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Sensorimotor Feedback Control Dysfunction as a Marker of Posttraumatic Stress Disorder 作为创伤后应激障碍标志的感觉运动反馈控制功能障碍
IF 4.8 2区 医学 Q1 NEUROSCIENCES Pub Date : 2025-11-01 DOI: 10.1016/j.bpsc.2024.07.010
Jonathon R. Howlett , Heekyeong Park , Martin P. Paulus

Background

Posttraumatic stress disorder (PTSD) is characterized not only by its direct association with traumatic events but also by a potential deficit in inhibitory control across emotional, cognitive, and sensorimotor domains. Recent research has shown that a continuous sensorimotor feedback control task, the rapid assessment of motor processing paradigm, can yield reliable measures of individual sensorimotor control performance. This study used this paradigm to investigate control deficits in PTSD compared with both a healthy volunteer group and a non-PTSD psychiatric comparison group.

Methods

We examined control processing using the rapid assessment of motor processing paradigm in a sample of 40 individuals with PTSD, matched groups of 40 individuals with mood and anxiety complaints, and 40 healthy control participants. We estimated Kp (drive) and Kd (damping) parameters using a proportional-derivative control modeling approach.

Results

The Kp parameter was lower in the PTSD group than in the healthy control (Cohen’s d = 0.86) and mood and anxiety (Cohen’s d = 0.63) groups. After controlling for color-word inhibition, Kp remained lower in the PTSD group than in the healthy control (Cohen’s d = 0.79) and mood and anxiety (Cohen’s d = 0.62) groups. Mediation analysis showed that Kd significantly mediated the relationship between PTSD and control deficits in the Kp parameter, with 96% of the effect being mediated by Kd.

Conclusions

These findings underscore the potential of using dynamic control paradigms to elucidate the control dysfunctions in PTSD and suggest that different psychiatric conditions may distinctly influence subcomponents of sensorimotor control.
背景:创伤后应激障碍(PTSD创伤后应激障碍(PTSD)的特点不仅在于它与创伤事件的直接联系,还在于它在情绪、认知和感觉运动领域的抑制控制方面可能存在缺陷。最近的研究表明,一种连续的感觉运动反馈控制任务--运动处理快速评估(RAMP)范式--可以对个体的感觉运动控制表现进行可靠的测量。本研究利用该范式调查了创伤后应激障碍患者相对于健康志愿者和非创伤后应激障碍精神疾病对比组的控制缺陷:方法:我们使用 RAMP 范式对 40 名创伤后应激障碍患者以及 40 名情绪和焦虑(MA)症状患者和 40 名健康对照组(HC)进行了控制处理研究。我们使用比例-衍生(PD)控制模型方法估算了Kp(驱动)和Kd(阻尼)参数:结果:与 HC 组(Cohen's d = 0.86)和 MA 组(Cohen's d = 0.63)相比,创伤后应激障碍组的 Kp 参数较低。在对颜色词抑制进行控制后,创伤后应激障碍组的 Kp 仍低于 HC 组(Cohen's d = 0.79)和 MA 组(Cohen's d = 0.62)。中介分析表明,Kd对创伤后应激障碍与Kp参数控制缺陷之间的关系有明显的中介作用,96%的影响由Kd中介:这些发现强调了使用动态控制范式来阐明创伤后应激障碍中的控制功能障碍的潜力,并表明不同的精神疾病可能会对感觉运动控制的子组件产生不同的影响。
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引用次数: 0
Editorial Board Page 编委会页面
IF 4.8 2区 医学 Q1 NEUROSCIENCES Pub Date : 2025-11-01 DOI: 10.1016/S2451-9022(25)00313-1
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引用次数: 0
Does Reward Insensitivity in Anhedonia Result From Limitations in Cognitive Capacity? 快感缺乏症的奖励不敏感是认知能力限制的结果吗?
IF 4.8 2区 医学 Q1 NEUROSCIENCES Pub Date : 2025-11-01 DOI: 10.1016/j.bpsc.2025.09.008
Vanessa M. Brown
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引用次数: 0
Computationally Informed Insights Into Anhedonia and Treatment by Kappa Opioid Receptor Antagonism 通过k-阿片受体拮抗剂对快感缺乏症和治疗的计算信息见解。
IF 4.8 2区 医学 Q1 NEUROSCIENCES Pub Date : 2025-11-01 DOI: 10.1016/j.bpsc.2025.05.011
Bilal A. Bari , Andrew D. Krystal , Diego A. Pizzagalli , Samuel J. Gershman

