Pub Date : 2026-01-03DOI: 10.1016/j.jpsychires.2026.01.004
Kristoffer Bele Ødegård , Martin Øverlien Myhre , Ole Klungsøyr , Lars Mehlum , Anita Johanna Tørmoen , Fredrik A. Walby
Background
The month following discharge from inpatient mental health treatment is the period associated with the highest short-term risk of suicide. The nature of this risk is not well understood. We aim to assess a potential short term causal effect of discharge on suicide risk using a novel counterfactual framework for causal inference.
Methods
National registry linkage study with individuals 18 years or older who died by suicide from 1.1.2018 to 31.12.2022 and was discharged in the last year (N = 731). We used a Case-crossover design comparing risk at a case-time and five randomly selected control-times within subjects and employed the Mantel-Haenszel estimator.
Results
We found an effect of discharge on the Incidence Rate Ratio (IRR) for suicide within 14 days (IRR = 5.48 95 % CI:4.37–6.72). Comparing the first four weeks, the IRR was 6.32 (95 % CI 4.87–8.00) for the first week, with significantly reduced risk for subsequent weeks.
Conclusion
Our findings are consistent with a causal effect of discharge on short-term suicide risk, under the assumptions described and controlling for confounders not addressed in prior studies. Recognizing this risk as causal enhances our understanding of the suicides that happen shortly after discharge and emphasizes the importance of identifying realistic targets for intervention in the post discharge period, which can then be evaluated through clinical trials.
{"title":"Discharge from mental health service admissions as a short-term causal risk factor for suicide: A case-crossover study","authors":"Kristoffer Bele Ødegård , Martin Øverlien Myhre , Ole Klungsøyr , Lars Mehlum , Anita Johanna Tørmoen , Fredrik A. Walby","doi":"10.1016/j.jpsychires.2026.01.004","DOIUrl":"10.1016/j.jpsychires.2026.01.004","url":null,"abstract":"<div><h3>Background</h3><div>The month following discharge from inpatient mental health treatment is the period associated with the highest short-term risk of suicide. The nature of this risk is not well understood. We aim to assess a potential short term causal effect of discharge on suicide risk using a novel counterfactual framework for causal inference.</div></div><div><h3>Methods</h3><div>National registry linkage study with individuals 18 years or older who died by suicide from 1.1.2018 to 31.12.2022 and was discharged in the last year (N = 731). We used a Case-crossover design comparing risk at a case-time and five randomly selected control-times within subjects and employed the Mantel-Haenszel estimator.</div></div><div><h3>Results</h3><div>We found an effect of discharge on the Incidence Rate Ratio (IRR) for suicide within 14 days (IRR = 5.48 95 % CI:4.37–6.72). Comparing the first four weeks, the IRR was 6.32 (95 % CI 4.87–8.00) for the first week, with significantly reduced risk for subsequent weeks.</div></div><div><h3>Conclusion</h3><div>Our findings are consistent with a causal effect of discharge on short-term suicide risk, under the assumptions described and controlling for confounders not addressed in prior studies. Recognizing this risk as causal enhances our understanding of the suicides that happen shortly after discharge and emphasizes the importance of identifying realistic targets for intervention in the post discharge period, which can then be evaluated through clinical trials.</div></div>","PeriodicalId":16868,"journal":{"name":"Journal of psychiatric research","volume":"194 ","pages":"Pages 174-180"},"PeriodicalIF":3.2,"publicationDate":"2026-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145917841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-03DOI: 10.1016/j.jpsychires.2026.01.005
Ke Wang, Shan Cai, Xin-Rong Duanmu, Chen-Yu Ma, Rui Yan, Yan-Rui Cui, Lin Zhou, Liu-Liu Xu
Objective
Quetiapine is an atypical antipsychotic with a broad spectrum of use including anti-anxiety and mood stabilizing properties and has proved effective in mood disorders, such as major depressive disorder and bipolar depression. An integration of cognitive behavioral therapy (CBT) with pharmacological treatment has shown to outperform drugs alone in reducing suicide risk for patients with mood disorders. In this study, we investigated the effect of adding cognitive behavioral therapy (CBT) to quetiapine on suicide risk, depressive symptoms, and coping style in adult patients with mood disorders.
Methods
One hundred and thirty-seven patients were randomized to QUE group (n = 70) and QUE + CBT group (n = 67). The primary outcome was suicide risk assessed by the Nurses’ Global Assessment of Suicide Risk (NGASR) scale. The secondary outcomes were depressive symptoms assessed by the 24-item Hamilton Depression Rating Scale (HDRS-24) and coping style assessed by the Simplified Coping Style Questionnaire (SCSQ).
