首页 > 最新文献

Biological psychiatry global open science最新文献

英文 中文
A Window of Opportunity: Unraveling How Puberty Relates to Psychotic-Like Experiences During Adolescence 机会之窗:揭示青春期如何与青春期的精神病样经历相关
IF 3.7 Q2 NEUROSCIENCES Pub Date : 2026-03-01 Epub Date: 2026-01-17 DOI: 10.1016/j.bpsgos.2025.100687
Mark Curtis
{"title":"A Window of Opportunity: Unraveling How Puberty Relates to Psychotic-Like Experiences During Adolescence","authors":"Mark Curtis","doi":"10.1016/j.bpsgos.2025.100687","DOIUrl":"10.1016/j.bpsgos.2025.100687","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100687"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145978092","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}
引用次数: 0
The Occipital-Fronto-Limbic Circuit of Body Dysmorphic Disorder: A Systematic Review and Meta-Analysis of Neuroimaging Studies 身体畸形障碍的枕额边缘回路:神经影像学研究的系统回顾和荟萃分析。
IF 3.7 Q2 NEUROSCIENCES Pub Date : 2026-03-01 Epub Date: 2025-12-17 DOI: 10.1016/j.bpsgos.2025.100676
Yihui Cheng , Emalee Burrows , Ludvic Zrinzo , Harith Akram , Trevor W. Robbins , Himanshu Tyagi

Background

Body dysmorphic disorder (BDD) is a severe psychiatric disorder characterized by excessive preoccupation with perceived flaws in appearance. In this review, we aim to synthesize the latest findings on the neurobiology of BDD and propose an updated BDD neurocircuitry model.

Methods

A systematic search identified 38 peer-reviewed original articles, and the protocol was registered (CRD42024553665). Qualitative thematic analysis was conducted, and activation likelihood estimation (ALE) meta-analysis was performed to quantify brain activation patterns.

Results

Brain regions with significant morphometric divergence in patients with BDD were predominantly located in primary and secondary visual processing areas and temporal-limbic and frontal-striatal networks despite overall heterogeneous findings. The electroencephalography studies suggested early visual processing and attentional abnormalities. The ALE analysis revealed a general hyperactivation over the frontotemporal region and hypoactivation over parieto-occipital regions. Although BDD shared similar connectivity patterns in frontostriatal and arbitration networks with obsessive-compulsive disorder, it was further characterized by bottom-up and top-down interaction between the ventral visual stream and temporal-limbic network compared with anorexia nervosa. Neurotransmitters such as serotonin, dopamine, and oxytocin play a key role in the pathophysiology of BDD, suggesting a complex interplay of neural circuits and neurotransmitters underlying the disorder.

