Pub Date : 2025-02-01DOI: 10.1016/S2451-9022(25)00007-2
{"title":"Guide for Authors","authors":"","doi":"10.1016/S2451-9022(25)00007-2","DOIUrl":"10.1016/S2451-9022(25)00007-2","url":null,"abstract":"","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"10 2","pages":"Pages A5-A10"},"PeriodicalIF":5.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143167046","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 : 2025-02-01DOI: 10.1016/j.bpsc.2024.08.019
Jingxian He , Mercy Chepngetich Bore , Heng Jiang , Xianyang Gan , Junjie Wang , Jialin Li , Xiaolei Xu , Lan Wang , Kun Fu , Liyuan Li , Bo Zhou , Keith Kendrick , Benjamin Becker
Background
Pain empathy represents a fundamental building block of several social functions, which have been demonstrated to be impaired across various mental disorders by accumulating evidence from case-control functional magnetic resonance imaging studies. However, it remains unclear whether the dysregulations are underpinned by robust neural alterations across mental disorders.
Methods
This study utilized coordinate-based meta-analyses to quantitatively determine robust markers of altered pain empathy across mental disorders. To support the interpretation of the findings, exploratory network-level and behavioral meta-analyses were conducted.
Results
Quantitative analysis of 11 case-control functional magnetic resonance imaging studies with data from 296 patients and 229 control participants revealed that patients with mental disorders exhibited increased pain empathic reactivity in the left anterior cingulate gyrus, adjacent medial prefrontal cortex, and right middle temporal gyrus but decreased activity in the left cerebellum IV/V and left middle occipital gyrus compared with control participants. The hyperactive regions showed network-level interactions with the core default mode network and were associated with affective and social cognitive domains.
Conclusions
The findings suggest that pain empathic alterations across mental disorders are underpinned by excessive empathic reactivity in brain systems involved in empathic distress and social processes, highlighting a shared therapeutic target to normalize basal social dysfunctions in mental disorders.
{"title":"Neural Basis of Pain Empathy Dysregulations in Mental Disorders: A Preregistered Neuroimaging Meta-Analysis","authors":"Jingxian He , Mercy Chepngetich Bore , Heng Jiang , Xianyang Gan , Junjie Wang , Jialin Li , Xiaolei Xu , Lan Wang , Kun Fu , Liyuan Li , Bo Zhou , Keith Kendrick , Benjamin Becker","doi":"10.1016/j.bpsc.2024.08.019","DOIUrl":"10.1016/j.bpsc.2024.08.019","url":null,"abstract":"<div><h3>Background</h3><div>Pain empathy represents a fundamental building block of several social functions, which have been demonstrated to be impaired across various mental disorders by accumulating evidence from case-control functional magnetic resonance imaging studies. However, it remains unclear whether the dysregulations are underpinned by robust neural alterations across mental disorders.</div></div><div><h3>Methods</h3><div>This study utilized coordinate-based meta-analyses to quantitatively determine robust markers of altered pain empathy across mental disorders. To support the interpretation of the findings, exploratory network-level and behavioral meta-analyses were conducted.</div></div><div><h3>Results</h3><div>Quantitative analysis of 11 case-control functional magnetic resonance imaging studies with data from 296 patients and 229 control participants revealed that patients with mental disorders exhibited increased pain empathic reactivity in the left anterior cingulate gyrus, adjacent medial prefrontal cortex, and right middle temporal gyrus but decreased activity in the left cerebellum IV/V and left middle occipital gyrus compared with control participants. The hyperactive regions showed network-level interactions with the core default mode network and were associated with affective and social cognitive domains.</div></div><div><h3>Conclusions</h3><div>The findings suggest that pain empathic alterations across mental disorders are underpinned by excessive empathic reactivity in brain systems involved in empathic distress and social processes, highlighting a shared therapeutic target to normalize basal social dysfunctions in mental disorders.</div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"10 2","pages":"Pages 127-137"},"PeriodicalIF":5.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142303309","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 : 2025-02-01DOI: 10.1016/j.bpsc.2024.07.013
Francesco L. Donati , Ahmad Mayeli , Bruno Andry Nascimento Couto , Kamakashi Sharma , Sabine Janssen , Robert J. Krafty , Adenauer G. Casali , Fabio Ferrarelli
Background
Abnormalities in dorsolateral prefrontal cortex (DLPFC) oscillations are neurophysiological signatures of schizophrenia thought to underlie its cognitive deficits. Transcranial magnetic stimulation with electroencephalography (TMS-EEG) provides a measure of cortical oscillations unaffected by sensory relay functionality and/or patients’ level of engagement, which are important confounding factors in schizophrenia. Previous TMS–EEG work showed reduced fast, gamma-range oscillations and a slowing of the main DLPFC oscillatory frequency, or natural frequency, in chronic schizophrenia. However, it is unclear whether this DLPFC natural frequency slowing is present in early-course schizophrenia (EC-SCZ) and is associated with symptom severity and cognitive dysfunction.