Results
The QUE + CBT group showed a significantly lower percentage with high suicide risk in the modified intention-to-treat population than the QUE group after 12-week intervention (χ2 = 5.50; p = 0.02). The analysis of covariance (ANCOVA) controlling for baseline scores indicated a significantly main effect of treatment in scores of NGASR [F(1, 135) = 25.30, p < 0.01, partial η2 = 0.16], HDRS-24 [F(1, 135) = 27.00, p < 0.01, partial η2 = 0.17], positive coping [F(1, 135) = 10.00, p < 0.01, partial η2 = 0.07] and negative coping of SCSQ [F(1, 135) = 26.70, p < 0.01, partial η2 = 0.17], suggesting that lower scores of NGASR and HDRS-24, a higher positive coping score, and a lower negative coping score in the QUE + CBT group than in the QUE group after 12-week intervention.
Conclusion
These results suggest that adding CBT to quetiapine could decrease suicide risk, improve depressive symptoms, and enhance coping style for adult patients with mood disorders.
目的：喹硫平是一种非典型抗精神病药物，具有广泛的抗焦虑和情绪稳定特性，已被证明对情绪障碍（如重度抑郁症和双相抑郁症）有效。认知行为疗法（CBT）与药物治疗相结合，在降低情绪障碍患者自杀风险方面的效果优于单独使用药物。在本研究中，我们研究了认知行为疗法（CBT）与喹硫平联合治疗对成年情绪障碍患者自杀风险、抑郁症状和应对方式的影响。方法：137例患者随机分为QUE组（n = 70）和QUE + CBT组（n = 67）。主要结果是自杀风险评估护士全球自杀风险评估（NGASR）量表。次要结局采用24项汉密尔顿抑郁评定量表（HDRS-24）评估抑郁症状，采用简化应对方式问卷（SCSQ）评估应对方式。结果：干预12周后，QUE + CBT组在修改意向治疗人群中的高自杀风险百分比明显低于QUE组（χ2 = 5.50; p = 0.02）。控制基线得分的协方差分析（ANCOVA）显示，治疗对NGASR得分[F(1,135) = 25.30, p 2 = 0.16]、HDRS-24得分[F(1,135) = 27.00, p 2 = 0.17]、积极应对[F(1,135) = 10.00, p 2 = 0.07]、SCSQ消极应对[F(1,135) = 26.70, p 2 = 0.17]有显著的主效应，提示NGASR和HDRS-24得分越低，积极应对得分越高。干预12周后，QUE + CBT组的消极应对得分低于QUE组。结论：在喹硫平基础上加用CBT可降低成年心境障碍患者自杀风险，改善抑郁症状，改善应对方式。
{"title":"Effect of adding cognitive behavioral therapy to quetiapine on suicide risk, depressive symptoms, and coping style in adult patients with mood disorders","authors":"Ke Wang, Shan Cai, Xin-Rong Duanmu, Chen-Yu Ma, Rui Yan, Yan-Rui Cui, Lin Zhou, Liu-Liu Xu","doi":"10.1016/j.jpsychires.2026.01.005","DOIUrl":"10.1016/j.jpsychires.2026.01.005","url":null,"abstract":"<div><h3>Objective</h3><div>Quetiapine is an atypical antipsychotic with a broad spectrum of use including anti-anxiety and mood stabilizing properties and has proved effective in mood disorders, such as major depressive disorder and bipolar depression. An integration of cognitive behavioral therapy (CBT) with pharmacological treatment has shown to outperform drugs alone in reducing suicide risk for patients with mood disorders. In this study, we investigated the effect of adding cognitive behavioral therapy (CBT) to quetiapine on suicide risk, depressive symptoms, and coping style in adult patients with mood disorders.</div></div><div><h3>Methods</h3><div>One hundred and thirty-seven patients were randomized to QUE group (n = 70) and QUE + CBT group (n = 67). The primary outcome was suicide risk assessed by the Nurses’ Global Assessment of Suicide Risk (NGASR) scale. The secondary outcomes were depressive symptoms assessed by the 24-item Hamilton Depression Rating Scale (HDRS-24) and coping style assessed by the Simplified Coping Style Questionnaire (SCSQ).</div></div><div><h3>Results</h3><div>The QUE + CBT group showed a significantly lower percentage with high suicide risk in the modified intention-to-treat population than the QUE group after 12-week intervention (χ<sup>2</sup> = 5.50; p = 0.02). The analysis of covariance (ANCOVA) controlling for baseline scores indicated a significantly main effect of treatment in scores of NGASR [F(1, 135) = 25.30, p < 0.01, partial η<sup>2</sup> = 0.16], HDRS-24 [F(1, 135) = 27.00, p < 0.01, partial η<sup>2</sup> = 0.17], positive coping [F(1, 135) = 10.00, p < 0.01, partial η<sup>2</sup> = 0.07] and negative coping of SCSQ [F(1, 135) = 26.70, p < 0.01, partial η<sup>2</sup> = 0.17], suggesting that lower scores of NGASR and HDRS-24, a higher positive coping score, and a lower negative coping score in the QUE + CBT group than in the QUE group after 12-week intervention.</div></div><div><h3>Conclusion</h3><div>These results suggest that adding CBT to quetiapine could decrease suicide risk, improve depressive symptoms, and enhance coping style for adult patients with mood disorders.</div></div>","PeriodicalId":16868,"journal":{"name":"Journal of psychiatric research","volume":"194 ","pages":"Pages 145-150"},"PeriodicalIF":3.2,"publicationDate":"2026-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145912053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
SARS-CoV-2 infection has been implicated in hippocampal damage, contributing to the pathogenesis of dysexecutive syndrome observed in post-COVID-19 patients. Given the growing prevalence of long-COVID worldwide, understanding how SARS-CoV-2 affects hippocampal structure and function has become an urgent scientific and clinical priority. The hippocampus—crucial for memory, emotional regulation, and executive functioning—is especially susceptible to viral-driven neuroinflammatory cascades. SARS-CoV-2 triggers astrocyte and microglia activation, disrupts blood–brain barrier integrity, and induces cytokine-mediated neurotoxicity, ultimately impairing neuroplasticity and neurogenesis. These mechanisms converge to produce cognitive and affective disturbances—most notably fatigue, apathy, low mood, and executive dysfunction—that typify dysexecutive syndrome in long-COVID.
