Progress in Neuro-Psychopharmacology & Biological Psychiatry最新文献_第7页

Involvement of dimethylarginine dimethylaminohydrolase type 1 (DDAH1) in addiction and social stress phenotypes: Insights from proteomic, metabolomic and functional studies 二甲基精氨酸二甲氨基水解酶1型（DDAH1）参与成瘾和社会应激表型：来自蛋白质组学、代谢组学和功能研究的见解

IF 3.9 2区医学 Q1 CLINICAL NEUROLOGY

Progress in Neuro-Psychopharmacology & Biological Psychiatry

Pub Date : 2025-11-27 DOI: 10.1016/j.pnpbp.2025.111568

Miroslav N. Nenov , Lisa A. Briand

Nitric oxide synthase (NOS) plays a role in substance use related neurotoxicity and addictive phenotypes. Inhibition of nitric oxide (NO) production can prevent negative phenotypes associated with drugs intake. Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NOS. ADMA levels are regulated by dimethylarginine dimethylaminohydrolase type 1 (DDAH1). Numerous evidence suggests that drugs of abuse can increase DDAH1 levels, leading to reduction of ADMA levels, and in turn, causing neurotoxicity associated with NO overproduction. Yet, this data is sparse, and very little mechanistic evidence exists. Here, we review the literature on the impact of substances of abuse and social stress, as a condition implicated in addictive phenotypes, on DDAH1 levels in the brain. This review highlights five things: first, psychostimulants can increase brain DDAH1 levels and DDAH1-ADMA-NOS signaling axis could underlay neurotoxicity and addictive behaviors driven by psychostimulants. Second, opioids can also significantly increase brain DDAH1 levels, yet currently no mechanistic studies exist to determine the consequences of that increase. Three, the nicotine and alcohol studies are inconclusive as results are often complicated with comorbidities associated with cardiovascular impairments, liver toxicity and aging. Four, studies on cannabinoids are insufficient, more data is needed. Finally, social stress affects DDAH1 levels and anti-depressants can reverse this effect, but mechanistic data is lacking. In conclusion, proteomic, metabolomic and functional studies suggest that DDAH1 may play a role in addiction and conditions related to social stress. Further investigation is necessary to elucidate the specific function of DDAH1 in addiction and social stress phenotypes.

一氧化氮合酶（NOS）在药物使用相关的神经毒性和成瘾表型中起作用。抑制一氧化氮（NO）的产生可以防止与药物摄入相关的负表型。不对称二甲基精氨酸（ADMA）是一种内源性NOS抑制剂，ADMA水平受二甲基精氨酸二甲氨基水解酶1型（DDAH1）调控。大量证据表明，滥用药物可增加DDAH1水平，导致ADMA水平降低，进而引起与NO过量产生相关的神经毒性。然而，这些数据是稀疏的，几乎没有机械证据存在。在这里，我们回顾了滥用物质和社会压力对大脑中DDAH1水平的影响的文献，作为成瘾表型的一种情况。这篇综述强调了五个方面：第一，精神兴奋剂可以增加大脑DDAH1水平，DDAH1- adma - nos信号轴可能是精神兴奋剂驱动的神经毒性和成瘾行为的基础。其次，阿片类药物也可以显著增加大脑DDAH1水平，但目前还没有机制研究来确定这种增加的后果。第三，尼古丁和酒精的研究是不确定的，因为结果往往伴随着与心血管损伤、肝毒性和衰老相关的合并症。四是大麻素的研究不足，需要更多的数据。最后，社会压力影响DDAH1水平，抗抑郁药物可以逆转这种影响，但缺乏机制数据。总之，蛋白质组学、代谢组学和功能研究表明，DDAH1可能在成瘾和与社会压力相关的疾病中发挥作用。需要进一步研究阐明DDAH1在成瘾和社会应激表型中的具体功能。

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引用次数: 0

Mitochondrial metabolic reprogramming of microglia in neuroinflammation: Implications for major depressive disorder 神经炎症中小胶质细胞的线粒体代谢重编程：对重度抑郁症的影响