Methods
We applied TMS–EEG to the left DLPFC in 30 individuals with EC-SCZ and 28 healthy control participants. Goal-directed working memory performance was assessed using the AX–Continuous Performance Task. The EEG frequency with the highest cumulative power at the stimulation site, or natural frequency, was extracted. We also calculated the local relative spectral power as the average power in each frequency band divided by the broadband power.
Results
Compared with the healthy control group, the EC-SCZ group had reduced DLPFC natural frequency (p = .0000002, Cohen’s d = −2.32) and higher DLPFC beta-range relative spectral power (p = .0003, Cohen’s d = 0.77). In the EC-SCZ group, the DLPFC natural frequency was inversely associated with negative symptoms. Across all participants, the beta band relative spectral power negatively correlated with AX–Continuous Performance Task performance.
Conclusions
DLPFC oscillatory slowing is an early pathophysiological biomarker of schizophrenia that is associated with its symptom severity and cognitive impairments. Future work should assess whether noninvasive neurostimulation, including repetitive TMS, can ameliorate prefrontal oscillatory deficits and related clinical functions in patients with EC-SCZ.
{"title":"Prefrontal Oscillatory Slowing in Early-Course Schizophrenia Is Associated With Worse Cognitive Performance and Negative Symptoms: A Transcranial Magnetic Stimulation–Electroencephalography Study","authors":"Francesco L. Donati , Ahmad Mayeli , Bruno Andry Nascimento Couto , Kamakashi Sharma , Sabine Janssen , Robert J. Krafty , Adenauer G. Casali , Fabio Ferrarelli","doi":"10.1016/j.bpsc.2024.07.013","DOIUrl":"10.1016/j.bpsc.2024.07.013","url":null,"abstract":"<div><h3>Background</h3><div>Abnormalities in dorsolateral prefrontal cortex (DLPFC) oscillations are neurophysiological signatures of schizophrenia thought to underlie its cognitive deficits. Transcranial magnetic stimulation with electroencephalography (TMS-EEG) provides a measure of cortical oscillations unaffected by sensory relay functionality and/or patients’ level of engagement, which are important confounding factors in schizophrenia. Previous TMS–EEG work showed reduced fast, gamma-range oscillations and a slowing of the main DLPFC oscillatory frequency, or natural frequency, in chronic schizophrenia. However, it is unclear whether this DLPFC natural frequency slowing is present in early-course schizophrenia (EC-SCZ) and is associated with symptom severity and cognitive dysfunction.</div></div><div><h3>Methods</h3><div>We applied TMS–EEG to the left DLPFC in 30 individuals with EC-SCZ and 28 healthy control participants. Goal-directed working memory performance was assessed using the AX–Continuous Performance Task. The EEG frequency with the highest cumulative power at the stimulation site, or natural frequency, was extracted. We also calculated the local relative spectral power as the average power in each frequency band divided by the broadband power.</div></div><div><h3>Results</h3><div>Compared with the healthy control group, the EC-SCZ group had reduced DLPFC natural frequency (<em>p</em> = .0000002, Cohen’s <em>d</em> = −2.32) and higher DLPFC beta-range relative spectral power (<em>p</em> = .0003, Cohen’s <em>d</em> = 0.77). In the EC-SCZ group, the DLPFC natural frequency was inversely associated with negative symptoms. Across all participants, the beta band relative spectral power negatively correlated with AX–Continuous Performance Task performance.</div></div><div><h3>Conclusions</h3><div>DLPFC oscillatory slowing is an early pathophysiological biomarker of schizophrenia that is associated with its symptom severity and cognitive impairments. Future work should assess whether noninvasive neurostimulation, including repetitive TMS, can ameliorate prefrontal oscillatory deficits and related clinical functions in patients with EC-SCZ.</div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"10 2","pages":"Pages 158-166"},"PeriodicalIF":5.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141768230","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 : 2025-02-01DOI: 10.1016/j.bpsc.2024.10.013
Anna Suleri , Tonya White , Lot de Witte , Frederieke Gigase , Charlotte A.M. Cecil , Vincent W.V. Jaddoe , Michael Breen , Manon H.J. Hillegers , Ryan L. Muetzel , Veerle Bergink
Background
Maternal immune activation (MIA) has been hypothesized to have an adverse effect on child neurodevelopment, but only a few neuroimaging studies have been performed to date, mostly in neonates. In this population-based cohort study, we investigated the association between MIA and multiple neuroimaging modalities depicting brain development from childhood to adolescence.