This review synthesizes current evidence from clinical and experimental studies, integrating findings on viral neurotropism, hippocampal hypometabolism, and astrocyte-mediated neurodegeneration. Distinctions between depressive symptoms driven by neuroinflammation and classical depressive disorders are clarified to improve diagnostic accuracy and guide personalized treatment. Emerging data on the neuroprotective role of COVID-19 vaccination—particularly its capacity to modulate microglial activation and support hippocampal neurogenesis—are also examined. Overall, the findings underscore the need for targeted therapeutic strategies aimed at modulating neuroinflammation and supporting hippocampal plasticity, including cognitive rehabilitation approaches.
Longitudinal studies are essential to elucidate the enduring impact of SARS-CoV-2 on hippocampal function and to inform effective clinical interventions.
{"title":"Astrocyte-mediated hippocampal damage in the pathogenesis of dysexecutive syndrome following COVID-19: A narrative review","authors":"Antonino Messina , Fabrizio Bella , Giuliana Maccarone , Gabriele Avincola , Maria Salvina Signorelli","doi":"10.1016/j.jpsychires.2026.01.007","DOIUrl":"10.1016/j.jpsychires.2026.01.007","url":null,"abstract":"<div><div>SARS-CoV-2 infection has been implicated in hippocampal damage, contributing to the pathogenesis of dysexecutive syndrome observed in post-COVID-19 patients. Given the growing prevalence of long-COVID worldwide, understanding how SARS-CoV-2 affects hippocampal structure and function has become an urgent scientific and clinical priority. The hippocampus—crucial for memory, emotional regulation, and executive functioning—is especially susceptible to viral-driven neuroinflammatory cascades. SARS-CoV-2 triggers astrocyte and microglia activation, disrupts blood–brain barrier integrity, and induces cytokine-mediated neurotoxicity, ultimately impairing neuroplasticity and neurogenesis. These mechanisms converge to produce cognitive and affective disturbances—most notably fatigue, apathy, low mood, and executive dysfunction—that typify dysexecutive syndrome in long-COVID.</div><div>This review synthesizes current evidence from clinical and experimental studies, integrating findings on viral neurotropism, hippocampal hypometabolism, and astrocyte-mediated neurodegeneration. Distinctions between depressive symptoms driven by neuroinflammation and classical depressive disorders are clarified to improve diagnostic accuracy and guide personalized treatment. Emerging data on the neuroprotective role of COVID-19 vaccination—particularly its capacity to modulate microglial activation and support hippocampal neurogenesis—are also examined. Overall, the findings underscore the need for targeted therapeutic strategies aimed at modulating neuroinflammation and supporting hippocampal plasticity, including cognitive rehabilitation approaches.</div><div>Longitudinal studies are essential to elucidate the enduring impact of SARS-CoV-2 on hippocampal function and to inform effective clinical interventions.</div></div>","PeriodicalId":16868,"journal":{"name":"Journal of psychiatric research","volume":"194 ","pages":"Pages 164-173"},"PeriodicalIF":3.2,"publicationDate":"2026-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145912068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-03DOI: 10.1016/j.jpsychires.2026.01.008
Ye Tu , Shenrui Li , Shaodi Guan , Yueyang Xin , Hong Tao , Zhiqiang Zhou , Shaofang Wang , Hongwei Jiang , Hui Xu
Background
Schizophrenia, a debilitating neuropsychiatric disorder with profound socioeconomic consequences, manifests characteristic cortical thinning patterns observable through neuroimaging. While structural magnetic resonance imaging (MRI) studies consistently demonstrate these anatomical disturbances, their molecular signatures remain poorly understood.
Methods
We employed an integrative neuroimaging-transcriptomic approach, combining structural MRI data from 50 schizophrenia patients and 125 healthy controls with postmortem gene expression profiles from the Allen Human Brain Atlas. Spatial relationships between transcriptional patterns and cortical thickness variations were quantified using partial least squares regression. Subsequent analyses included gene ontology enrichment, cell-type deconvolution, and protein-protein interaction network.