Conclusions

This comprehensive review of up-to-date neurobiological studies of individuals with BDD reveals differences in brain structure and functionality compared with control participants. The proposed neurocircuitry model expands on the previous understanding of BDD neurobiology and elucidates the interconnection between the visual processing, temporal-limbic, and frontostriatal networks and their clinical implications. This review provides theoretical support for future neuromodulation target identification.
背景:身体畸形障碍(BDD)是一种严重的精神障碍,其特征是过度关注感知到的外表缺陷。在本文中,我们旨在综合BDD神经生物学的最新研究成果,并提出一个更新的BDD神经回路模型。方法:系统检索38篇经同行评审的原创文章,注册方案(CRD42024553665)。进行定性主题分析,并进行激活似然估计(ALE)元分析来量化大脑激活模式。结果:在BDD患者中存在显著形态差异的脑区域主要位于初级和次级视觉处理区以及颞边缘和额纹状体网络,尽管总体上存在异质性。脑电图研究提示早期的视觉处理和注意力异常。ALE分析揭示了额颞区普遍的过度激活和顶枕区低激活。虽然BDD与强迫症在额纹状体和仲裁网络中具有相似的连接模式,但与厌食症神经相比,BDD进一步表现为腹侧视觉流与颞边缘网络自下而上和自上而下的相互作用。神经递质如血清素、多巴胺和催产素在BDD的病理生理中起着关键作用,表明神经回路和神经递质之间存在复杂的相互作用。结论:这项对BDD患者最新神经生物学研究的综合综述揭示了与对照组相比,BDD患者的大脑结构和功能存在差异。提出的神经回路模型扩展了先前对BDD神经生物学的理解,并阐明了视觉处理、颞边缘和额纹状体网络之间的联系及其临床意义。这一综述为今后神经调节靶点的识别提供了理论支持。
{"title":"The Occipital-Fronto-Limbic Circuit of Body Dysmorphic Disorder: A Systematic Review and Meta-Analysis of Neuroimaging Studies","authors":"Yihui Cheng ,&nbsp;Emalee Burrows ,&nbsp;Ludvic Zrinzo ,&nbsp;Harith Akram ,&nbsp;Trevor W. Robbins ,&nbsp;Himanshu Tyagi","doi":"10.1016/j.bpsgos.2025.100676","DOIUrl":"10.1016/j.bpsgos.2025.100676","url":null,"abstract":"<div><h3>Background</h3><div>Body dysmorphic disorder (BDD) is a severe psychiatric disorder characterized by excessive preoccupation with perceived flaws in appearance. In this review, we aim to synthesize the latest findings on the neurobiology of BDD and propose an updated BDD neurocircuitry model.</div></div><div><h3>Methods</h3><div>A systematic search identified 38 peer-reviewed original articles, and the protocol was registered (<span><span>CRD42024553665</span><svg><path></path></svg></span>). Qualitative thematic analysis was conducted, and activation likelihood estimation (ALE) meta-analysis was performed to quantify brain activation patterns.</div></div><div><h3>Results</h3><div>Brain regions with significant morphometric divergence in patients with BDD were predominantly located in primary and secondary visual processing areas and temporal-limbic and frontal-striatal networks despite overall heterogeneous findings. The electroencephalography studies suggested early visual processing and attentional abnormalities. The ALE analysis revealed a general hyperactivation over the frontotemporal region and hypoactivation over parieto-occipital regions. Although BDD shared similar connectivity patterns in frontostriatal and arbitration networks with obsessive-compulsive disorder, it was further characterized by bottom-up and top-down interaction between the ventral visual stream and temporal-limbic network compared with anorexia nervosa. Neurotransmitters such as serotonin, dopamine, and oxytocin play a key role in the pathophysiology of BDD, suggesting a complex interplay of neural circuits and neurotransmitters underlying the disorder.</div></div><div><h3>Conclusions</h3><div>This comprehensive review of up-to-date neurobiological studies of individuals with BDD reveals differences in brain structure and functionality compared with control participants. The proposed neurocircuitry model expands on the previous understanding of BDD neurobiology and elucidates the interconnection between the visual processing, temporal-limbic, and frontostriatal networks and their clinical implications. This review provides theoretical support for future neuromodulation target identification.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100676"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146204132","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}
引用次数: 0
μ Opioid Modulation of Sensorimotor Functional Connectivity in Autism: Insights From a Pharmacological Neuroimaging Investigation Using Tianeptine μ阿片类药物对自闭症感觉运动功能连通性的调节:来自使用天奈肽的药理神经影像学研究的见解
IF 3.7 Q2 NEUROSCIENCES Pub Date : 2026-03-01 Epub Date: 2025-12-04 DOI: 10.1016/j.bpsgos.2025.100663
Mihail Dimitrov , Nichol M.L. Wong , Sydney Leaman , Lucas G.S. França , Ioannis Valasakis , Jason He , David J. Lythgoe , James L. Findon , Robert H. Wichers , Vladimira Stoencheva , Dene M. Robertson , Sarah Blainey , Glynis Ivin , Štefan Holiga , Mark D. Tricklebank , Dafnis Batalle , Declan G.M. Murphy , Gráinne M. McAlonan , Eileen Daly

Background

Reproducible patterns of atypical functional connectivity (FC) of sensorimotor and higher-order networks have previously been identified in the autistic brain. However, the neurosignaling pathways underpinning these differences remain unclear. The μ opioid system is involved in sensory processing as well as social and reward behaviors and has been implicated in autism, suggesting a potential role in shaping the autistic brain. Therefore, we tested the hypothesis that there is atypical involvement of the μ opioid system in these networks in autism.

Methods

We used a placebo-controlled, double-blind, randomized, crossover study design to compare the effects of a single dose of the μ opioid receptor agonist tianeptine in autistic (n = 20) and nonautistic (n = 21) males on FC of sensorimotor and frontoparietal networks.

Results

We found that tianeptine increased FC of a sensorimotor network previously characterized by atypically low FC in autism. The connectivity of the frontoparietal network was not significantly shifted.