Methods
We used data of mother-child pairs from the Generation R Study. To define our exposure, we measured interleukin (IL) 1β, IL-6, IL-17a, IL-23, interferon gamma, and C-reactive protein at 2 time points during pregnancy. Because levels of these 5 cytokines were highly correlated, we were able to compute a cytokine index. We used multiple brain imaging modalities as outcomes, including global and regional measures of brain morphology (structural magnetic resonance imaging, volume; n = 3295), white matter microstructure (diffusion magnetic resonance imaging, fractional anisotropy and mean diffusivity; n = 3267), and functional connectivity (functional magnetic resonance imaging, graph theory measures, and network-level connectivity; n = 2914) in the children at ages 10 and 14 years. We performed mixed effects models using child’s age as a continuous time variable.
Results
We found no significant effect of time on any neuroimaging outcomes in children over time, and there was no time × MIA interaction. These associations were similar for the cytokine index, C-reactive protein, and individual cytokines. We observed no evidence for differential effects of timing of prenatal MIA or child sex after multiple testing correction.
Conclusions
In this longitudinal population-based study, we found no evidence for an association between MIA and child brain development in the general population. Our findings differ from previous research in neonates that have shown structural and functional brain abnormalities after MIA.
背景：母体免疫激活（MIA）被认为会对儿童的神经发育产生不良影响，但迄今为止仅开展了少数几项神经影像学研究，其中大部分是针对新生儿的。在这项基于人群的队列研究中，我们调查了 MIA 与描述儿童至青少年时期大脑发育的多种神经影像模式之间的关联：我们使用了 R 世代研究中的母子对数据。为了确定我们的暴露，我们在怀孕期间的两个时间点测量了IL-1β、IL-6、IL-17a、IL-23和IFN-γ以及CRP。鉴于这五种细胞因子的水平高度相关，我们可以计算出细胞因子指数。我们使用了多种脑成像模式作为研究结果，包括在儿童平均 10 岁和 14 岁时对大脑形态（结构磁共振成像，体积，n=3,295）、白质微结构（扩散磁共振成像，FA 和 MD，n=3,267）和功能连接（功能磁共振成像，图论测量和网络级连接，n=2,914）的整体和区域测量。我们使用儿童年龄作为连续时间变量，建立了混合效应模型：结果：我们发现，随着时间的推移，MIA 与儿童的任何神经影像结果之间都没有明显的关联或时间交互作用。细胞因子指数、CRP 和单个细胞因子也存在类似的关联。经过多重检验校正后，我们没有观察到产前 MIA 时间或儿童性别的不同影响：这项以人群为基础的纵向研究没有发现 MIA 与普通人群中儿童大脑发育有关的证据。我们的研究结果与之前对新生儿进行的研究不同，这些新生儿在经历 MIA 后会出现大脑结构和功能异常。
{"title":"Maternal Immune Activation and Child Brain Development: A Longitudinal Population-Based Multimodal Neuroimaging Study","authors":"Anna Suleri , Tonya White , Lot de Witte , Frederieke Gigase , Charlotte A.M. Cecil , Vincent W.V. Jaddoe , Michael Breen , Manon H.J. Hillegers , Ryan L. Muetzel , Veerle Bergink","doi":"10.1016/j.bpsc.2024.10.013","DOIUrl":"10.1016/j.bpsc.2024.10.013","url":null,"abstract":"<div><h3>Background</h3><div>Maternal immune activation (MIA) has been hypothesized to have an adverse effect on child neurodevelopment, but only a few neuroimaging studies have been performed to date, mostly in neonates. In this population-based cohort study, we investigated the association between MIA and multiple neuroimaging modalities depicting brain development from childhood to adolescence.