Background

Anhedonia, the loss of pleasure, is prevalent and impairing. Parsing its computational basis promises to explain its transdiagnostic character. One manifestation of anhedonia, reward insensitivity, may be linked to limited memory. Furthermore, the need to economize on limited memory engenders a perseverative bias toward frequently chosen actions. Anhedonia may also be linked with deviations from optimal perseveration for a given memory capacity, a pattern that causes inefficiency because it results in less reward for the same memory cost.

Methods

To test these hypotheses, we applied a theory of optimal decision making under memory constraints that decomposes behavior into a memory component and an efficiency component. We applied this theory to behavior on the Probabilistic Reward Task, a reward learning paradigm that has been validated in anhedonia, and performed secondary analysis of a randomized controlled trial testing kappa opioid receptor (KOR) antagonism for anhedonia (n = 24 KOR; n = 31 placebo), as well as analyses of 3 other datasets (n = 100, 66, 24, respectively). We fit a resource-bounded reinforcement learning model to behavior.

Results

Across clinical and nonclinical populations, anhedonia was associated with deficits in efficiency but not memory. The reinforcement learning models demonstrated that deficits in efficiency arise from the inability to perseverate optimally. KOR antagonism, which likely elevates tonic dopamine, increases both memory and efficiency, and the model demonstrated that this arises from increased reward sensitivity and perseveration.

Conclusions

Therefore, KOR antagonism has distinct cognitive effects, only one related to anhedonia. These findings have potential implications for the applications of KOR antagonists.
背景:快感缺乏,即快乐的丧失,是一种普遍且有害的现象。分析其计算基础有望解释其跨诊断特性。快感缺乏的一种表现——奖励不敏感——可能与记忆有限有关。此外,为了节省有限的记忆,人们对频繁选择的行为产生了持久的偏见。快感缺乏症也可能与对给定记忆容量的最佳持久性的偏离有关,这种模式导致效率低下,因为它导致相同记忆成本的奖励更少。方法:为了验证这些假设,我们应用记忆约束下的最优决策理论,将行为分解为记忆成分和效率成分。我们将这一理论应用于概率奖励任务(Probabilistic Reward Task)的行为,这是一种奖励学习范式,在快感缺乏症中得到了验证,并对一项随机对照试验进行了二次分析,该试验测试了κ-阿片受体(KOR)对快感缺乏症的拮抗作用(N=24 KOR;N=31安慰剂),以及其他三个数据集的分析(N=100, 66, 24)。我们将资源有限的强化学习模型应用于行为。结果:在临床和非临床人群中,快感缺乏与效率缺陷有关,但与记忆缺陷无关。强化学习模型表明,效率的缺陷来自于无法保持最佳状态。KOR拮抗剂可能会增加强直性多巴胺,从而增加记忆和效率,该模型表明,这是由于奖励敏感性和持久性的增加。结论:因此,KOR拮抗剂具有明显的认知作用,只有一种与快感缺乏有关。这些发现对KOR拮抗剂的应用具有潜在的意义。
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引用次数: 0
The Desegregation of Neural Networks During Worry Induction in Late Life: An Effective Connectivity Analysis 晚年焦虑诱导中神经网络的去隔离——一种有效的连通性分析。
IF 4.8 2区 医学 Q1 NEUROSCIENCES Pub Date : 2025-11-01 DOI: 10.1016/j.bpsc.2025.04.010
Andrew R. Gerlach , Helmet T. Karim , Kevin Kahru , Dana L. Tudorascu , James J. Gross , Meryl A. Butters , Carmen Andreescu

Background

Severe worry is a core component of anxiety and depressive disorders and is independently associated with significant morbidity and mortality. However, the neural basis of worry is poorly understood. We investigated effective connectivity (EC) using functional magnetic resonance imaging of a naturalistic worry induction and reappraisal task in late life.