Conclusions

Our findings suggest that μ opioid neurosignaling may contribute to functional brain differences in the sensorimotor network in autism. Given that sensorimotor system alterations are thought to be central to autism and contribute to other core autistic features, as well as adaptability and mental health, further research is warranted to explore the translational potential of μ opioid modulation in autism.
背景:感觉运动和高阶网络的非典型功能连接(FC)的可复制模式已经在自闭症大脑中被发现。然而,支撑这些差异的神经信号通路仍不清楚。μ阿片系统参与感觉加工以及社会和奖励行为,并与自闭症有关,这表明在塑造自闭症大脑中具有潜在作用。因此,我们验证了μ阿片系统在自闭症中参与这些网络的非典型假设。方法采用安慰剂对照、双盲、随机、交叉研究设计,比较单剂量μ阿片受体激动剂天奈肽对自闭症(20例)和非自闭症(21例)男性感觉运动网络和额顶叶网络FC的影响。结果我们发现,在自闭症患者中,天奈肽增加了一个感觉运动网络的FC。额顶叶网络的连通性没有明显改变。结论μ阿片神经信号可能与自闭症患者感觉运动网络的脑功能差异有关。考虑到感觉运动系统的改变被认为是自闭症的核心,并有助于其他核心自闭症特征,以及适应性和心理健康,进一步的研究需要探索μ阿片调节在自闭症中的转化潜力。
{"title":"μ Opioid Modulation of Sensorimotor Functional Connectivity in Autism: Insights From a Pharmacological Neuroimaging Investigation Using Tianeptine","authors":"Mihail Dimitrov ,&nbsp;Nichol M.L. Wong ,&nbsp;Sydney Leaman ,&nbsp;Lucas G.S. França ,&nbsp;Ioannis Valasakis ,&nbsp;Jason He ,&nbsp;David J. Lythgoe ,&nbsp;James L. Findon ,&nbsp;Robert H. Wichers ,&nbsp;Vladimira Stoencheva ,&nbsp;Dene M. Robertson ,&nbsp;Sarah Blainey ,&nbsp;Glynis Ivin ,&nbsp;Štefan Holiga ,&nbsp;Mark D. Tricklebank ,&nbsp;Dafnis Batalle ,&nbsp;Declan G.M. Murphy ,&nbsp;Gráinne M. McAlonan ,&nbsp;Eileen Daly","doi":"10.1016/j.bpsgos.2025.100663","DOIUrl":"10.1016/j.bpsgos.2025.100663","url":null,"abstract":"<div><h3>Background</h3><div>Reproducible patterns of atypical functional connectivity (FC) of sensorimotor and higher-order networks have previously been identified in the autistic brain. However, the neurosignaling pathways underpinning these differences remain unclear. The μ opioid system is involved in sensory processing as well as social and reward behaviors and has been implicated in autism, suggesting a potential role in shaping the autistic brain. Therefore, we tested the hypothesis that there is atypical involvement of the μ opioid system in these networks in autism.</div></div><div><h3>Methods</h3><div>We used a placebo-controlled, double-blind, randomized, crossover study design to compare the effects of a single dose of the μ opioid receptor agonist tianeptine in autistic (<em>n</em> = 20) and nonautistic (<em>n</em> = 21) males on FC of sensorimotor and frontoparietal networks.</div></div><div><h3>Results</h3><div>We found that tianeptine increased FC of a sensorimotor network previously characterized by atypically low FC in autism. The connectivity of the frontoparietal network was not significantly shifted.</div></div><div><h3>Conclusions</h3><div>Our findings suggest that μ opioid neurosignaling may contribute to functional brain differences in the sensorimotor network in autism. Given that sensorimotor system alterations are thought to be central to autism and contribute to other core autistic features, as well as adaptability and mental health, further research is warranted to explore the translational potential of μ opioid modulation in autism.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100663"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146038038","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}
引用次数: 0
Persistent Alterations of Brain and Behavior in Children With Low Prenatal Alcohol Exposure 产前低酒精暴露儿童大脑和行为的持续改变
IF 3.7 Q2 NEUROSCIENCES Pub Date : 2026-03-01 Epub Date: 2025-10-31 DOI: 10.1016/j.bpsgos.2025.100648
Xiangyu Long , Catherine Lebel

Background

Heavy prenatal alcohol exposure (PAE) is associated with alterations in behavior and cognitive and brain development. However, the effects of low levels of PAE on the brain and behavior remain unclear. In the current study, we aimed to investigate longitudinal changes in the brain and behavior in children with low levels of PAE compared with well-matched unexposed children.

Methods

Children (n = 108, mean [SD] = 9.52 [0.50] years at baseline) with PAE (0.97 ± 0.90 drinks/wk) and control children (n = 108, 9.52 [0.50] years at baseline) matched on socioeconomic status were selected from the ABCD (Adolescent Brain Cognitive Development) Study and were followed over 4 years with magnetic resonance imaging and Child Behavior Checklist (CBCL) scores. No children had adverse exposures to other substances.

Results

Compared with unexposed children, children with low levels of PAE had persistently higher CBCL scores (worse behavior) and higher intracranial volumes over time.