IF 3.9 2区医学 Q1 CLINICAL NEUROLOGY

Progress in Neuro-Psychopharmacology & Biological Psychiatry

Pub Date : 2025-11-26 DOI: 10.1016/j.pnpbp.2025.111566

Yu-Fei Wang, Cong-Ya Chen, Xuan Yang, Lan Lei, Yi Zhang

Major depressive disorder (MDD) is a recurrent episodic mood disorder characterized by persistent low mood and loss of interest. The pathogenesis of major depressive disorder (MDD) involves a neuroinflammatory response, neurotransmitter dysfunction, blood-brain barrier disruption, oxidative stress, and mitochondrial dysfunction. Neuroinflammation, caused by the overactivation of microglia, is considered a key factor in the development of the disease. Metabolic reprogramming has been shown to play a crucial role in microglial activation and executive function. In MDD, microglia have the potential to become activated and transform into either pro-inflammatory or anti-inflammatory phenotypes. These variations in cellular phenotypes lead to differences in cellular energy metabolism. Mitochondria are involved in the energy metabolism of microglia and have intricate connections with microglia-mediated metabolic reprogramming and neuroinflammation. However, the specific changes in the metabolic reprogramming of microglia in depression, the numerous signaling pathways and cytokines involved, and the mechanisms by which they mediate phenotypic transitions remain unclear. Therefore, this review summarizes the metabolic reprogramming of microglia in MDD, as well as the involved signaling pathways, mitochondrial involvement and cytokines, and elaborates on their interaction with phenotypic transformation. The effects of drugs on regulating immune metabolic reprogramming to suppress neuroinflammation were summarized, providing potential for new research approaches in the treatment of MDD.

重度抑郁障碍（MDD）是一种复发性发作性情绪障碍，其特征是持续的情绪低落和兴趣丧失。重度抑郁症（MDD）的发病机制涉及神经炎症反应、神经递质功能障碍、血脑屏障破坏、氧化应激和线粒体功能障碍。由小胶质细胞过度激活引起的神经炎症被认为是该疾病发展的关键因素。代谢重编程已被证明在小胶质细胞激活和执行功能中起着至关重要的作用。在MDD中，小胶质细胞有可能被激活并转化为促炎或抗炎表型。这些细胞表型的变化导致细胞能量代谢的差异。线粒体参与小胶质细胞的能量代谢，并与小胶质细胞介导的代谢重编程和神经炎症有复杂的联系。然而，抑郁症中小胶质细胞代谢重编程的具体变化，所涉及的众多信号通路和细胞因子，以及它们介导表型转变的机制尚不清楚。因此，本文综述了MDD中小胶质细胞的代谢重编程，以及相关的信号通路、线粒体参与和细胞因子，并阐述了它们与表型转化的相互作用。综述了药物调节免疫代谢重编程抑制神经炎症的作用，为MDD治疗提供了新的研究途径。

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引用次数: 0

Mechanistic insights into the antidepressant potential of plant-derived flavonoids: A preclinical review 植物源黄酮类化合物抗抑郁潜能的机制研究：临床前综述。

IF 3.9 2区医学 Q1 CLINICAL NEUROLOGY

Progress in Neuro-Psychopharmacology & Biological Psychiatry

Pub Date : 2025-11-22 DOI: 10.1016/j.pnpbp.2025.111567

Yingjun Cui , Zenovia Ursuliak , H.P. Vasantha Rupasinghe

Flavonoid-based phytomedicines are emerging as promising therapies for combating various disorders, including depression. Depression is a common and serious medical illness that negatively affects the quality of life. It has become a leading cause of disability worldwide. Flavonoids are ubiquitous biologically active phytochemicals in medicinal plants, herbs, fruits, vegetables, teas, and wines. There is a negative association between total flavonoid intake and depression symptoms in humans. This review aims to discuss the recent in vivo and in vitro studies on the effects of dietary flavonoids in depression models and assays to identify the molecular pathways that underlie their actions. Here, we briefly introduce the pathophysiology of depression, the diagnosis of depression, and the models for studying depression. The discovered potential antidepressant flavonoids include flavonols (quercetin, quercitrin, kaemferol, and heptamethoxyflavone), flavones (luteolin, baicalin, apigenin, and cymaroside), isoflavones (ononin), flavanones (pinocembrin), and anthocyanins (callistephin). These plant-derived flavonoids have been shown to reduce neuronal damage in the hippocampus, decrease neurotransmitter depletion, attenuate hypothalamic-pituitary-adrenal axis hyperactivation, inhibit inflammation in the central nervous system, and regulate gut microbiota. The key signaling pathways regulated by flavonoids include brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinase B (TrkB), and nuclear factor kappa-B (NF-κB). Clearly, there is a need to conduct human dietary intervention studies to validate the beneficial physiological functions of flavonoids on the prevention and management of depression.