Methods

A total of 112 participants age >50 years with varying worry severity completed a personalized, in-scanner worry induction and reappraisal task. We calculated voxelwise EC in neutral, worry, and reappraisal conditions with generalized psychophysiological interactions using seeds in the subgenual anterior cingulate cortex (ACC), dorsal ACC, and left and right amygdalae and used paired t tests to compare conditions. We assessed clusters for association with in-scanner worry severity using linear regression.

Results

During the worry condition, EC increased between the subgenual ACC and the default mode network (DMN) and major hubs of the executive control and salience networks. Left amygdala EC to the posterior cingulate also increased during worry, and dorsal ACC connectivity to primary sensory and motor regions decreased. Reappraisal reduced subgenual and dorsal ACC EC observed during worry and the EC between the left amygdala and regions of the dorsal attention network. Broadly, left amygdala EC was robustly associated with in-scanner worry severity.

Conclusions

Worry induction robustly engaged the DMN and increased connectivity with other high-order associative networks, potentially subsuming cortical resources. Reappraisal reduced these connectivities and disengaged the amygdala from areas associated with top-down attention. These findings could inform targets for neuromodulatory treatment of severe worry in older adults.
背景:严重忧虑是焦虑和抑郁障碍的核心组成部分,与显著的发病率和死亡率独立相关。然而,人们对焦虑的神经基础知之甚少。本研究利用功能性磁共振成像(fMRI)研究了晚年自然焦虑诱导和再评价任务的有效连通性。方法:112名年龄在50岁至50岁之间的不同焦虑严重程度的参与者完成了个性化的扫描内焦虑诱导和重新评估任务。我们利用亚掌前扣带皮层(ACC)、背侧扣带皮层和左右杏仁核中的种子计算了中性、焦虑和重评价条件下具有广义心理生理相互作用的体素型EC,并使用配对t检验来比较条件。我们使用线性回归评估了与扫描仪内担忧严重程度的关联。结果:在焦虑状态下,亚一般ACC与默认模式网络(DMN)以及执行控制和显著性网络的主要枢纽之间的EC增加。在焦虑时,左杏仁核与后扣带的连接也增加,而背侧ACC与主要感觉和运动区域的连接减少。重新评估减少了亚属和背侧的前扣带皮层在焦虑和左杏仁核和背侧注意网络区域之间的前扣带皮层。总的来说,左杏仁核EC与扫描内焦虑严重程度密切相关。结论:焦虑诱导与DMN密切相关,并增加了与其他高阶关联网络的连通性,可能包含皮层资源。重新评估减少了这些连接,并使杏仁核与自上而下的注意力相关的区域分离。这些发现可以为老年人严重忧虑的神经调节治疗提供靶点。
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引用次数: 0
Guide for Authors 作者指南
IF 4.8 2区 医学 Q1 NEUROSCIENCES Pub Date : 2025-11-01 DOI: 10.1016/S2451-9022(25)00317-9
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引用次数: 0
Polygenic Risks for Depression and Neural Responses to Reward and Punishment in Young Adults 年轻人抑郁和奖惩神经反应的多基因风险。
IF 4.8 2区 医学 Q1 NEUROSCIENCES Pub Date : 2025-11-01 DOI: 10.1016/j.bpsc.2025.05.008
Yu Chen , Huey-Ting Li , Xingguang Luo , Guangfei Li , Jaime S. Ide , Chiang-Shan R. Li

Background

Extensive research has shown aberrant reward and punishment processing in people with depression. Genetic risks contribute to depression, but whether or how these risks of depression may affect behavioral and neural responses to reward and punishment remains unclear.