Conclusions

Our results provide further evidence of alterations in the brain and behavior associated with low levels of PAE across early adolescence, highlighting the importance of prevention and early intervention even with low levels of PAE.
产前重度酒精暴露(PAE)与行为、认知和大脑发育的改变有关。然而,低水平PAE对大脑和行为的影响尚不清楚。在目前的研究中,我们的目的是调查低水平PAE儿童与良好匹配的未暴露儿童的大脑和行为的纵向变化。方法从ABCD(青少年大脑认知发展)研究中选取社会经济地位匹配的PAE(0.97±0.90饮料/周)患儿(n = 108,平均[SD] = 9.52[0.50]岁)和对照患儿(n = 108, 9.52[0.50]岁),采用磁共振成像和儿童行为检查表(CBCL)评分进行4年的随访。没有儿童对其他物质有不良接触。结果与未接触PAE的儿童相比,随着时间的推移,低水平PAE儿童的CBCL评分持续较高(行为更差),颅内容量也持续增加。结论我们的研究结果进一步证明了青春期早期PAE水平低与大脑和行为的改变有关,强调了在PAE水平低的情况下预防和早期干预的重要性。
{"title":"Persistent Alterations of Brain and Behavior in Children With Low Prenatal Alcohol Exposure","authors":"Xiangyu Long ,&nbsp;Catherine Lebel","doi":"10.1016/j.bpsgos.2025.100648","DOIUrl":"10.1016/j.bpsgos.2025.100648","url":null,"abstract":"<div><h3>Background</h3><div>Heavy prenatal alcohol exposure (PAE) is associated with alterations in behavior and cognitive and brain development. However, the effects of low levels of PAE on the brain and behavior remain unclear. In the current study, we aimed to investigate longitudinal changes in the brain and behavior in children with low levels of PAE compared with well-matched unexposed children.</div></div><div><h3>Methods</h3><div>Children (<em>n</em> = 108, mean [SD] = 9.52 [0.50] years at baseline) with PAE (0.97 ± 0.90 drinks/wk) and control children (<em>n</em> = 108, 9.52 [0.50] years at baseline) matched on socioeconomic status were selected from the ABCD (Adolescent Brain Cognitive Development) Study and were followed over 4 years with magnetic resonance imaging and Child Behavior Checklist (CBCL) scores. No children had adverse exposures to other substances.</div></div><div><h3>Results</h3><div>Compared with unexposed children, children with low levels of PAE had persistently higher CBCL scores (worse behavior) and higher intracranial volumes over time.</div></div><div><h3>Conclusions</h3><div>Our results provide further evidence of alterations in the brain and behavior associated with low levels of PAE across early adolescence, highlighting the importance of prevention and early intervention even with low levels of PAE.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100648"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145885174","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}
引用次数: 0
Behavioral and Prefrontal Circuit Deficits in a Newly Developed Setbp1 Haploinsufficiency Mouse Model 新建立的Setbp1单倍功能不全小鼠模型中的行为和前额叶回路缺陷
IF 3.7 Q2 NEUROSCIENCES Pub Date : 2026-03-01 Epub Date: 2025-12-09 DOI: 10.1016/j.bpsgos.2025.100666
MacKenzie A. Howard, Mendee A. Geist, Gregory J. Ordemann, Alena Kizimenko, Dominic M. Balice, F. Isaac Guillén, Emmanuella Bassey, Polina Lyuboslavsky, Audrey C. Brumback

Background

SET binding protein 1 (SETBP1) regulates the cell cycle, gene transcription, and other vital intracellular processes. SETBP1 loss-of-function variants cause the neurodevelopmental disorders SETBP1-haploinsufficiency disorder and SETBP1-related disorders (SETBP1-HD and SETBP1-RD), which are characterized by attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), intellectual disability/developmental delay, and other neurological disabilities. Here we sought to characterize behavioral, physiological, and cell morphology phenotypes of a newly developed mouse model of SETBP1-HD.

Methods

We used open field, 3-chamber, and Y-maze behavioral tests to measure activity, social interest, and spatial learning, respectively. We used whole-cell current clamp recordings from medial prefrontal cortex (mPFC) layer-5 extratelencephalic projection neurons in ex vivo slices to measure cell intrinsic and spike properties. We used morphological reconstruction to measure dendritic arborization in recorded neurons.

Results

Setbp1+/− mice exhibited hyperactivity, decreased social interest, and increased olfactory exploration in behavioral tests. Ex vivo electrophysiology revealed hypoexcitability in layer-5 extratelencephalic projection neurons in the mPFC. Morphological reconstruction revealed changes to the way branch points and length are distributed within the apical dendritic arbor of these prefrontal pyramidal neurons without changes in overall length or branch number.