</div></div><div><h3>Methods</h3><div>We used data of mother-child pairs from the Generation R Study. To define our exposure, we measured interleukin (IL) 1β, IL-6, IL-17a, IL-23, interferon gamma, and C-reactive protein at 2 time points during pregnancy. Because levels of these 5 cytokines were highly correlated, we were able to compute a cytokine index. We used multiple brain imaging modalities as outcomes, including global and regional measures of brain morphology (structural magnetic resonance imaging, volume; <em>n</em> = 3295), white matter microstructure (diffusion magnetic resonance imaging, fractional anisotropy and mean diffusivity; <em>n</em> = 3267), and functional connectivity (functional magnetic resonance imaging, graph theory measures, and network-level connectivity; <em>n</em> = 2914) in the children at ages 10 and 14 years. We performed mixed effects models using child’s age as a continuous time variable.</div></div><div><h3>Results</h3><div>We found no significant effect of time on any neuroimaging outcomes in children over time, and there was no time × MIA interaction. These associations were similar for the cytokine index, C-reactive protein, and individual cytokines. We observed no evidence for differential effects of timing of prenatal MIA or child sex after multiple testing correction.</div></div><div><h3>Conclusions</h3><div>In this longitudinal population-based study, we found no evidence for an association between MIA and child brain development in the general population. Our findings differ from previous research in neonates that have shown structural and functional brain abnormalities after MIA.</div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"10 2","pages":"Pages 222-235"},"PeriodicalIF":5.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142570460","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 : 2025-02-01DOI: 10.1016/j.bpsc.2024.06.007
Riddhi J. Pitliya , Kreshnik Burani , Brady D. Nelson , Greg Hajcak , Jingwen Jin
Background
The mechanisms that link neural and behavioral indices of reduced reward sensitivity in depression, particularly in children, remain unclear. Reward positivity (RewP), a neural index of reward processing, has been consistently associated with depression. Separately, recent studies using the drift-diffusion model on behavioral data have delineated computational indices of reward sensitivity. Therefore, in the current study, we examined whether RewP is a neural mediator of drift-diffusion model–based indices of reward processing in predicting pediatric depression across varying levels of symptom severity.
Methods
A community sample of 166 girls, ages 8 to 14 years, completed 2 tasks. The first was a reward guessing task from which RewP was computed using electroencephalography; the second was a probabilistic reward-based decision-making task. On this second task, drift-diffusion model analysis was applied to behavioral data to quantify the efficiency of accumulating reward-related evidence (drift rate) and potential baseline bias (starting point) toward the differently rewarded choices. Depression severity was measured using the self-report Children’s Depression Inventory.
Results
RewP was correlated with drift rate, but not starting point bias, toward the more rewarded choice. Furthermore, RewP completely mediated the association between a slower drift rate toward the more rewarded option and higher depression symptom severity.
Conclusions
Our findings suggest that reduced neural sensitivity to reward feedback may be a neural mechanism that underlies behavioral insensitivity to reward in children and adolescents with higher depression symptom severity, offering novel insights into the relationship between neural and computational indices of reward processing in this context.