以黄酮类化合物为基础的植物药物正在成为对抗包括抑郁症在内的各种疾病的有希望的治疗方法。抑郁症是一种常见的严重的医学疾病，会对生活质量产生负面影响。它已成为世界范围内致残的主要原因。类黄酮是一种普遍存在于药用植物、草药、水果、蔬菜、茶和酒中的具有生物活性的植物化学物质。人类摄入总黄酮与抑郁症状呈负相关。本文综述了近年来关于膳食类黄酮在抑郁症模型中的作用的体内和体外研究，并分析了其作用的分子途径。本文简要介绍了抑郁症的病理生理学、抑郁症的诊断以及抑郁症的研究模型。已发现的潜在抗抑郁药物黄酮类化合物包括黄酮醇（槲皮素、槲皮素、山奈酚和七甲基黄酮）、黄酮（木犀草素、黄芩苷、芹菜素和cymaroside）、异黄酮（芥子草苷）、黄酮（松皮素）和花青素（石蒜素）。这些植物衍生的类黄酮已被证明可以减少海马神经元损伤，减少神经递质耗损，减轻下丘脑-垂体-肾上腺轴过度激活，抑制中枢神经系统炎症，调节肠道微生物群。黄酮类化合物调节的关键信号通路包括脑源性神经营养因子(BDNF)/原肌球蛋白相关激酶B （TrkB）和核因子κB （NF-κB）。显然，有必要进行人类饮食干预研究，以验证黄酮类化合物在预防和管理抑郁症方面的有益生理功能。

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引用次数: 0

Cognitive outcomes following psilocybin-assisted therapy in treatment-resistant depression: A post-hoc analysis of a randomized, waitlist-controlled trial 对难治性抑郁症进行裸盖菇素辅助治疗后的认知结果：一项随机、候补对照试验的事后分析。

IF 3.9 2区医学 Q1 CLINICAL NEUROLOGY

Progress in Neuro-Psychopharmacology & Biological Psychiatry

Pub Date : 2025-11-22 DOI: 10.1016/j.pnpbp.2025.111565

Danica E. Johnson , Shakila Meshkat , Erica S. Kaczmarek , Jennifer S. Rabin , Ryan M. Brudner , Noah Chisamore , Zoe Doyle , Jordan Bawks , Jeremy Riva-Cambrin , Rodrigo B. Mansur , Orly Lipsitz , Roger S. McIntyre , Krista L. Lanctôt , Joshua D. Rosenblat

Background

Cognitive difficulties within treatment-resistant unipolar and bipolar depression (TRD; TRBD) often do not improve with conventional pharmacotherapies. Psilocybin-assisted psychotherapy (PAP) has shown promise as a novel intervention for TRD; however, few studies have assessed its effects on cognition in this population.

Methods

This retrospective post hoc analysis included 26 adults with TRD or TRBD from an open-label trial of PAP. Cognition was assessed with the Digit Symbol Substitution Test (DSST) and Trail Making Test Part A and B (TMT-A/B) at baseline, one-day, and two-weeks post-treatment. Linear mixed models (LMMs) evaluated change over time, and reliable change indices (RCIs) with binomial tests assessed whether the proportion of participants showing meaningful improvement exceeded chance.

Results

Significant improvements were observed on all cognitive measures over time (all p < .05). After adjusting for depressive symptoms, gains on the TMT-A (p < .001), TMT-B (p < .001), and TMTB – A (p = .005) remained significant. In contrast, DSST improvements were attenuated (p = .069). RCIs showed that 4.2 %–12.5 % of participants achieved meaningful improvement, but these rates did not significantly exceed chance expectations.