Conclusions

These data show that Setbp1+/− mice exhibit phenotypes parallel to the ADHD and ASD that are common in patients with SETBP1-HD. Additionally, we identified cellular changes to a key control center for attention, social behavior, and cognitive function that may elucidate the mechanism that underlies the neuropsychiatric disabilities of this disorder.
set结合蛋白1 (SETBP1)调节细胞周期、基因转录和其他重要的细胞内过程。SETBP1功能缺失变异体导致神经发育障碍SETBP1-单倍功能不全障碍和SETBP1相关疾病(SETBP1- hd和SETBP1- rd),其特征是注意缺陷/多动障碍(ADHD)、自闭症谱系障碍(ASD)、智力残疾/发育迟缓和其他神经系统残疾。在这里,我们试图描述新开发的SETBP1-HD小鼠模型的行为,生理和细胞形态学表型。方法采用开场、3室和y迷宫行为测试,分别测量小鼠的活动、社会兴趣和空间学习能力。我们在离体切片中使用来自内侧前额叶皮层(mPFC)第5层脑外投射神经元的全细胞电流钳记录来测量细胞的内在特性和峰值特性。我们使用形态学重建来测量记录神经元的树突树突化。结果setbp1 +/−小鼠在行为测试中表现出多动症,社交兴趣下降,嗅觉探索增加。离体电生理显示,mPFC第5层脑外投射神经元低兴奋性。形态学重建显示,这些前额锥体神经元顶端树突乔木内分支点和长度的分布方式发生了变化,但总体长度和分支数量没有变化。这些数据表明,Setbp1+/−小鼠表现出与Setbp1 - hd患者常见的ADHD和ASD相似的表型。此外,我们发现了一个控制注意力、社会行为和认知功能的关键控制中心的细胞变化,这可能阐明了这种疾病的神经精神残疾的机制。
{"title":"Behavioral and Prefrontal Circuit Deficits in a Newly Developed Setbp1 Haploinsufficiency Mouse Model","authors":"MacKenzie A. Howard,&nbsp;Mendee A. Geist,&nbsp;Gregory J. Ordemann,&nbsp;Alena Kizimenko,&nbsp;Dominic M. Balice,&nbsp;F. Isaac Guillén,&nbsp;Emmanuella Bassey,&nbsp;Polina Lyuboslavsky,&nbsp;Audrey C. Brumback","doi":"10.1016/j.bpsgos.2025.100666","DOIUrl":"10.1016/j.bpsgos.2025.100666","url":null,"abstract":"<div><h3>Background</h3><div>SET binding protein 1 (<em>SETBP1</em>) regulates the cell cycle, gene transcription, and other vital intracellular processes. <em>SETBP1</em> loss-of-function variants cause the neurodevelopmental disorders <em>SETBP1</em>-haploinsufficiency disorder and <em>SETBP1</em>-related disorders (<em>SETBP1</em>-HD and <em>SETBP1</em>-RD), which are characterized by attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), intellectual disability/developmental delay, and other neurological disabilities. Here we sought to characterize behavioral, physiological, and cell morphology phenotypes of a newly developed mouse model of <em>SETBP1</em>-HD.</div></div><div><h3>Methods</h3><div>We used open field, 3-chamber, and Y-maze behavioral tests to measure activity, social interest, and spatial learning, respectively. We used whole-cell current clamp recordings from medial prefrontal cortex (mPFC) layer-5 extratelencephalic projection neurons in ex vivo slices to measure cell intrinsic and spike properties. We used morphological reconstruction to measure dendritic arborization in recorded neurons.</div></div><div><h3>Results</h3><div><em>Setbp1</em><sup><em>+/−</em></sup> mice exhibited hyperactivity, decreased social interest, and increased olfactory exploration in behavioral tests. Ex vivo electrophysiology revealed hypoexcitability in layer-5 extratelencephalic projection neurons in the mPFC. Morphological reconstruction revealed changes to the way branch points and length are distributed within the apical dendritic arbor of these prefrontal pyramidal neurons without changes in overall length or branch number.</div></div><div><h3>Conclusions</h3><div>These data show that <em>Setbp1</em><sup><em>+/−</em></sup> mice exhibit phenotypes parallel to the ADHD and ASD that are common in patients with <em>SETBP1</em>-HD. Additionally, we identified cellular changes to a key control center for attention, social behavior, and cognitive function that may elucidate the mechanism that underlies the neuropsychiatric disabilities of this disorder.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100666"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146078100","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}
引用次数: 0
Parsing Socioeconomic Effects on Treatment Trajectory and Reward Processing in Depression 抑郁症治疗轨迹和奖励加工的社会经济效应分析
IF 3.7 Q2 NEUROSCIENCES Pub Date : 2026-03-01 Epub Date: 2026-01-17 DOI: 10.1016/j.bpsgos.2025.100686
Kristina T. Legget
{"title":"Parsing Socioeconomic Effects on Treatment Trajectory and Reward Processing in Depression","authors":"Kristina T. Legget","doi":"10.1016/j.bpsgos.2025.100686","DOIUrl":"10.1016/j.bpsgos.2025.100686","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100686"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145978093","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}
引用次数: 0
Metabolism and the Mind: Investigating the Link Between Glucose Control and Reinforcement Learning in Humans 代谢与心智:研究人类葡萄糖控制与强化学习之间的联系
IF 3.7 Q2 NEUROSCIENCES Pub Date : 2026-03-01 Epub Date: 2025-10-29 DOI: 10.1016/j.bpsgos.2025.100645
Hugo Fleming , Martyna K. Stasiak , Isabel Lau , Annalise Whines , Sara Z. Mehrhof , Camilla L. Nord

Background

Signals from the body profoundly influence cognition. This process is known as interoception, and has been extensively studied in the cardiac, respiratory, and gastric domains; in contrast, metabolic influences remain poorly understood. Here, we focus on the link between glucose control and cognition, motivated by the observation that there is substantial, unexplained comorbidity between type 2 diabetes and depression. In rodents, insulin modulates dopamine signaling in the ventral striatum. We therefore hypothesized that, in humans, differences in glucose control would be associated with altered reward learning.

