before lithium, episodes (p = .009), depressive episodes (p = .006), and depressive episodes/year (p = .010) were more common in patients with an FH of AD. Manic episodes (p = .020) were more common in patients with no FH of AD. On lithium, episodes (p = .010), episodes/year (p = .001), depressive episodes (p < .001), and depressive episodes/year (p < .001) were more common in patients with an FH of AD. FH of suicide was present only among patients with an FH of AD (p < .001).
Conclusions
BD patients with an FH of AD have a more severe form of BD with a special effect on SAs, AOO, episodes, and lithium response in BD.
{"title":"Bipolar Disorder VII: Family History and Its Relationship With Suicide Attempts, Severity, and the Prophylactic Effect of Lithium Treatment in a Long-Term Follow-Up Study of Bipolar Disorder","authors":"Per-Olof Nylander , Erik Lexne , Christer Lehman , Lars Brudin , Finn Bengtsson","doi":"10.1016/j.bpsgos.2025.100608","DOIUrl":"10.1016/j.bpsgos.2025.100608","url":null,"abstract":"<div><h3>Background</h3><div>Family history (FH) of affective disorders (ADs) is important for the course of bipolar disorder (BD).</div></div><div><h3>Methods</h3><div>In a long-term study (mean 25 years), 192 patients with BD diagnosed by DSM-IV criteria were recruited from lithium dispensaries. Differences between patients with and without an FH of ADs were studied.</div></div><div><h3>Results</h3><div>Patients with an FH of AD had poorer lithium response (<em>p</em> = .027), earlier age of onset (AOO) (<em>p</em> < .001), were younger (<em>p</em> = .009), made suicide attempts (SAs) earlier after onset (<em>p</em> = .012), and had more episodes/year (<em>p</em> = .017) and depressive episodes/year (<em>p</em> = .010) before SA. SAs were more common (<em>p</em> = .028) in patients with an FH of AD. SAs were more common (<em>p</em> = .001) before lithium treatment, and SAs (<em>p</em> < .001) were only present in patients with an FH of AD within the first 5 years after AOO. Patients with an FH of AD had more episodes (<em>p</em> = .009), episodes/year (<em>p</em> = .002), depressive episodes (<em>p</em> < .001), and depressive episodes/year (<em>p</em> < .001) during their lifetime. Before lithium, episodes (<em>p</em> = .009), depressive episodes (<em>p</em> = .006), and depressive episodes/year (<em>p</em> = .010) were more common in patients with an FH of AD. Manic episodes (<em>p</em> = .020) were more common in patients with no FH of AD. On lithium, episodes (<em>p</em> = .010), episodes/year (<em>p</em> = .001), depressive episodes (<em>p</em> < .001), and depressive episodes/year (<em>p</em> < .001) were more common in patients with an FH of AD. FH of suicide was present only among patients with an FH of AD (<em>p</em> < .001).</div></div><div><h3>Conclusions</h3><div>BD patients with an FH of AD have a more severe form of BD with a special effect on SAs, AOO, episodes, and lithium response in BD.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 1","pages":"Article 100608"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145324651","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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