Conclusion

PAP was associated with modest, short-term improvements in performance on measures of processing speed and executive function among individuals with TRD. While these changes appeared independent of mood, they did not consistently exceed expected practice effects. These findings highlight the need for adequately powered, controlled trials to clarify whether observed cognitive changes reflect genuine procognitive effects of psilocybin or are attributable to non-specific influences such as test familiarity or concurrent mood improvements.

背景：难治性单极和双相抑郁症（TRD； TRBD）的认知困难通常不能通过常规药物治疗得到改善。裸盖菇素辅助心理治疗（PAP）作为一种治疗TRD的新型干预手段已显示出前景；然而，很少有研究评估它对这一人群认知能力的影响。方法：这项回顾性事后分析包括26名来自开放标签PAP试验的TRD或TRBD成人。在基线、治疗后一天和两周，通过数字符号替代测试（DSST）和轨迹测试A部分和B部分（TMT-A/B）评估认知。线性混合模型（lmm）评估随时间的变化，采用二项检验的可靠变化指数（rci）评估显示有意义改善的参与者比例是否超过机会。结果：随着时间的推移，所有认知测量都有显著的改善（p均为 ）。结论：PAP与TRD患者在处理速度和执行功能方面的表现有适度的短期改善有关。虽然这些变化似乎与情绪无关，但它们并不总是超过预期的练习效果。这些发现强调需要足够有力的对照试验来澄清观察到的认知变化是反映了裸盖菇素真正的前认知效应，还是归因于非特异性影响，如测试熟悉度或同时的情绪改善。

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引用次数: 0

Aging increases susceptibility to high-fat diet-induced neurobehavioral and mitochondrial dysfunction in zebrafish 衰老增加了斑马鱼对高脂肪饮食诱导的神经行为和线粒体功能障碍的易感性

IF 3.9 2区医学 Q1 CLINICAL NEUROLOGY

Progress in Neuro-Psychopharmacology & Biological Psychiatry

Pub Date : 2025-11-20 DOI: 10.1016/j.pnpbp.2025.111564

Victor L. Picolo , Letícia A. Tavares , Whitney R. Santos , Nathasha P. Lopes , Ethiane R. dos Santos , Wembley R. Vilela , Angelica Amato , Paula Q. Bellozi , Jair T. Goulart , Cesar K. Grisolia , Daniel Ardisson-Araújo , Andreza F. de Bem

Aging and unhealthy eating habits independently and synergistically disrupt central nervous system (CNS) homeostasis, increasing susceptibility to neurological and behavioral disorders. Mitochondria plays a critical role in maintaining neuronal survival and activity, representing a central player in the pathogenesis of neurodegenerative diseases. Here, we used zebrafish as a model to investigate how aging and a high-fat diet (HFD) affect brain bioenergetics and behavior. Young (4–6 months) and aged (17–22 months) male zebrafish were fed either a standard diet or an HFD based on boiled chicken egg yolk for 14 days. Brain mitochondria was evaluated using high-resolution respirometry, transmission electron microscopy (TEM), and qRT-PCR. HFD impaired the metabolic health of both young and aged animals, promoting weight gain, increased abdominal length, and elevated fasting glucose levels. Aging intensified the HFD detrimental effects on behavior: aged HFD-fed zebrafish displayed increased anxiety-like behavior in the novel tank test, and impaired cognitive performance in the T-maze test. Notably, HFD had no significant effect on aggressive behavior regardless of age. Mitochondrial responses to HFD differed by age: while cerebral bioenergetic function declined in young fish, aged animals showed an opposite trend. TEM analysis revealed increased accumulation of fragmented mitochondria in HFD group, indicating potential mitochondrial dysfunction. RT-qPCR showed upregulation of genes involved in the electron transport chain, especially in aged zebrafish. In conclusion, our findings demonstrate an age-dependent vulnerability to the effects of HFD on both neurobehavioral and mitochondrial parameters.