Methods

To test this hypothesis, we recruited 48 participants from the general population, who each completed a glucose tolerance test, a monetary reward learning task known to relate to dopamine function, and mental health questionnaires. We fitted an established reinforcement learning model to the task data to obtain computational parameters characterizing participants’ learning, and then examined the associations between these parameters and their glucose control.

Results

We discovered that poorer glucose control was associated with greater reliance on recent rewards during learning, which was in turn associated with higher levels of depression symptoms. There was also more modest evidence for the association between glucose control and depression symptoms.

Conclusions

Together, our results identify a specific neurocognitive process, reward learning, by which metabolic information may influence cognition, and which may explain the link between metabolic diseases such as type 2 diabetes and depression.
来自身体的信号深刻地影响着认知。这一过程被称为内感受,并在心脏、呼吸和胃领域得到了广泛的研究;相比之下,代谢的影响仍然知之甚少。在这里,我们关注葡萄糖控制和认知之间的联系,动机是观察到2型糖尿病和抑郁症之间存在大量无法解释的合并症。在啮齿类动物中,胰岛素调节腹侧纹状体中的多巴胺信号。因此,我们假设,在人类中,葡萄糖控制的差异可能与奖赏学习的改变有关。为了验证这一假设,我们从普通人群中招募了48名参与者,他们每个人都完成了葡萄糖耐量测试,一项已知与多巴胺功能相关的金钱奖励学习任务,以及心理健康问卷。我们将已建立的强化学习模型拟合到任务数据中,以获得表征参与者学习的计算参数,然后检查这些参数与他们的血糖控制之间的关系。结果:我们发现,较差的血糖控制与学习过程中对近期奖励的依赖程度较高有关,而这又与较高程度的抑郁症状有关。也有更温和的证据表明血糖控制和抑郁症状之间存在关联。总之,我们的研究结果确定了一个特定的神经认知过程,即奖励学习,代谢信息可能通过该过程影响认知,并可能解释代谢性疾病(如2型糖尿病和抑郁症)之间的联系。
{"title":"Metabolism and the Mind: Investigating the Link Between Glucose Control and Reinforcement Learning in Humans","authors":"Hugo Fleming ,&nbsp;Martyna K. Stasiak ,&nbsp;Isabel Lau ,&nbsp;Annalise Whines ,&nbsp;Sara Z. Mehrhof ,&nbsp;Camilla L. Nord","doi":"10.1016/j.bpsgos.2025.100645","DOIUrl":"10.1016/j.bpsgos.2025.100645","url":null,"abstract":"<div><h3>Background</h3><div>Signals from the body profoundly influence cognition. This process is known as interoception, and has been extensively studied in the cardiac, respiratory, and gastric domains; in contrast, metabolic influences remain poorly understood. Here, we focus on the link between glucose control and cognition, motivated by the observation that there is substantial, unexplained comorbidity between type 2 diabetes and depression. In rodents, insulin modulates dopamine signaling in the ventral striatum. We therefore hypothesized that, in humans, differences in glucose control would be associated with altered reward learning.</div></div><div><h3>Methods</h3><div>To test this hypothesis, we recruited 48 participants from the general population, who each completed a glucose tolerance test, a monetary reward learning task known to relate to dopamine function, and mental health questionnaires. We fitted an established reinforcement learning model to the task data to obtain computational parameters characterizing participants’ learning, and then examined the associations between these parameters and their glucose control.</div></div><div><h3>Results</h3><div>We discovered that poorer glucose control was associated with greater reliance on recent rewards during learning, which was in turn associated with higher levels of depression symptoms. There was also more modest evidence for the association between glucose control and depression symptoms.</div></div><div><h3>Conclusions</h3><div>Together, our results identify a specific neurocognitive process, reward learning, by which metabolic information may influence cognition, and which may explain the link between metabolic diseases such as type 2 diabetes and depression.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100645"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145798675","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}
引用次数: 0
Bridging the Poles: What the Transcranial Magnetic Stimulation Evidence Tells Us About Bipolar Depression 桥接两极:经颅磁刺激证据告诉我们关于双相抑郁症
IF 3.7 Q2 NEUROSCIENCES Pub Date : 2026-03-01 Epub Date: 2025-12-10 DOI: 10.1016/j.bpsgos.2025.100657
Véronique Desbeaumes Jodoin
{"title":"Bridging the Poles: What the Transcranial Magnetic Stimulation Evidence Tells Us About Bipolar Depression","authors":"Véronique Desbeaumes Jodoin","doi":"10.1016/j.bpsgos.2025.100657","DOIUrl":"10.1016/j.bpsgos.2025.100657","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100657"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145712294","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}
引用次数: 0
Considerations for Neural Cannabis Cue-Reactivity Studies in Individuals With Cannabis Use Disorder 大麻使用障碍患者神经大麻线索反应性研究的考虑
IF 3.7 Q2 NEUROSCIENCES Pub Date : 2026-03-01 Epub Date: 2026-01-12 DOI: 10.1016/j.bpsgos.2025.100669
Erica N. Grodin , Kaitlin McManus
{"title":"Considerations for Neural Cannabis Cue-Reactivity Studies in Individuals With Cannabis Use Disorder","authors":"Erica N. Grodin ,&nbsp;Kaitlin McManus","doi":"10.1016/j.bpsgos.2025.100669","DOIUrl":"10.1016/j.bpsgos.2025.100669","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100669"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145978094","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}
引用次数: 0
Increased Tumor Necrosis Factor Superfamily Members in Neuroinflammatory Schizophrenia and Bipolar Disorder Midbrains 神经炎性精神分裂症和双相情感障碍中脑肿瘤坏死因子超家族成员增加
IF 3.7 Q2 NEUROSCIENCES Pub Date : 2026-03-01 Epub Date: 2025-11-01 DOI: 10.1016/j.bpsgos.2025.100650
Gerardo Mendez-Victoriano , Yunting Zhu , Layla Neuhaus , Suhaana Shaik , Frank Middleton , Yuji Kondo , Amir Fayyazuddin , Daniel Hoeppner , Sofía Puvogel , Astrid Alsema , Laura Kracht , Mitsuyuki Matsumoto , Bart J.L. Eggen , Adam K. Walker , Maree J. Webster , Iris E.C. Sommer , Cynthia S. Weickert