Results
Schizophrenia patients demonstrated significant cortical thinning in limbic and paralimbic regions critical for emotional processing, including anterior cingulate and insular cortices. Imaging transcriptomic analyses revealed strong associations between cortical alterations and schizophrenia-risk genes STON2, ANK3, and KCNN3. Enriched biological pathways included stress-responsive signaling, calcium homeostasis, and synaptic plasticity. Cell-type analyses implicated excitatory and inhibitory neurons, together with microglia, while network analysis identified KCNB1, PTGS2, and TPT1 as central molecular hubs.
Conclusions
This study reveals specific molecular correlates of cortical thinning in schizophrenia, highlighting biological mechanisms that may contribute to structural abnormalities. The identified genes and pathways offer potential therapeutic targets for addressing both neuroanatomical changes and affective disturbances in schizophrenia.
{"title":"Imaging transcriptomics identifies gene signatures associated with cortical thinning in schizophrenia","authors":"Ye Tu , Shenrui Li , Shaodi Guan , Yueyang Xin , Hong Tao , Zhiqiang Zhou , Shaofang Wang , Hongwei Jiang , Hui Xu","doi":"10.1016/j.jpsychires.2026.01.008","DOIUrl":"10.1016/j.jpsychires.2026.01.008","url":null,"abstract":"<div><h3>Background</h3><div>Schizophrenia, a debilitating neuropsychiatric disorder with profound socioeconomic consequences, manifests characteristic cortical thinning patterns observable through neuroimaging. While structural magnetic resonance imaging (MRI) studies consistently demonstrate these anatomical disturbances, their molecular signatures remain poorly understood.</div></div><div><h3>Methods</h3><div>We employed an integrative neuroimaging-transcriptomic approach, combining structural MRI data from 50 schizophrenia patients and 125 healthy controls with postmortem gene expression profiles from the Allen Human Brain Atlas. Spatial relationships between transcriptional patterns and cortical thickness variations were quantified using partial least squares regression. Subsequent analyses included gene ontology enrichment, cell-type deconvolution, and protein-protein interaction network.</div></div><div><h3>Results</h3><div>Schizophrenia patients demonstrated significant cortical thinning in limbic and paralimbic regions critical for emotional processing, including anterior cingulate and insular cortices. Imaging transcriptomic analyses revealed strong associations between cortical alterations and schizophrenia-risk genes <em>STON2, ANK3,</em> and <em>KCNN3</em>. Enriched biological pathways included stress-responsive signaling, calcium homeostasis, and synaptic plasticity. Cell-type analyses implicated excitatory and inhibitory neurons, together with microglia, while network analysis identified KCNB1, PTGS2, and TPT1 as central molecular hubs.</div></div><div><h3>Conclusions</h3><div>This study reveals specific molecular correlates of cortical thinning in schizophrenia, highlighting biological mechanisms that may contribute to structural abnormalities. The identified genes and pathways offer potential therapeutic targets for addressing both neuroanatomical changes and affective disturbances in schizophrenia.</div></div>","PeriodicalId":16868,"journal":{"name":"Journal of psychiatric research","volume":"194 ","pages":"Pages 151-163"},"PeriodicalIF":3.2,"publicationDate":"2026-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145912036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-03DOI: 10.1016/j.jpsychires.2026.01.001
K. Wolfova , B.H. Strand , J. Weiss , P. Brennan Kearns , T. Mekonnen , Y. Stern , H.-P. Kohler , V.F. Skirbekk , S.E. Tom
Objectives
We explored the relationship between the number of children and cognitive outcomes in later life in a large cohort of older females and males from Norway.
Design
Cross-sectional analysis using multinomial logistic regression.
Settings
The Norwegian HUNT4 70+ Study.
Participants
Males and females aged ≥70 years.
Measurments
The exposure was the number of biological children (none, one, two, three, or four or more). The primary outcome was categorized as dementia, mild cognitive impairment (MCI), or no cognitive impairment.
Results
Among 9263 participants (mean age 78 years; 54 % females), those without children had higher risk of dementia (relative risk ratio [RRR] 1.82, 95 % confidence interval [CI] 1.37 to 2.42) and MCI (RRR 1.31, 95 % CI 1.08 to 1.59) compared to those who had two children, adjusting for age and sex. Similar pattern was observed for those with one child, whereas those with three children did not have an increased MCI or dementia risk. Having four or more children was marginally associated with higher dementia risk (RRR 1.22, 95 % CI 1.00–1.49), but not with MCI risk. This association was attenuated after adjusting for education and marital status, whereas those without children and with one child had still higher risk. In sex-stratified analysis, having no children was associated with higher risk of dementia only in males.
Conclusions
The weak association with high parity, along with the increased dementia risk observed in males without children, contrasts with previous findings. Our results highlight the need for further investigation into the social mechanisms linking reproductive history to cognitive health.