衰老和不健康的饮食习惯独立和协同破坏中枢神经系统（CNS）稳态，增加神经和行为障碍的易感性。线粒体在维持神经元存活和活动中起着关键作用，在神经退行性疾病的发病机制中起着核心作用。在这里，我们使用斑马鱼作为模型来研究衰老和高脂肪饮食（HFD）如何影响大脑生物能量学和行为。幼龄（4-6个月）和老年（17-22个月）雄性斑马鱼分别饲喂标准饲料或以煮鸡蛋黄为基础的高热量饲料14天。使用高分辨率呼吸仪、透射电镜（TEM）和qRT-PCR评估脑线粒体。HFD损害了幼龄和老年动物的代谢健康，促进体重增加、腹部长度增加和空腹血糖水平升高。衰老加剧了HFD对行为的有害影响：喂食HFD的年老斑马鱼在新型水箱测试中表现出焦虑样行为增加，在t -迷宫测试中表现出认知能力受损。值得注意的是，无论年龄大小，高脂肪饮食对攻击行为没有显著影响。线粒体对HFD的反应因年龄而异：幼鱼的大脑生物能量功能下降，老年动物则呈现相反的趋势。透射电镜分析显示，HFD组线粒体碎片积累增加，提示可能存在线粒体功能障碍。RT-qPCR显示参与电子传递链的基因上调，尤其是在老年斑马鱼中。总之，我们的研究结果表明，HFD对神经行为和线粒体参数的影响具有年龄依赖性。

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引用次数: 0

Enriched environment restores depressive- and anxiety-like behaviors in mice with early life stress exposure by reversing striatal function, structure and metabolism 丰富的环境通过逆转纹状体功能、结构和代谢，恢复早期生活压力暴露小鼠的抑郁和焦虑样行为。

IF 3.9 2区医学 Q1 CLINICAL NEUROLOGY

Progress in Neuro-Psychopharmacology & Biological Psychiatry

Pub Date : 2025-11-15 DOI: 10.1016/j.pnpbp.2025.111562

Ziqi An , Kai Tang , Baoxing Ren , Quan Tao , Chuanjun Tong , Xinyuan Zhang , Lina Zhao , Jiaming Liu , Yanqiu Feng

Early life stress (ELS) has been widely recognized as a major risk factor for the development of depression and anxiety in humans. While clinical studies have established this association, the underlying neural mechanisms remain elusive. To address this gap, rodent models such as maternal separation have been employed to mimic ELS and to explore its long-term effects on the brain and behavior. Environmental enrichment (EE) has further been proposed as a potential intervention to counteract the detrimental consequences of ELS, but its efficacy and underlying mechanisms remain insufficiently characterized. In this study, we utilized multi-parametric magnetic resonance imaging combined with behavioral tests to systematically evaluate the long-term effects of ELS exposure and subsequent EE intervention on brain signatures and behavioral changes in adult male and female ELS mice. ELS mice exhibited depressive- and anxiety-like behaviors, along with increased brain activity in the striatum. These behavioral changes were accompanied by reductions in gray matter volume, white matter integrity and metabolite ratios in the striatum. Importantly, EE intervention effectively reversed the behavioral impairments by restoring the alterations in brain function, structure, and metabolism, especially in the striatum. This study provides comprehensive insights into the detrimental effects of early life stress on brain and behavioral outcomes and reveals that these negative effects can be mitigated by EE intervention. Our findings identify the striatum as a critical region involved in these processes.

早期生活压力（ELS）已被广泛认为是人类抑郁和焦虑发展的主要危险因素。虽然临床研究已经建立了这种联系，但潜在的神经机制仍然难以捉摸。为了解决这一差距，啮齿类动物模型，如母亲分离，已被用来模拟ELS和探索其对大脑和行为的长期影响。环境富集（Environmental enrichment， EE）已被进一步提出作为一种潜在的干预措施，以抵消ELS的有害后果，但其有效性和潜在机制尚未得到充分的研究。在这项研究中，我们利用多参数磁共振成像结合行为测试，系统评估ELS暴露和随后的EE干预对成年雄性和雌性ELS小鼠脑特征和行为变化的长期影响。ELS小鼠表现出抑郁和焦虑样行为，同时纹状体的大脑活动增加。这些行为变化伴随着纹状体灰质体积、白质完整性和代谢物比率的减少。重要的是，情感表达干预通过恢复大脑功能、结构和代谢，尤其是纹状体的改变，有效地逆转了行为障碍。这项研究为早期生活压力对大脑和行为结果的有害影响提供了全面的见解，并揭示了这些负面影响可以通过情感表达干预来减轻。我们的发现确定纹状体是参与这些过程的关键区域。