Methods

We curated the data of 879 young adults performing a gambling task during brain imaging from the Human Connectome Project. Depression severity was assessed with the Achenbach Adult Self Report. Polygenic risk scores (PRSs) for depression were computed for all participants. With published routines and at a corrected threshold, we evaluated how brain responses to reward and punishment were associated with depression scores and PRSs in a linear regression in all, male, and female participants, with age, sex (for all), race, and drinking severity as covariates.

Results

The results showed broad frontal, parietal, and occipital cortical activation in negative correlation with PRSs during both reward and punishment processing. Notably, posterior cingulate cortical activation was specifically associated with PRS-related punishment processing. In addition, men and women displayed both shared and distinct neural responses to PRS-related reward and punishment processing.

Conclusions

These findings highlight the influence of genetic risks for depression on neural responses to reward and punishment and provide insights into genetically informed markers of depression.
背景:广泛的研究表明抑郁症患者的奖惩加工异常。遗传风险会导致抑郁,但这些抑郁风险是否或如何影响对奖励和惩罚的行为和神经反应仍不清楚。方法:我们整理了879名年轻人在人类连接组项目的脑成像过程中执行赌博任务的数据。用Achenbach成人自我报告评估抑郁严重程度。计算所有受试者抑郁症的多基因风险评分(PRS)。根据已公布的程序和校正阈值,我们评估了所有男性和女性受试者的大脑对奖励和惩罚的反应与抑郁评分和PRS的线性回归,并将年龄、性别(所有人)、种族和饮酒严重程度作为协变量。结果:在奖惩加工过程中,前额叶、顶叶和枕叶皮层的广泛激活与PRS呈负相关。值得注意的是,后扣带皮层的激活与prs相关的惩罚加工特别相关。此外,男性和女性对与prs相关的奖惩处理表现出共同的和不同的神经反应。结论:这些发现强调了抑郁症的遗传风险对奖励和惩罚的神经反应的影响,并为抑郁症的遗传标记提供了见解。
{"title":"Polygenic Risks for Depression and Neural Responses to Reward and Punishment in Young Adults","authors":"Yu Chen ,&nbsp;Huey-Ting Li ,&nbsp;Xingguang Luo ,&nbsp;Guangfei Li ,&nbsp;Jaime S. Ide ,&nbsp;Chiang-Shan R. Li","doi":"10.1016/j.bpsc.2025.05.008","DOIUrl":"10.1016/j.bpsc.2025.05.008","url":null,"abstract":"<div><h3>Background</h3><div>Extensive research has shown aberrant reward and punishment processing in people with depression. Genetic risks contribute to depression, but whether or how these risks of depression may affect behavioral and neural responses to reward and punishment remains unclear.</div></div><div><h3>Methods</h3><div>We curated the data of 879 young adults performing a gambling task during brain imaging from the Human Connectome Project. Depression severity was assessed with the Achenbach Adult Self Report. Polygenic risk scores (PRSs) for depression were computed for all participants. With published routines and at a corrected threshold, we evaluated how brain responses to reward and punishment were associated with depression scores and PRSs in a linear regression in all, male, and female participants, with age, sex (for all), race, and drinking severity as covariates.</div></div><div><h3>Results</h3><div>The results showed broad frontal, parietal, and occipital cortical activation in negative correlation with PRSs during both reward and punishment processing. Notably, posterior cingulate cortical activation was specifically associated with PRS-related punishment processing. In addition, men and women displayed both shared and distinct neural responses to PRS-related reward and punishment processing.</div></div><div><h3>Conclusions</h3><div>These findings highlight the influence of genetic risks for depression on neural responses to reward and punishment and provide insights into genetically informed markers of depression.</div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"10 11","pages":"Pages 1155-1165"},"PeriodicalIF":4.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144144870","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}
引用次数: 0
Ketosis Elevates Antioxidants and Markers of Energy Metabolism: A Proton Magnetic Resonance Spectroscopy Study 酮症提高抗氧化剂和能量代谢标志物:1H磁共振光谱研究。
IF 4.8 2区 医学 Q1 NEUROSCIENCES Pub Date : 2025-11-01 DOI: 10.1016/j.bpsc.2025.06.009
Helena van Nieuwenhuizen , Botond B. Antal , Antoine Hone-Blanchet , Andrew Lithen , Liam McMahon , Sofia Nikolaidou , Zeming Kuang , Kieran Clarke , Bruce G. Jenkins , Douglas L. Rothman , Lilianne R. Mujica-Parodi , Eva-Maria Ratai

Background

Ketosis is known to alter the balance of neuroactive amino acids and enhance neural function compared with a glycolytic condition. However, its influence on other metabolites, such as antioxidants and neural energy markers, and the mechanisms by which ketosis improves neural function remain unclear.