Background

Neuroinflammation is a key neuropathological finding in schizophrenia and bipolar disorder, as increased cytokines are found in the midbrain of these individuals. However, the most upregulated inflammatory cytokines and most activated downstream signaling pathway(s) are unidentified.

Methods

We aimed to identify the most robust transcriptional change in the schizophrenia midbrain by bulk RNA sequencing (RNA-seq) and to confirm the cellular source and magnitude of change by single-nucleus RNA-seq, reverse transcriptase–polymerase chain reaction (RT-PCR), and immunohistochemistry in 61 healthy controls, 63 schizophrenia cases, and 33 bipolar disorder cases stratified into low- and high-inflammation groups.

Results

By RNA-seq, the TNF superfamily (TNFSF) pathway messenger RNAs (mRNAs) were among the most changed in high-inflammation schizophrenia (all ps ≤ .01), with TNFSF receptors (TNFR1, TNFR2, and FAS) being most highly expressed in astrocytes and microglia. Using RT-PCR, we confirmed that 5 TNFSF receptor mRNAs (TNFR1, TNFR2, DR4, FAS, and TWEAKR, all ps ≤ .01) were increased in high-inflammation schizophrenia/bipolar disorder cases compared with low-inflammation controls. Furthermore, the means for mRNA encoding cell death–related proteins acting downstream of TNF receptors (P53, CASP1, CASP7, CASP8; all ps ≤ .05) were increased in high-inflammation schizophrenia, as were mRNAs encoding proteins regulating cell survival (BCL2 and MCL1, all ps ≤ .01). All 5 TNFSF receptor mRNAs positively correlated with effector protein mRNAs (all ps ≤ .05) and with the astrocyte-related marker GFAP mRNA (all ps ≤ .001).