目的：我们对来自挪威的一大群老年男女进行研究，探讨子女数量与晚年认知结局之间的关系。设计采用多项逻辑回归进行横断面分析。挪威HUNT4 70+研究。参与者：年龄≥70岁的男女。暴露量是指亲生子女的数量（没有、一个、两个、三个、四个或更多）。主要结局分为痴呆、轻度认知障碍（MCI）或无认知障碍。结果在9263名参与者中（平均年龄78岁，女性占54%），与有两个孩子的参与者相比，没有孩子的参与者患痴呆（相对风险比[RRR] 1.82, 95%可信区间[CI] 1.37至2.42）和MCI （RRR 1.31, 95% CI 1.08至1.59）的风险更高，调整了年龄和性别。有一个孩子的人也观察到了类似的模式，而有三个孩子的人则没有增加轻度认知障碍或痴呆的风险。有4个或4个以上孩子与较高的痴呆风险有轻微关联（RRR 1.22, 95% CI 1.00-1.49），但与轻度认知障碍风险无关。在调整了教育程度和婚姻状况后，这种关联减弱了，而没有孩子和只有一个孩子的人的风险仍然更高。在性别分层分析中，没有孩子的男性患痴呆症的风险更高。结论：在没有孩子的男性中观察到的高胎次与痴呆风险增加的弱关联，与先前的研究结果形成了对比。我们的研究结果强调需要进一步研究生殖史与认知健康之间的社会机制。
{"title":"Reproductive history and cognitive health among older Norwegian females and males: the population-based HUNT Study","authors":"K. Wolfova , B.H. Strand , J. Weiss , P. Brennan Kearns , T. Mekonnen , Y. Stern , H.-P. Kohler , V.F. Skirbekk , S.E. Tom","doi":"10.1016/j.jpsychires.2026.01.001","DOIUrl":"10.1016/j.jpsychires.2026.01.001","url":null,"abstract":"<div><h3>Objectives</h3><div>We explored the relationship between the number of children and cognitive outcomes in later life in a large cohort of older females and males from Norway.</div></div><div><h3>Design</h3><div>Cross-sectional analysis using multinomial logistic regression.</div></div><div><h3>Settings</h3><div>The Norwegian HUNT4 70+ Study.</div></div><div><h3>Participants</h3><div>Males and females aged ≥70 years.</div></div><div><h3>Measurments</h3><div>The exposure was the number of biological children (none, one, two, three, or four or more). The primary outcome was categorized as dementia, mild cognitive impairment (MCI), or no cognitive impairment.</div></div><div><h3>Results</h3><div>Among 9263 participants (mean age 78 years; 54 % females), those without children had higher risk of dementia (relative risk ratio [RRR] 1.82, 95 % confidence interval [CI] 1.37 to 2.42) and MCI (RRR 1.31, 95 % CI 1.08 to 1.59) compared to those who had two children, adjusting for age and sex. Similar pattern was observed for those with one child, whereas those with three children did not have an increased MCI or dementia risk. Having four or more children was marginally associated with higher dementia risk (RRR 1.22, 95 % CI 1.00–1.49), but not with MCI risk. This association was attenuated after adjusting for education and marital status, whereas those without children and with one child had still higher risk. In sex-stratified analysis, having no children was associated with higher risk of dementia only in males.</div></div><div><h3>Conclusions</h3><div>The weak association with high parity, along with the increased dementia risk observed in males without children, contrasts with previous findings. Our results highlight the need for further investigation into the social mechanisms linking reproductive history to cognitive health.</div></div>","PeriodicalId":16868,"journal":{"name":"Journal of psychiatric research","volume":"194 ","pages":"Pages 181-187"},"PeriodicalIF":3.2,"publicationDate":"2026-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145927689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-03DOI: 10.1016/j.jpsychires.2026.01.003
Rachel M. Ranney , Beth E. Cohen , Hui Shen , Katherine J. Hoggatt , Shira Maguen
This study aimed to investigate associations between social determinants of health (SDoH, the conditions in which people live) and receipt of psychotherapy among Veterans with posttraumatic stress disorder (PTSD) engaged in care at the Veterans Health Administration. Past research has identified disparities in receipt of PTSD care related to demographics, but there is a lack of research on disparities related to SDoH. This study investigated three SDoH: homelessness, socioeconomic disadvantage, and rurality. Using VHA electronic health records, we included Veterans with a PTSD diagnosis from 2015 to 2018, a total of 435,381 Veterans, and reviewed receipt of PTSD psychotherapy through 2019. In regression models accounting for demographics, trauma exposure, and mental and physical health factors, we found that Veterans who had experienced lifetime homelessness were more likely to receive any PTSD psychotherapy and a minimally adequate dose of PTSD psychotherapy (eight sessions within a 24-week period). We found that Veterans with greater socioeconomic disadvantage and Veterans who resided in rural areas were less likely to receive a minimally adequate dose of PTSD psychotherapy. These findings suggest that efforts are needed to promote engagement with mental healthcare for rural Veterans and those with greater socioeconomic disadvantage.