Methods

Here, we measured the neurochemical effects of acute ketosis on key brain metabolites (neurotransmitters, antioxidants, and energy markers) in the human brain using ultra-high-field proton magnetic resonance spectroscopy (1H-MRS) and investigated the subsequent impact on neural function, measured via dynamic functional connectivity, using resting-state functional magnetic resonance imaging (rs-fMRI). In a within-subjects design, 63 healthy adults (30 female) from across the lifespan underwent 1H-MRS and rs-fMRI scans before and after consuming individually weight-dosed and calorically matched ketone monoester or glucose drinks.

Results

Ketone monoester administration, but not glucose, significantly elevated cerebral antioxidants and energy markers while decreasing GABA (gamma-aminobutyric acid), glutamate, and glutamine levels in the posterior cingulate cortex. Notably, increased energy markers, specifically an increase in total creatine, correlated with greater improvements in neural function measured using rs-fMRI.

Conclusions

Our results integrate metabolic and functional neuroimaging findings, offering a comprehensive understanding of ketosis-induced changes in brain chemistry and functional network dynamics. These insights clarify potential mechanisms by which ketosis imparts its neural benefits and provide valuable information to assist the development of novel treatment strategies for a variety of psychiatric and neurodegenerative disorders.
背景:与糖酵解相比,酮症可以改变神经活性氨基酸的平衡,增强神经功能。然而,其对其他代谢物的影响,如抗氧化剂和神经能量标记物,以及酮症改善神经功能的机制尚不清楚。方法:在这里,我们使用超高场1H磁共振光谱(MRS)测量急性酮症对人脑关键脑代谢物(神经递质、抗氧化剂和能量标记物)的神经化学影响,并使用静息状态功能磁共振成像(rsfMRI)通过动态功能连接测量对神经功能的后续影响。在受试者内部设计中,63名健康成年人(30名女性)在饮用按体重剂量和热量匹配的酮单酯或葡萄糖饮料前后接受了1H磁共振成像和rsfMRI扫描。结果:给药酮单酯,而不是葡萄糖,显著提高大脑抗氧化剂和能量标志物,同时降低GABA,谷氨酸和谷氨酰胺在后扣带皮层的水平。值得注意的是,能量标记物的增加,特别是总肌酸的增加,与rsfMRI测量的神经功能的更大改善相关。结论:我们的研究结果整合了代谢和功能神经影像学结果,为酮症诱导的脑化学和功能网络动力学变化提供了全面的理解。这些见解阐明了酮症赋予其神经益处的潜在机制,并为协助开发各种精神和神经退行性疾病的新治疗策略提供了有价值的信息。临床试验注册:代谢约束下的动态连接,ClinicalTrials.gov ID NCT04840095, https://clinicaltrials.gov/study/NCT04840095。
{"title":"Ketosis Elevates Antioxidants and Markers of Energy Metabolism: A Proton Magnetic Resonance Spectroscopy Study","authors":"Helena van Nieuwenhuizen ,&nbsp;Botond B. Antal ,&nbsp;Antoine Hone-Blanchet ,&nbsp;Andrew Lithen ,&nbsp;Liam McMahon ,&nbsp;Sofia Nikolaidou ,&nbsp;Zeming Kuang ,&nbsp;Kieran Clarke ,&nbsp;Bruce G. Jenkins ,&nbsp;Douglas L. Rothman ,&nbsp;Lilianne R. Mujica-Parodi ,&nbsp;Eva-Maria Ratai","doi":"10.1016/j.bpsc.2025.06.009","DOIUrl":"10.1016/j.bpsc.2025.06.009","url":null,"abstract":"<div><h3>Background</h3><div>Ketosis is known to alter the balance of neuroactive amino acids and enhance neural function compared with a glycolytic condition. However, its influence on other metabolites, such as antioxidants and neural energy markers, and the mechanisms by which ketosis improves neural function remain unclear.