Conclusions

Our results suggest that TNFSF transcripts represent the main activated inflammatory pathway in the midbrains of people with schizophrenia, which overlaps somewhat with bipolar disorder. These findings highlight the need for anti-inflammatory interventions targeting TNF/TNFSF receptors to test for therapeutic benefits in psychiatric patients displaying elevated inflammation.
神经炎症是精神分裂症和双相情感障碍的关键神经病理学发现,因为在这些个体的中脑中发现了增加的细胞因子。然而,最上调的炎症细胞因子和最激活的下游信号通路尚未确定。方法我们旨在通过大量RNA测序(RNA-seq)确定精神分裂症中脑中最强烈的转录变化,并通过单核RNA-seq、逆转录聚合酶链反应(RT-PCR)和免疫组织化学确认61名健康对照者、63名精神分裂症患者和33名双相情感障碍患者分为低炎症组和高炎症组的细胞来源和变化程度。结果通过RNA-seq分析,TNF超家族(TNFSF)通路信使rna (mrna)在高炎症性精神分裂症中变化最大(均ps≤0.01),其中TNFSF受体(TNFR1、TNFR2和FAS)在星形胶质细胞和小胶质细胞中表达最高。通过RT-PCR,我们证实了5种TNFSF受体mrna (TNFR1、TNFR2、DR4、FAS和TWEAKR,所有ps≤0.01)在高炎症性精神分裂症/双相情感障碍患者中比低炎症性对照组增加。此外,在高炎症性精神分裂症中,编码TNF受体下游细胞死亡相关蛋白的mRNA (P53、CASP1、CASP7、CASP8,所有ps≤0.05)的均值升高,编码细胞存活蛋白的mRNA (BCL2和MCL1,所有ps≤0.01)的均值升高。5种TNFSF受体mRNA均与效应蛋白mRNA呈正相关(均ps≤0.05),与星形胶质细胞相关标志物GFAP mRNA呈正相关(均ps≤0.001)。结论TNFSF转录本是精神分裂症患者中脑激活的主要炎症通路,与双相情感障碍有一定的重叠。这些发现强调了针对TNF/TNFSF受体的抗炎干预的必要性,以测试对表现出炎症升高的精神病患者的治疗效果。
{"title":"Increased Tumor Necrosis Factor Superfamily Members in Neuroinflammatory Schizophrenia and Bipolar Disorder Midbrains","authors":"Gerardo Mendez-Victoriano ,&nbsp;Yunting Zhu ,&nbsp;Layla Neuhaus ,&nbsp;Suhaana Shaik ,&nbsp;Frank Middleton ,&nbsp;Yuji Kondo ,&nbsp;Amir Fayyazuddin ,&nbsp;Daniel Hoeppner ,&nbsp;Sofía Puvogel ,&nbsp;Astrid Alsema ,&nbsp;Laura Kracht ,&nbsp;Mitsuyuki Matsumoto ,&nbsp;Bart J.L. Eggen ,&nbsp;Adam K. Walker ,&nbsp;Maree J. Webster ,&nbsp;Iris E.C. Sommer ,&nbsp;Cynthia S. Weickert","doi":"10.1016/j.bpsgos.2025.100650","DOIUrl":"10.1016/j.bpsgos.2025.100650","url":null,"abstract":"<div><h3>Background</h3><div>Neuroinflammation is a key neuropathological finding in schizophrenia and bipolar disorder, as increased cytokines are found in the midbrain of these individuals. However, the most upregulated inflammatory cytokines and most activated downstream signaling pathway(s) are unidentified.</div></div><div><h3>Methods</h3><div>We aimed to identify the most robust transcriptional change in the schizophrenia midbrain by bulk RNA sequencing (RNA-seq) and to confirm the cellular source and magnitude of change by single-nucleus RNA-seq, reverse transcriptase–polymerase chain reaction (RT-PCR), and immunohistochemistry in 61 healthy controls, 63 schizophrenia cases, and 33 bipolar disorder cases stratified into low- and high-inflammation groups.</div></div><div><h3>Results</h3><div>By RNA-seq, the TNF superfamily (TNFSF) pathway messenger RNAs (mRNAs) were among the most changed in high-inflammation schizophrenia (all <em>p</em>s ≤ .01), with TNFSF receptors (<em>TNFR1</em>, <em>TNFR2</em>, and <em>FAS</em>) being most highly expressed in astrocytes and microglia. Using RT-PCR, we confirmed that 5 TNFSF receptor mRNAs (<em>TNFR</em><em>1</em>, <em>TNFR</em><em>2</em>, <em>DR4</em>, <em>FAS</em>, and <em>TWEAKR</em>, all <em>p</em>s ≤ .01) were increased in high-inflammation schizophrenia/bipolar disorder cases compared with low-inflammation controls. Furthermore, the means for mRNA encoding cell death–related proteins acting downstream of TNF receptors (<em>P53</em>, <em>CASP1</em>, <em>CASP7</em>, <em>CASP8</em>; all <em>p</em>s ≤ .05) were increased in high-inflammation schizophrenia, as were mRNAs encoding proteins regulating cell survival (<em>BCL2</em> and <em>MCL1</em>, all <em>p</em>s ≤ .01). All 5 TNFSF receptor mRNAs positively correlated with effector protein mRNAs (all <em>p</em>s ≤ .05) and with the astrocyte-related marker <em>GFAP</em> mRNA (all <em>p</em>s ≤ .001).</div></div><div><h3>Conclusions</h3><div>Our results suggest that TNFSF transcripts represent the main activated inflammatory pathway in the midbrains of people with schizophrenia, which overlaps somewhat with bipolar disorder. These findings highlight the need for anti-inflammatory interventions targeting TNF/TNFSF receptors to test for therapeutic benefits in psychiatric patients displaying elevated inflammation.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"6 2","pages":"Article 100650"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939220","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}
引用次数: 0
期刊
Biological psychiatry global open science
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1