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引用次数: 0

Sirtuin 3, a mitochondrial metabolic enzyme, links the mitochondrial function to neurophysiology in depression Sirtuin 3是一种线粒体代谢酶，将线粒体功能与抑郁症的神经生理学联系起来

IF 3.9 2区医学 Q1 CLINICAL NEUROLOGY

Progress in Neuro-Psychopharmacology & Biological Psychiatry

Pub Date : 2025-11-14 DOI: 10.1016/j.pnpbp.2025.111563

Cong-Ya Chen , Ya-Ting Wang , Ling-Jie Liu , Yi Zhang

Depression, characterized by sustained low moods and even suicidal tendencies, has been intimately linked with mitochondrial dysfunction. This dysfunction is significantly connected with various psychiatric disorders, suggesting its potential role in the pathogenesis and progression of depression. Sirtuin 3 (SIRT3), a potent deacetylase enzyme primarily located within mitochondria, orchestrates mitochondrial function and mitigates various dysfunctions, e.g., insufficient cellular energy supply and oxidative stress. Insufficient cellular energy supply and oxidative stress disrupt normal neuroplasticity and neuroinflammation in the nervous system, as well as disturbances of the hypothalamic-pituitary-adrenal axis in peripheral systems. This review aims to elucidate that SIRT3 can be a potential target for depression, thereby summarizing the mechanisms by which SIRT3 is involved in the pathogenesis and progression of depression by regulating mitochondrial function.

抑郁症以持续的情绪低落甚至自杀倾向为特征，与线粒体功能障碍密切相关。这种功能障碍与多种精神疾病密切相关，提示其在抑郁症的发病和发展中可能起作用。Sirtuin 3 （SIRT3）是一种主要位于线粒体内的强效去乙酰酶，可调节线粒体功能并减轻各种功能障碍，如细胞能量供应不足和氧化应激。细胞能量供应不足和氧化应激破坏神经系统正常的神经可塑性和神经炎症，以及外周系统的下丘脑-垂体-肾上腺轴的紊乱。本文旨在阐明SIRT3可能是抑郁症的潜在靶点，从而总结SIRT3通过调节线粒体功能参与抑郁症发病和进展的机制。

引用次数: 0

Electroencephalography source-space functional connectivity reveals frequency-specific brain network dysfunctions in obsessive-compulsive disorder 脑电图源空间功能连接揭示强迫症中频率特异性脑网络功能障碍。

IF 3.9 2区医学 Q1 CLINICAL NEUROLOGY

Progress in Neuro-Psychopharmacology & Biological Psychiatry

Pub Date : 2025-11-14 DOI: 10.1016/j.pnpbp.2025.111561

Ke Chen , Yian Xiao , Siya Zhu , Fuyao Cao , Qiangyan Che , Yueling Liu , Ke Wan , Xuemeng Chen , Wanying Zhang , Jiarui Ye , Zhisen Li , Fengqiong Yu , Kai Wang , Chunyan Zhu

Background

Obsessive-compulsive disorder (OCD) is characterized by disruptions in large-scale brain networks. However, the role of high-frequency neural synchrony in these abnormalities remains unclear. Elucidating frequency-specific alterations may offer critical insights into the neurophysiological mechanisms underlying brain network dysfunction in OCD.

Methods

We analyzed resting-state electroencephalography data from 88 OCD patients and 100 healthy controls (HCs), and constructed source-space functional connectivity networks using weighted phase lag index. Graph-theoretical metrics including global and local efficiency were computed to quantify network topology. Machine learning with support vector machines was applied to classify OCD patients and HCs using multi-frequency network features.

Results

Compared to HCs, OCD patients exhibited increased beta-band connectivity between the default mode network (DMN) and frontoparietal network (FPN). Beta-band connectivity within the FPN was correlated with compulsive symptoms. Additionally, reduced global efficiency and local efficiency in the right visual cortex was observed in the beta band. Low-frequency (dela and theta) network topology metrics also correlated with anxiety severity. Classification analysis integrating multi-frequency features achieved an accuracy of 87.9 %.