{"title":"Reward-Related Brain Activity Mediates the Relationship Between Decision-Making Deficits and Pediatric Depression Symptom Severity","authors":"Riddhi J. Pitliya , Kreshnik Burani , Brady D. Nelson , Greg Hajcak , Jingwen Jin","doi":"10.1016/j.bpsc.2024.06.007","DOIUrl":"10.1016/j.bpsc.2024.06.007","url":null,"abstract":"<div><h3>Background</h3><div>The mechanisms that link neural and behavioral indices of reduced reward sensitivity in depression, particularly in children, remain unclear. Reward positivity (RewP), a neural index of reward processing, has been consistently associated with depression. Separately, recent studies using the drift-diffusion model on behavioral data have delineated computational indices of reward sensitivity. Therefore, in the current study, we examined whether RewP is a neural mediator of drift-diffusion model–based indices of reward processing in predicting pediatric depression across varying levels of symptom severity.</div></div><div><h3>Methods</h3><div>A community sample of 166 girls, ages 8 to 14 years, completed 2 tasks. The first was a reward guessing task from which RewP was computed using electroencephalography; the second was a probabilistic reward-based decision-making task. On this second task, drift-diffusion model analysis was applied to behavioral data to quantify the efficiency of accumulating reward-related evidence (drift rate) and potential baseline bias (starting point) toward the differently rewarded choices. Depression severity was measured using the self-report Children’s Depression Inventory.</div></div><div><h3>Results</h3><div>RewP was correlated with drift rate, but not starting point bias, toward the more rewarded choice. Furthermore, RewP completely mediated the association between a slower drift rate toward the more rewarded option and higher depression symptom severity.</div></div><div><h3>Conclusions</h3><div>Our findings suggest that reduced neural sensitivity to reward feedback may be a neural mechanism that underlies behavioral insensitivity to reward in children and adolescents with higher depression symptom severity, offering novel insights into the relationship between neural and computational indices of reward processing in this context.</div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"10 2","pages":"Pages 138-147"},"PeriodicalIF":5.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141473528","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 : 2025-01-01DOI: 10.1016/j.bpsc.2024.08.005
Nora Maria Raschle , Réka Borbás , Plamina Dimanova , Eva Unternaehrer , Gregor Kohls , Stephane De Brito , Graeme Fairchild , Christine M. Freitag , Kerstin Konrad , Christina Stadler
Background
Emotion regulation skills are linked to corticolimbic brain activity (e.g., dorsolateral prefrontal cortex [dlPFC] and limbic regions) and enable an individual to control their emotional experiences, thus allowing healthy social functioning. Disruptions in emotion regulation skills are reported in neuropsychiatric disorders, including conduct disorder or oppositional defiant disorder (CD/ODD). Clinically recognized means to ameliorate emotion regulation deficits observed in CD/ODD include cognitive or dialectical behavioral skills therapy as implemented in the START NOW program. However, the role of emotion regulation and its neural substrates in symptom severity and prognosis following treatment of adolescent CD/ODD has not been investigated.
Methods
Cross-sectional data including functional magnetic resonance imaging responses during emotion regulation (N = 114; average age = 15 years), repeated-measures assessments of symptom severity (pretreatment, posttreatment, long-term follow-up), and functional magnetic resonance imaging data collected prior to and following the START NOW randomized controlled trial (n = 44) for female adolescents with CD/ODD were analyzed using group comparisons and multiple regression.
Results
First, behavioral and neural correlates of emotion regulation were disrupted in female adolescents with CD/ODD. Second, ODD symptom severity was negatively associated with dlPFC/precentral gyrus activity during regulation. Third, treatment-related symptom changes were predicted by pretreatment ODD symptom severity and regulatory dlPFC/precentral activity. Additionally, pretreatment dlPFC/precentral activity and ODD symptom severity predicted long-term reductions in symptom severity following treatment for participants who received the START NOW treatment.
Conclusions
Our findings demonstrate the important role that emotion regulation skills play in the characteristics of CD/ODD and show that regulatory dlPFC/precentral activity is positively associated with treatment response in female adolescents with CD/ODD.