{"title":"Social determinants of health associated with receipt of psychotherapy for veterans with posttraumatic stress disorder","authors":"Rachel M. Ranney , Beth E. Cohen , Hui Shen , Katherine J. Hoggatt , Shira Maguen","doi":"10.1016/j.jpsychires.2026.01.003","DOIUrl":"10.1016/j.jpsychires.2026.01.003","url":null,"abstract":"<div><div>This study aimed to investigate associations between social determinants of health (SDoH, the conditions in which people live) and receipt of psychotherapy among Veterans with posttraumatic stress disorder (PTSD) engaged in care at the Veterans Health Administration. Past research has identified disparities in receipt of PTSD care related to demographics, but there is a lack of research on disparities related to SDoH. This study investigated three SDoH: homelessness, socioeconomic disadvantage, and rurality. Using VHA electronic health records, we included Veterans with a PTSD diagnosis from 2015 to 2018, a total of 435,381 Veterans, and reviewed receipt of PTSD psychotherapy through 2019. In regression models accounting for demographics, trauma exposure, and mental and physical health factors, we found that Veterans who had experienced lifetime homelessness were more likely to receive any PTSD psychotherapy and a minimally adequate dose of PTSD psychotherapy (eight sessions within a 24-week period). We found that Veterans with greater socioeconomic disadvantage and Veterans who resided in rural areas were less likely to receive a minimally adequate dose of PTSD psychotherapy. These findings suggest that efforts are needed to promote engagement with mental healthcare for rural Veterans and those with greater socioeconomic disadvantage.</div></div>","PeriodicalId":16868,"journal":{"name":"Journal of psychiatric research","volume":"194 ","pages":"Pages 188-195"},"PeriodicalIF":3.2,"publicationDate":"2026-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145927688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Major depressive disorder (MDD) affects approximately 280 million people worldwide, yet its neurobiological mechanisms remain largely unclear. Anti-myelin basic protein (anti-MBP) antibodies, markers of autoimmune activity, have been associated with various neuropsychiatric conditions, but their role in depression is poorly understood. This study examined the associations between serum anti-MBP levels, depression severity, functioning, and hippocampal volume, and compared anti-MBP levels between patients with MDD and healthy controls.
Methods
Thirty patients diagnosed with MDD who applied to the psychiatry outpatient clinic of Farabi Hospital and 30 healthy controls matched for age, gender and education were included. All participants were assessed using the Hamilton Depression Rating Scale (HAM-D), the Montgomery-Åsberg Depression Rating Scale (MADRS), and the Functioning Assessment Short Test (FAST). Venous blood samples were collected to determine anti-MBP levels. Hippocampal volumes were assessed using T1-weighted magnetic resonance imaging.
Results
Linear regression analysis in the total sample of participants demonstrated that anti-MBP levels were significantly associated with a decrease in total (p = 0.020), right (p = 0.013), and left (p = 0.046) hippocampal volume. Furthermore, ROC analysis revealed that anti-MBP levels could distinguish MDD patients from healthy controls with high diagnostic accuracy.
Conclusions
These results suggest a potential association between anti-MBP antibodies and neuroimmune alterations in depression. Across all participants, age- and sex-adjusted regression analyses showed an inverse association between anti-MBP and hippocampal volume. Notably, anti-MBP levels were higher in patients, suggesting its potential utility as a biomarker candidate for future studies in MDD. Consistently, ROC analysis performed well in discriminating between patients and controls.