</div></div><div><h3>Methods</h3><div>Here, we measured the neurochemical effects of acute ketosis on key brain metabolites (neurotransmitters, antioxidants, and energy markers) in the human brain using ultra-high-field proton magnetic resonance spectroscopy (<sup>1</sup>H-MRS) and investigated the subsequent impact on neural function, measured via dynamic functional connectivity, using resting-state functional magnetic resonance imaging (rs-fMRI). In a within-subjects design, 63 healthy adults (30 female) from across the lifespan underwent <sup>1</sup>H-MRS and rs-fMRI scans before and after consuming individually weight-dosed and calorically matched ketone monoester or glucose drinks.</div></div><div><h3>Results</h3><div>Ketone monoester administration, but not glucose, significantly elevated cerebral antioxidants and energy markers while decreasing GABA (gamma-aminobutyric acid), glutamate, and glutamine levels in the posterior cingulate cortex. Notably, increased energy markers, specifically an increase in total creatine, correlated with greater improvements in neural function measured using rs-fMRI.</div></div><div><h3>Conclusions</h3><div>Our results integrate metabolic and functional neuroimaging findings, offering a comprehensive understanding of ketosis-induced changes in brain chemistry and functional network dynamics. These insights clarify potential mechanisms by which ketosis imparts its neural benefits and provide valuable information to assist the development of novel treatment strategies for a variety of psychiatric and neurodegenerative disorders.</div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"10 11","pages":"Pages 1186-1196"},"PeriodicalIF":4.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144602535","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}
引用次数: 0
Structural Brain Differences in the Alzheimer’s Disease Continuum: Insights Into the Heterogeneity From a Large Multisite Neuroimaging Consortium 阿尔茨海默氏症连续症的大脑结构差异:从大型多站点神经成像联盟中洞察异质性。
IF 4.8 2区 医学 Q1 NEUROSCIENCES Pub Date : 2025-10-01 DOI: 10.1016/j.bpsc.2024.07.019
Tavia E. Evans , Natalia Vilor-Tejedor , Gregory Operto , Carles Falcon , Albert Hofman , Agustin Ibáñez , Sudha Seshadari , Louis C.S. Tan , Michael Weiner , Suverna Alladi , Udunna Anazodo , Juan Domingo Gispert , Alzheimer’s Disease Neuroimaging Initiative, Australian Imaging Biomarkers and Lifestyle flagship study of ageing, Hieab H.H. Adams

Background

Neurodegenerative diseases require collaborative, multisite research to comprehensively grasp their complex and diverse pathological progression; however, there is caution in aggregating global data due to data heterogeneity. In the current study, we investigated brain structure across stages of Alzheimer’s disease (AD) and how relationships vary across sources of heterogeneity.

Methods

Using 6 international datasets (N > 27,000), associations of structural neuroimaging markers were investigated in relation to the AD continuum via meta-analysis. We investigated whether associations varied across elements of magnetic resonance imaging acquisition, study design, and populations.

Results

Modest differences in associations were found depending on how data were acquired; however, patterns were similar. Preliminary results suggested that neuroimaging marker–AD relationships differ across ethnic groups.