{"title":"Losing Control: Prefrontal Emotion Regulation Is Related to Symptom Severity and Predicts Treatment-Related Symptom Change in Adolescent Girls With Conduct Disorder","authors":"Nora Maria Raschle , Réka Borbás , Plamina Dimanova , Eva Unternaehrer , Gregor Kohls , Stephane De Brito , Graeme Fairchild , Christine M. Freitag , Kerstin Konrad , Christina Stadler","doi":"10.1016/j.bpsc.2024.08.005","DOIUrl":"10.1016/j.bpsc.2024.08.005","url":null,"abstract":"<div><h3>Background</h3><div>Emotion regulation skills are linked to corticolimbic brain activity (e.g., dorsolateral prefrontal cortex [dlPFC] and limbic regions) and enable an individual to control their emotional experiences, thus allowing healthy social functioning. Disruptions in emotion regulation skills are reported in neuropsychiatric disorders, including conduct disorder or oppositional defiant disorder (CD/ODD). Clinically recognized means to ameliorate emotion regulation deficits observed in CD/ODD include cognitive or dialectical behavioral skills therapy as implemented in the START NOW program. However, the role of emotion regulation and its neural substrates in symptom severity and prognosis following treatment of adolescent CD/ODD has not been investigated.</div></div><div><h3>Methods</h3><div>Cross-sectional data including functional magnetic resonance imaging responses during emotion regulation (<em>N</em> = 114; average age = 15 years), repeated-measures assessments of symptom severity (pretreatment, posttreatment, long-term follow-up), and functional magnetic resonance imaging data collected prior to and following the START NOW randomized controlled trial (<em>n</em> = 44) for female adolescents with CD/ODD were analyzed using group comparisons and multiple regression.</div></div><div><h3>Results</h3><div>First, behavioral and neural correlates of emotion regulation were disrupted in female adolescents with CD/ODD. Second, ODD symptom severity was negatively associated with dlPFC/precentral gyrus activity during regulation. Third, treatment-related symptom changes were predicted by pretreatment ODD symptom severity and regulatory dlPFC/precentral activity. Additionally, pretreatment dlPFC/precentral activity and ODD symptom severity predicted long-term reductions in symptom severity following treatment for participants who received the START NOW treatment.</div></div><div><h3>Conclusions</h3><div>Our findings demonstrate the important role that emotion regulation skills play in the characteristics of CD/ODD and show that regulatory dlPFC/precentral activity is positively associated with treatment response in female adolescents with CD/ODD.</div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"10 1","pages":"Pages 80-93"},"PeriodicalIF":5.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142057540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01DOI: 10.1016/j.bpsc.2024.08.004
Lotte Veddum , Vibeke Bliksted , Yuan Zhou , Anna Krogh Andreassen , Christina Bruun Knudsen , Aja Neergaard Greve , Nanna Lawaetz Steffensen , Merete Birk , Nicoline Hemager , Julie Marie Brandt , Maja Gregersen , Line Korsgaard Johnsen , Kit Melissa Larsen , William Frans Christiaan Baaré , Kathrine Skak Madsen , Hartwig Roman Siebner , Kerstin Jessica Plessen , Anne Amalie Elgaard Thorup , Leif Østergaard , Merete Nordentoft , Martin Dietz
Background
Schizophrenia and bipolar disorder are characterized by social cognitive impairments, and recent research has identified alterations of the social brain. However, it is unknown whether familial high risk (FHR) of these disorders is associated with neurobiological alterations already present in childhood.
Methods
As part of the Danish High Risk and Resilience Study–VIA 11, we examined children at FHR of schizophrenia (n = 121, 50% female) or bipolar disorder (n = 75, 47% female) and population-based control children (PBCs) (n = 128, 48% female). Using functional magnetic resonance imaging and dynamic causal modeling, we investigated brain activation and effective connectivity during the social cognition paradigm from the Human Connectome Project.
Results
We found similar activation of the mentalizing network across groups, including visual area V5, the dorsomedial prefrontal cortex, and the posterior superior temporal sulcus (pSTS). Nonetheless, both FHR groups showed aberrant brain connectivity in the form of increased feedforward connectivity from left V5 to pSTS compared with PBCs. Children at FHR of schizophrenia had reduced intrinsic connectivity in bilateral V5 compared with PBCs, whereas children at FHR of bipolar disorder showed increased reciprocal connectivity between the left dorsomedial prefrontal cortex and the pSTS, increased intrinsic connectivity in the right pSTS, and reduced feedforward connectivity from the right pSTS to the dorsomedial prefrontal cortex compared with PBCs.