Limitation

The majority of patients in our sample were receiving pharmacological treatment, and the effects of medication could not be fully controlled.

Conclusion

These findings reveal frequency-specific disruptions in brain networks underlying OCD symptoms and demonstrate the potential of electrophysiological connectome biomarkers for diagnosis. These results support frequency-targeted neuromodulation strategies for personalized OCD treatment.

背景：强迫症（OCD）的特征是大规模大脑网络的中断。然而，高频神经同步在这些异常中的作用仍不清楚。阐明频率特异性改变可能为强迫症脑网络功能障碍的神经生理机制提供重要见解。方法：分析88例强迫症患者和100例健康对照的静息状态脑电图数据，采用加权相位滞后指数构建源空间功能连接网络。计算了包括全局和局部效率在内的图理论度量来量化网络拓扑。将机器学习与支持向量机结合，利用多频网络特征对强迫症患者和hc进行分类。结果：与正常人相比，强迫症患者表现出默认模式网络（DMN）和额顶叶网络（FPN）之间的β波段连通性增加。FPN内的β波段连通性与强迫症状相关。此外，在β带观察到右侧视觉皮层的整体效率和局部效率降低。低频（δ和θ）网络拓扑指标也与焦虑严重程度相关。结合多频特征的分类分析准确率达到87.9% %。局限性：我们样本中的大多数患者都在接受药物治疗，药物的作用不能完全控制。结论：这些发现揭示了强迫症症状背后的大脑网络频率特异性中断，并证明了电生理连接组生物标志物在诊断方面的潜力。这些结果支持频率靶向神经调节策略用于个性化强迫症治疗。

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引用次数: 0

Gray matter volumes of the superior temporal gyrus link preterm birth and developmentally disordered eye gazing patterns in toddlers at eighteen months 颞上回灰质体积与早产和18个月大的幼儿眼睛注视模式发育障碍有关。

IF 3.9 2区医学 Q1 CLINICAL NEUROLOGY

Progress in Neuro-Psychopharmacology & Biological Psychiatry

Pub Date : 2025-11-11 DOI: 10.1016/j.pnpbp.2025.111560

Yanan Su , Guangfei Li , Shanmei Wang , Dongmei Hao , Clara S. Li , Yiyao Ye-Lin , Xiaolin Wang , Ruolin Zhang , Lin Yang , Chiang-Shan R. Li

Background

Preterm birth involves structural brain changes and increases the risk of neurodevelopmental disorders, including social cognitive dysfunction as implicated in autism spectrum disorder (ASD). However, it remains unclear whether or how volumetric brain changes may impact the risk of social cognitive dysfunction in toddlers of preterm birth.

Methods

We curated data of 569 toddlers approximately 18 months of age, including 76 with preterm (PB) and 493 with term (TB) birth, from the developing Human Connectome Project. We processed the imaging data, collected at birth, and investigated group differences in gray matter volume (GMV) of the brain and eye-tracking data collected at 18 months as well as the interrelationships amongst birth age, GMVs, and eye-tracking markers of ASD.

Results

In a covariance analysis with age at scan, total intracranial volume, sex, and number of embryos at gestation as covariates, PB demonstrated higher GMV in bilateral superior temporal gyri (STG). Right STG GMV's were negatively correlated with birth age and positively with the proportion of looking at faces and mouths in PB, but not in TB. Further, path analyses suggested right STG GMV at birth as a marker of preferential face and mouth viewing in PB at 18 months.

Conclusions

The findings associate earlier birth age with atypical volumetrics of the right STG and eye gazing patterns in preterm children at 18 months. Longitudinal studies are needed to examine whether these neural and behavioral markers may reflect risks of social cognitive dysfunction in children with neurodevelopmental disorders, including ASD.