Conclusions

Diversity in data offers unique insights into the neural substrate of AD; however, harmonized processing and transparency of data collection are needed. Global collaborations should embrace the inherent heterogeneity that exists in the data and quantify its contribution to research findings at the meta-analytical stage.
导言:神经退行性疾病需要多机构合作研究才能全面掌握其复杂多样的病理发展过程,但由于数据的异质性,在汇总全球数据时需要谨慎。本研究调查了阿尔茨海默病(AD)各阶段的大脑结构,以及不同异质性来源之间的关系:利用 6 个国际数据集(n>27,000),通过荟萃分析研究了神经影像结构标记与阿尔茨海默病连续性的关联。我们研究了磁共振成像采集、研究设计和人群等因素之间的关联是否存在差异:结果:根据数据获取方式的不同,相关性略有不同,但模式相似。初步结果表明,不同种族群体的神经影像标记物与AD的关系存在差异:讨论:数据的多样性为了解 AD 的神经基质提供了独特的视角,但数据收集的统一处理和透明度仍有待提高。全球合作应接受数据中存在的固有异质性,并在荟萃分析阶段量化其对研究结果的贡献。
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引用次数: 0
Beyond the Surface: Deep Transcranial Magnetic Stimulation Efficacy in Reducing Craving in Addictive Disorders: A Systematic Review and Meta-Analysis 表面之外:深度经颅磁刺激在减少成瘾障碍的渴望中的功效。系统回顾和荟萃分析。
IF 4.8 2区 医学 Q1 NEUROSCIENCES Pub Date : 2025-10-01 DOI: 10.1016/j.bpsc.2025.03.012
Lilia Del Mauro , Alessandra Vergallito , Francantonio Devoto , Gaia Locatelli , Gabriel Hassan , Leonor Josefina Romero Lauro

Background

Substance use disorders (SUDs) and gambling disorder (GD) are addictive diseases with a chronic course. Due to the limited efficacy of conventional treatments, there is growing interest in alternative approaches that target the altered neural circuits underlying these disorders. Deep transcranial magnetic stimulation (dTMS) has emerged as a promising neuromodulation technique capable of reaching deep and bilateral brain regions. However, no definite recommendation for its use in addiction treatment exists. In this study, we systematically reviewed and quantitatively analyzed dTMS effects in SUDs and GD.

Methods

Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, we screened 4 electronic databases up to February 2024 and selected relevant original English-language research articles. Seventeen articles were included in the systematic review and 12 in the meta-analysis. Because only a minority of studies used a sham-controlled design, we ran a main analysis computing the standardized mean change (SMCC) from pre to post real stimulation as the effect size, with self-reported craving scores as the outcome measure.

Results

The results showed a significant and large effect of real dTMS in reducing craving scores (SMCC = −1.26; 95% CI, −1.67 to −0.86; p < .001). High heterogeneity across studies was found at both quantitative and qualitative levels.

Conclusions

Results provide preliminary evidence supporting the effectiveness of dTMS for the treatment of SUDs. Current limitations and future directions are critically discussed, highlighting the need for further rigorous research to refine the therapeutic potential and develop consensus-based guidelines for dTMS clinical application.
背景:物质使用障碍(SUDs)和赌博障碍(GD)是一种慢性成瘾疾病。由于常规治疗的疗效有限,人们对针对这些疾病背后改变的神经回路的替代方法越来越感兴趣。深经颅磁刺激(dTMS)已成为一种很有前途的神经调节技术,能够到达深部和双侧脑区。然而,目前尚无明确的建议将其用于成瘾治疗。本研究系统回顾并定量分析了dTMS在sud和GD中的作用。方法:根据PRISMA指南,筛选截至2024年2月的4个电子数据库,并选择相关的英文原创研究文章。17篇论文被纳入系统评价。由于只有少数研究采用假对照设计,我们对12项研究的子集进行了荟萃分析,计算真实刺激前后的标准化平均变化(SMCC)作为效应大小,使用自我报告的渴望分数作为因变量。结果:结果显示,真正的dTMS在降低渴望评分方面有显著而大的效果(SMCC = - 1.26, 95% CI [-1.67, - 0.86], p)。结论:结果为dTMS治疗SUDs的有效性提供了初步证据。目前的局限性和未来的方向进行了批判性的讨论,强调需要进一步严格的研究,以完善治疗潜力,并为dTMS临床应用制定基于共识的指导方针。
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引用次数: 0
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Biological Psychiatry-Cognitive Neuroscience and Neuroimaging
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