Conclusions
Our results provide first-time evidence of aberrant brain connectivity in the mentalizing network of children at FHR of schizophrenia or FHR of bipolar disorder. Longitudinal research is warranted to clarify whether aberrant brain connectivity during mentalizing constitutes an endophenotype associated with the development of a mental disorder later in life.
{"title":"Brain Activation and Aberrant Effective Connectivity in the Mentalizing Network of Preadolescent Children at Familial High Risk of Schizophrenia or Bipolar Disorder","authors":"Lotte Veddum , Vibeke Bliksted , Yuan Zhou , Anna Krogh Andreassen , Christina Bruun Knudsen , Aja Neergaard Greve , Nanna Lawaetz Steffensen , Merete Birk , Nicoline Hemager , Julie Marie Brandt , Maja Gregersen , Line Korsgaard Johnsen , Kit Melissa Larsen , William Frans Christiaan Baaré , Kathrine Skak Madsen , Hartwig Roman Siebner , Kerstin Jessica Plessen , Anne Amalie Elgaard Thorup , Leif Østergaard , Merete Nordentoft , Martin Dietz","doi":"10.1016/j.bpsc.2024.08.004","DOIUrl":"10.1016/j.bpsc.2024.08.004","url":null,"abstract":"<div><h3>Background</h3><div>Schizophrenia and bipolar disorder are characterized by social cognitive impairments, and recent research has identified alterations of the social brain. However, it is unknown whether familial high risk (FHR) of these disorders is associated with neurobiological alterations already present in childhood.</div></div><div><h3>Methods</h3><div>As part of the Danish High Risk and Resilience Study–VIA 11, we examined children at FHR of schizophrenia (<em>n</em> = 121, 50% female) or bipolar disorder (<em>n</em> = 75, 47% female) and population-based control children (PBCs) (<em>n</em> = 128, 48% female). Using functional magnetic resonance imaging and dynamic causal modeling, we investigated brain activation and effective connectivity during the social cognition paradigm from the Human Connectome Project.</div></div><div><h3>Results</h3><div>We found similar activation of the mentalizing network across groups, including visual area V5, the dorsomedial prefrontal cortex, and the posterior superior temporal sulcus (pSTS). Nonetheless, both FHR groups showed aberrant brain connectivity in the form of increased feedforward connectivity from left V5 to pSTS compared with PBCs. Children at FHR of schizophrenia had reduced intrinsic connectivity in bilateral V5 compared with PBCs, whereas children at FHR of bipolar disorder showed increased reciprocal connectivity between the left dorsomedial prefrontal cortex and the pSTS, increased intrinsic connectivity in the right pSTS, and reduced feedforward connectivity from the right pSTS to the dorsomedial prefrontal cortex compared with PBCs.</div></div><div><h3>Conclusions</h3><div>Our results provide first-time evidence of aberrant brain connectivity in the mentalizing network of children at FHR of schizophrenia or FHR of bipolar disorder. Longitudinal research is warranted to clarify whether aberrant brain connectivity during mentalizing constitutes an endophenotype associated with the development of a mental disorder later in life.</div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"10 1","pages":"Pages 68-79"},"PeriodicalIF":5.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142057536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01DOI: 10.1016/j.bpsc.2024.09.009
Helmet T. Karim , Andrew Gerlach , Meryl A. Butters , Robert Krafty , Brian D. Boyd , Layla Banihashemi , Bennett A. Landman , Olusola Ajilore , Warren D. Taylor , Carmen Andreescu
Background
Late-life depression (LLD) has been associated cross-sectionally with lower brain structural volumes and accelerated brain aging compared with healthy control participants (HCs). There are few longitudinal studies on the neurobiological predictors of recurrence in LLD. We tested a machine learning brain age model and its prospective association with LLD recurrence risk.
Methods
We recruited individuals with LLD (n = 102) and HCs (n = 43) into a multisite, 2-year longitudinal study. Individuals with LLD were enrolled within 4 months of remission. Remitted participants with LLD underwent baseline neuroimaging and longitudinal clinical follow-up. Over 2 years, 43 participants with LLD relapsed and 59 stayed in remission. We used a previously developed machine learning brain age algorithm to compute brain age at baseline, and we evaluated brain age group differences (HC vs. LLD and HC vs. remitted LLD vs. relapsed LLD). We conducted a Cox proportional hazards model to evaluate whether baseline brain age predicted time to relapse.