背景：早产涉及大脑结构改变，增加神经发育障碍的风险，包括与自闭症谱系障碍（ASD）有关的社会认知功能障碍。然而，目前尚不清楚脑容量变化是否或如何影响早产儿社会认知功能障碍的风险。方法：我们收集了569名年龄约为18 个月的幼儿的数据，包括76名早产儿（PB）和493名足月新生儿（TB），这些数据来自正在发展的人类连接组项目。我们对出生时收集的成像数据进行了处理，并调查了18 个月时收集的大脑灰质体积（GMV）和眼动追踪数据的组间差异，以及出生年龄、GMV和ASD眼动追踪标志物之间的相互关系。结果：在以扫描年龄、颅内总容积、性别和妊娠胚胎数为协方差分析中，PB在双侧颞上回（STG）表现出更高的GMV。右侧STG GMV与出生年龄呈负相关，与注视面孔和嘴巴的比例呈正相关，而与TB无显著相关性。此外，通径分析表明，出生时右侧STG GMV是18 个月大的婴儿优先观看面部和嘴巴的标志。结论：研究结果将早产年龄与18 个月的早产儿右STG的非典型体积和眼睛凝视模式联系起来。需要进行纵向研究，以检查这些神经和行为标志物是否可以反映包括ASD在内的神经发育障碍儿童的社会认知功能障碍风险。

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引用次数: 0

Social cognition in women with eating disorders: Differences between the restrictive and purgative profiles 饮食失调妇女的社会认知：限制性和泻性特征之间的差异。

IF 3.9 2区医学 Q1 CLINICAL NEUROLOGY

Progress in Neuro-Psychopharmacology & Biological Psychiatry

Pub Date : 2025-11-08 DOI: 10.1016/j.pnpbp.2025.111556

P. de la Higuera-Gonzalez , A. Galvez-Merlin , B. Marcos-Diaz , A. Calvo , A. Carrasco-Diaz , W. Ayad-Ahmed , P. Mola-Cardenes , A. de la Torre-Luque , F. Ruiz-Guerrero , F. Polo-Montes , J.L. Carrasco-Perera , L. Beato-Fernandez , A. Gomez-del Barrio , M. Diaz-Marsa

Introduction

Difficulties in interpersonal interactions have been related to Social Cognition (SC) impairments in eating disorders (EDs). However, results do not account for differences between restrictive (rED) and purgative (pED) profiles and are just based on decoding tasks. This study assessed SC by Theory of Mind (ToM) abilities in ToM decoding and inference tasks between rED and pED patients and healthy women and its relationship with clinical variables.

Method

37 rED patients, 42 pED patients and 34 controls were evaluated using the Movie for the Assessment of Social Cognition (MASC) -ToM inference abilities- and the Reading the Mind in the Eyes revised version (RMET-R) - ToM decoding abilities-. Age, body mass index (BMI) and disorder's duration were considered as clinical variables. ANCOVA analyses were carried out to analyse differences between groups, controlling for impulsivity as a covariate. Group relationships between ToM and clinical variables were analysed through linear regression models.

Results

pED showed lower correct MASC responses (p < .01) and more overmentalising errors (p < .05) than controls, and for rED, differences overmentalising errors were close to significance (p = .051). For RMET-R, differences were related to impulsivity. Age (p < .01) and BMI p < .05) were related with correct MASC responses.

Conclusions

Patients with EDs show difficulties in ToM inference abilities, especially those with a purgative profile, with poorer performance related to clinical severity indices such as weight and age. Differences in ToM decoding appear to be related to impulsivity rather than clinical diagnosis.

人际交往困难与进食障碍患者的社会认知障碍有关。然而，结果并没有考虑限制性（rED）和泻性（pED）配置文件之间的差异，而只是基于解码任务。本研究通过心理理论（ToM）在rED和pED患者和健康女性的ToM解码和推理任务中的能力及其与临床变量的关系来评估SC。方法：对37例rED患者、42例pED患者和34例对照患者进行社会认知能力(MASC) -ToM推理能力测评和眼读心术(RMET-R) -ToM解码能力测评。年龄、身体质量指数（BMI）和疾病持续时间作为临床变量。进行ANCOVA分析以分析组间差异，控制冲动性作为协变量。通过线性回归模型分析ToM与临床变量的组间关系。结果：pED患者的正确MASC反应较低（p ）结论：ed患者在ToM推断能力方面存在困难，特别是那些有泻药病史的患者，其在体重和年龄等临床严重程度指标方面的表现较差。ToM解码的差异似乎与冲动有关，而不是与临床诊断有关。

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