{"title":"The relationship between Antibody levels against myelin basic protein in depressive disorder, neuroimaging, and functioning","authors":"Samet Öksüz , Aykut Karahan , Hüseyin Yaman , Selçuk Akkaya","doi":"10.1016/j.jpsychires.2025.12.048","DOIUrl":"10.1016/j.jpsychires.2025.12.048","url":null,"abstract":"<div><h3>Background</h3><div>Major depressive disorder (MDD) affects approximately 280 million people worldwide, yet its neurobiological mechanisms remain largely unclear. Anti-myelin basic protein (anti-MBP) antibodies, markers of autoimmune activity, have been associated with various neuropsychiatric conditions, but their role in depression is poorly understood. This study examined the associations between serum anti-MBP levels, depression severity, functioning, and hippocampal volume, and compared anti-MBP levels between patients with MDD and healthy controls.</div></div><div><h3>Methods</h3><div>Thirty patients diagnosed with MDD who applied to the psychiatry outpatient clinic of Farabi Hospital and 30 healthy controls matched for age, gender and education were included. All participants were assessed using the Hamilton Depression Rating Scale (HAM-D), the Montgomery-Åsberg Depression Rating Scale (MADRS), and the Functioning Assessment Short Test (FAST). Venous blood samples were collected to determine anti-MBP levels. Hippocampal volumes were assessed using T1-weighted magnetic resonance imaging.</div></div><div><h3>Results</h3><div>Linear regression analysis in the total sample of participants demonstrated that anti-MBP levels were significantly associated with a decrease in total (p = 0.020), right (p = 0.013), and left (p = 0.046) hippocampal volume. Furthermore, ROC analysis revealed that anti-MBP levels could distinguish MDD patients from healthy controls with high diagnostic accuracy.</div></div><div><h3>Conclusions</h3><div>These results suggest a potential association between anti-MBP antibodies and neuroimmune alterations in depression. Across all participants, age- and sex-adjusted regression analyses showed an inverse association between anti-MBP and hippocampal volume. Notably, anti-MBP levels were higher in patients, suggesting its potential utility as a biomarker candidate for future studies in MDD. Consistently, ROC analysis performed well in discriminating between patients and controls.</div></div>","PeriodicalId":16868,"journal":{"name":"Journal of psychiatric research","volume":"194 ","pages":"Pages 90-98"},"PeriodicalIF":3.2,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145863347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-24DOI: 10.1016/j.jpsychires.2025.12.035
Eric Hollander, Naomi Fineberg
{"title":"Dan J. Stein (1962–2025): A life dedicated to the science and care of the mind","authors":"Eric Hollander, Naomi Fineberg","doi":"10.1016/j.jpsychires.2025.12.035","DOIUrl":"10.1016/j.jpsychires.2025.12.035","url":null,"abstract":"","PeriodicalId":16868,"journal":{"name":"Journal of psychiatric research","volume":"194 ","pages":"Pages 69-70"},"PeriodicalIF":3.2,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145827943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-23DOI: 10.1016/j.jpsychires.2025.12.047
Brad A. MacNeil, Bailey Coon, Talia Gruber, Shainee Price, Magdalena Samela, Reece Sandercock, Emily Wilson
This study examined clinicians’ perspectives of family-based therapy (FBT) and psychiatric medication, and whether they would recommend these for treating their own child or another family member if they had an eating disorder (ED). Participants were 80 clinicians (45 women, 35 men; Mage = 31.7 years) who completed an e-survey that included questions about their profession, whether they use FBT, training, and length of time providing it. Participants also reported their main theoretical orientation, whether they recommend FBT to their patients, and if they would recommend it to their own child or another family member. Approximately 42.5 % were physicians or psychiatrists, 30.1 % nurses or nurse practitioners, and 27.6 % therapists (e.g., psychologist, social worker etc.). The average amount of time they had been providing treatment for EDs was 4.38 years (SD = 1.09). Treatment settings included hospitals (45 %), community mental health (31.3 %), private practice (15 %), and residential treatment (8.8 %). Most participants were FBT trained (98.8 %) by in person workshop with supervision (46.8 %), in person workshop only (31.6 %), or other (21.6 %; online training, self-paced reading). Engagement in consultation or supervision for FBT was reported by 83.8 % of clinicians. All providers endorsed recommending FBT to their patients or another family member if they had an ED, whereas 88.8 % would recommend it for their own child. A considerable proportion of clinicians (96.3 %) would agree to start their own family member on psychiatric medication if they had an ED. These results have important implications for training and dissemination of the FBT.
{"title":"Clinicians’ perspectives on family-based therapy (FBT) and psychiatric medication for eating disorders","authors":"Brad A. MacNeil, Bailey Coon, Talia Gruber, Shainee Price, Magdalena Samela, Reece Sandercock, Emily Wilson","doi":"10.1016/j.jpsychires.2025.12.047","DOIUrl":"10.1016/j.jpsychires.2025.12.047","url":null,"abstract":"<div><div>This study examined clinicians’ perspectives of family-based therapy (FBT) and psychiatric medication, and whether they would recommend these for treating their own child or another family member if they had an eating disorder (ED). Participants were 80 clinicians (45 women, 35 men; <em>M</em><sub><em>age</em></sub> = 31.7 years) who completed an e-survey that included questions about their profession, whether they use FBT, training, and length of time providing it. Participants also reported their main theoretical orientation, whether they recommend FBT to their patients, and if they would recommend it to their own child or another family member. Approximately 42.5 % were physicians or psychiatrists, 30.1 % nurses or nurse practitioners, and 27.6 % therapists (e.g., psychologist, social worker etc.). The average amount of time they had been providing treatment for EDs was 4.38 years (<em>SD</em> = 1.09). Treatment settings included hospitals (45 %), community mental health (31.3 %), private practice (15 %), and residential treatment (8.8 %). Most participants were FBT trained (98.8 %) by in person workshop with supervision (46.8 %), in person workshop only (31.6 %), or other (21.6 %; online training, self-paced reading). Engagement in consultation or supervision for FBT was reported by 83.8 % of clinicians. All providers endorsed recommending FBT to their patients or another family member if they had an ED, whereas 88.8 % would recommend it for their own child. A considerable proportion of clinicians (96.3 %) would agree to start their own family member on psychiatric medication if they had an ED. These results have important implications for training and dissemination of the FBT.</div></div>","PeriodicalId":16868,"journal":{"name":"Journal of psychiatric research","volume":"194 ","pages":"Pages 85-89"},"PeriodicalIF":3.2,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145856597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-23DOI: 10.1016/j.jpsychires.2025.12.044
Michael G. Wheaton , Rachel Van Boxtel , Carolyn I. Rodriguez
Purpose
Hoarding disorder (HD) involves difficulty discarding clutter. Existing treatments for HD (including cognitive-behavioral therapy [CBT]) yield only partial symptom reduction. Identifying factors that contribute to hoarding may inform potential treatment mechanisms. One such factor is intolerance of uncertainty (IU), the tendency to maladaptively respond to the unknown via fear, discomfort, and avoidance. While IU has been linked to hoarding symptoms, its role in treatment outcomes remains understudied.