Results
We found that brain age did not significantly differ between the HC and LLD groups or between the HC, remitted LLD, and relapsed LLD groups. Brain age did not significantly predict time to relapse.
Conclusions
In contrast to our hypothesis, we found that brain age did not differ between control participants without depression and individuals with remitted LLD, and brain age was not associated with subsequent recurrence. This is in contrast to existing literature which has identified baseline brain age differences in late life but consistent with work that has shown no differences between people who do and do not relapse on gross structural measures.
简介与健康对照组（HC）相比，晚年抑郁症（LLD）在横断面上与较低的脑结构体积和加速的脑衰老有关。有关晚年抑郁症复发的神经生物学预测因素的纵向研究很少。我们测试了机器学习（ML）脑年龄模型及其与LLD复发风险的前瞻性关联：我们招募了LLD患者（n=102）和HC患者（n=43）参与一项为期2年的多地点纵向研究。LLD患者在病情缓解后4个月内入组。缓解的LLD患者接受基线神经影像学检查和纵向临床随访。2年中，43名LLD患者复发（REL），59名患者保持缓解（REM）。我们使用之前开发的ML脑年龄算法计算基线时的脑年龄，并评估了脑年龄组差异（HC vs. LLD，HC vs. REM vs. REL）。我们采用 Cox 比例危险模型来评估基线脑龄是否能预测复发时间：结果：我们发现，脑年龄在 HC 组与 LLD 组以及 HC 组、REM 组和 REL 组之间没有明显差异。脑年龄对复发时间的预测作用也不明显：与我们的假设相反，我们发现非抑郁对照组和LLD缓解患者的脑年龄没有差异，而且脑年龄与随后的复发没有关联。这与现有文献中发现的晚年基线脑龄差异不同，但与那些显示复发和未复发者在结构测量上没有差异的研究结果一致。
{"title":"Brain Age Is Not a Significant Predictor of Relapse Risk in Late-Life Depression","authors":"Helmet T. Karim , Andrew Gerlach , Meryl A. Butters , Robert Krafty , Brian D. Boyd , Layla Banihashemi , Bennett A. Landman , Olusola Ajilore , Warren D. Taylor , Carmen Andreescu","doi":"10.1016/j.bpsc.2024.09.009","DOIUrl":"10.1016/j.bpsc.2024.09.009","url":null,"abstract":"<div><h3>Background</h3><div>Late-life depression (LLD) has been associated cross-sectionally with lower brain structural volumes and accelerated brain aging compared with healthy control participants (HCs). There are few longitudinal studies on the neurobiological predictors of recurrence in LLD. We tested a machine learning brain age model and its prospective association with LLD recurrence risk.</div></div><div><h3>Methods</h3><div>We recruited individuals with LLD (<em>n</em> = 102) and HCs (<em>n</em> = 43) into a multisite, 2-year longitudinal study. Individuals with LLD were enrolled within 4 months of remission. Remitted participants with LLD underwent baseline neuroimaging and longitudinal clinical follow-up. Over 2 years, 43 participants with LLD relapsed and 59 stayed in remission. We used a previously developed machine learning brain age algorithm to compute brain age at baseline, and we evaluated brain age group differences (HC vs. LLD and HC vs. remitted LLD vs. relapsed LLD). We conducted a Cox proportional hazards model to evaluate whether baseline brain age predicted time to relapse.</div></div><div><h3>Results</h3><div>We found that brain age did not significantly differ between the HC and LLD groups or between the HC, remitted LLD, and relapsed LLD groups. Brain age did not significantly predict time to relapse.</div></div><div><h3>Conclusions</h3><div>In contrast to our hypothesis, we found that brain age did not differ between control participants without depression and individuals with remitted LLD, and brain age was not associated with subsequent recurrence. This is in contrast to existing literature which has identified baseline brain age differences in late life but consistent with work that has shown no differences between people who do and do not relapse on gross structural measures.</div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"10 1","pages":"Pages 103-110"},"PeriodicalIF":5.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142334315","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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