Methods
41 adults with HD completed the Buried in Treasures (BIT+) Workshop (a 16-session manualized skills group using CBT principles, with 10 additional supervised in-home uncluttering practice). IU and HD symptom severity were assessed pre- and post-treatment.
Results
Pre-treatment IU did not significantly predict improvement in hoarding symptoms (β = .15, p = .31). However, IU significantly decreased following treatment (t = 2.23, p = .017). Smaller reductions in IU significantly predicted worse hoarding symptom outcomes, accounting for baseline severity (β = .41, p < .01).
Conclusions
Results suggest that high initial levels of IU may not prevent patients from benefiting from hoarding treatment via the BIT+, but that reduction in IU accounts for a significant increment in hoarding treatment gains. Given the room for improvement evident in HD treatments, future research might consider augmenting existing treatment with IU-specific interventions to boost treatment efficacy.
目的：囤积障碍（HD）涉及难以丢弃杂物。现有的HD治疗方法（包括认知行为疗法[CBT]）只能部分减轻症状。确定导致囤积的因素可能为潜在的治疗机制提供信息。其中一个因素是对不确定性的不耐受（IU），即通过恐惧、不适和回避对未知做出不适应反应的倾向。虽然IU与囤积症状有关，但其在治疗结果中的作用仍未得到充分研究。方法：41名成人HD患者完成了埋藏在宝藏（BIT+）工作坊（一个使用CBT原则的16次手工技能小组，另外有10次在家监督整理练习）。治疗前后分别评估IU和HD症状严重程度。结果：治疗前IU不能显著预测囤积症状的改善（β = 0.15, p = 0.31）。然而，治疗后IU显著降低（t = 2.23, p = 0.017）。较小的IU减少显著预测更糟糕的囤积症状结果，考虑到基线严重程度（β = 0.41, p）。结论：结果表明，高初始IU水平可能不会阻止患者从BIT+治疗中获益，但IU的减少可以显著增加囤积治疗的收益。鉴于HD治疗有明显的改进空间，未来的研究可能会考虑用iu特异性干预措施来增加现有治疗，以提高治疗效果。
{"title":"Intolerance of uncertainty as a factor in hoarding treatment","authors":"Michael G. Wheaton , Rachel Van Boxtel , Carolyn I. Rodriguez","doi":"10.1016/j.jpsychires.2025.12.044","DOIUrl":"10.1016/j.jpsychires.2025.12.044","url":null,"abstract":"<div><h3>Purpose</h3><div>Hoarding disorder (HD) involves difficulty discarding clutter. Existing treatments for HD (including cognitive-behavioral therapy [CBT]) yield only partial symptom reduction. Identifying factors that contribute to hoarding may inform potential treatment mechanisms. One such factor is intolerance of uncertainty (IU), the tendency to maladaptively respond to the unknown via fear, discomfort, and avoidance. While IU has been linked to hoarding symptoms, its role in treatment outcomes remains understudied.</div></div><div><h3>Methods</h3><div>41 adults with HD completed the Buried in Treasures (BIT+) Workshop (a 16-session manualized skills group using CBT principles, with 10 additional supervised in-home uncluttering practice). IU and HD symptom severity were assessed pre- and post-treatment.</div></div><div><h3>Results</h3><div>Pre-treatment IU did not significantly predict improvement in hoarding symptoms (β = .15, p = .31). However, IU significantly decreased following treatment (t = 2.23, p = .017). Smaller reductions in IU significantly predicted worse hoarding symptom outcomes, accounting for baseline severity (β = .41, <em>p</em> < .01).</div></div><div><h3>Conclusions</h3><div>Results suggest that high initial levels of IU may not prevent patients from benefiting from hoarding treatment via the BIT+, but that reduction in IU accounts for a significant increment in hoarding treatment gains. Given the room for improvement evident in HD treatments, future research might consider augmenting existing treatment with IU-specific interventions to boost treatment efficacy.</div></div>","PeriodicalId":16868,"journal":{"name":"Journal of psychiatric research","volume":"194 ","pages":"Pages 116-122"},"PeriodicalIF":3.2,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145863317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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