Neuroscience最新文献_第4页

Bridging ancient substances and modern psychiatry: the role of classic psychedelics in depression treatment 连接古代物质和现代精神病学：经典致幻剂在抑郁症治疗中的作用。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2026-01-22 DOI: 10.1016/j.neuroscience.2026.01.022

Guilherme Lodetti, Gislaine Zilli Réus, Eduardo Pacheco Rico

Pharmacotherapy for MDD is commonly prescribed to patients, yet fewer than half achieve remission. Moreover, many patients exhibit intolerant responses to pharmacological treatment, highlighting the need to explore new forms of therapy. The present work provides a narrative review of classic psychedelics as an alternative to MDD treatment. In addition, mechanisms by which psychedelics exert antidepressant effects are discussed. A literature review of recent studies regarding psychedelics used for the treatment of depressive disorders. The main search platform for relevant indexed articles used was PubMed, using keywords such as psychedelics, MDD, depression, and treatment. Studies have shown that classic psychedelics mainly bind to 5-HT2A receptors, increasing interaction between sensory and somatomotor brain networks. These substances play a significant role in treating psychiatric disorders. Also, classic psychedelics generate long-term behavioural responses comparable to traditional treatments. Therefore, they are strongly associated with the management of these conditions. Recent studies have shown that classic psychedelics yield favourable outcomes in alleviating symptoms of depression. This has been observed in clinical and experimental investigations. The improvement in mood is thought to arise from their influence on molecular targets associated with neuroplasticity, including the promotion of neurogenesis and the behavioural responses linked to downstream and upstream signalling pathways.

通常会给重度抑郁症患者开药物治疗，但只有不到一半的患者获得缓解。此外，许多患者对药物治疗表现出不耐受反应，强调需要探索新的治疗形式。目前的工作提供了一个叙述性的回顾经典迷幻药作为替代重度抑郁症治疗。此外，还讨论了致幻剂发挥抗抑郁作用的机制。关于迷幻药用于治疗抑郁症的最新研究的文献综述。相关索引文章的主要搜索平台是PubMed，关键词包括迷幻药、重度抑郁症、抑郁症和治疗。研究表明，经典迷幻药主要与5-HT2A受体结合，增加感觉和躯体运动脑网络之间的相互作用。这些物质在治疗精神疾病方面起着重要作用。此外，经典迷幻药产生的长期行为反应与传统疗法相当。因此，它们与这些条件的管理密切相关。最近的研究表明，经典迷幻药在缓解抑郁症状方面效果良好。这已在临床和实验研究中观察到。情绪的改善被认为是由于它们对与神经可塑性相关的分子靶标的影响，包括促进神经发生和与下游和上游信号通路相关的行为反应。

{"title":"Bridging ancient substances and modern psychiatry: the role of classic psychedelics in depression treatment","authors":"Guilherme Lodetti, Gislaine Zilli Réus, Eduardo Pacheco Rico","doi":"10.1016/j.neuroscience.2026.01.022","DOIUrl":"10.1016/j.neuroscience.2026.01.022","url":null,"abstract":"<div><div>Pharmacotherapy for MDD is commonly prescribed to patients, yet fewer than half achieve remission. Moreover, many patients exhibit intolerant responses to pharmacological treatment, highlighting the need to explore new forms of therapy. The present work provides a narrative review of classic psychedelics as an alternative to MDD treatment. In addition, mechanisms by which psychedelics exert antidepressant effects are discussed. A literature review of recent studies regarding psychedelics used for the treatment of depressive disorders. The main search platform for relevant indexed articles used was PubMed, using keywords such as psychedelics, MDD, depression, and treatment. Studies have shown that classic psychedelics mainly bind to 5-HT2A receptors, increasing interaction between sensory and somatomotor brain networks. These substances play a significant role in treating psychiatric disorders. Also, classic psychedelics generate long-term behavioural responses comparable to traditional treatments. Therefore, they are strongly associated with the management of these conditions. Recent studies have shown that classic psychedelics yield favourable outcomes in alleviating symptoms of depression. This has been observed in clinical and experimental investigations. The improvement in mood is thought to arise from their influence on molecular targets associated with neuroplasticity, including the promotion of neurogenesis and the behavioural responses linked to downstream and upstream signalling pathways.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"597 ","pages":"Pages 38-49"},"PeriodicalIF":2.8,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146044046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

An ALS-associated mutant SOD1 protein can be eliminated in microglia culture by selective autophagy. als相关的SOD1突变蛋白可以通过选择性自噬在小胶质细胞培养中消除。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2026-01-22 DOI: 10.1016/j.neuroscience.2026.01.017

Kumiko Murakami, Norihiro Sudou, Atushi Kurata, Motoko Kawaguchi-Niida

The acquired toxicity of the familial amyotrophic lateral sclerosis (ALS)-associated mutant Zn-superoxide dismutase 1 (SOD1) protein has been implicated in motoneuron death, and cytosolic aggregates or inclusions have been observed in the cytoplasm of motoneurons, astrocytes, and neuronal axons but not in that of microglia. This study elucidates the mechanisms by which mutant SOD1 does not aggregate in and is cleared by microglia. We generated pcDNA3-Venus-tagged SOD1 constructs: wild-type SOD1 and mutant SOD1 were used as controls, and the A4V, D90A, and G93A SOD1 mutants were used as disease-related constructs; these plasmids were introduced into the Ra2 microglia line for subsequent evaluation. In spinal cords collected from postsymptomatic G93A mice, very little aggregation of the mutant SOD1 protein was detected in microglia, consistent with previous reports. Our new findings, which were based on immunohistochemical, Western blot, and enzyme immunoassay analyses, revealed that the protein expression of mutant SOD1 in microglia is significantly lower than that of wild-type SOD1. Furthermore, we observed the recovery of mutant SOD1 protein levels in autophagy suppression experiments and its colocalization with WDFY3, a selective autophagy-related protein. These in vitro results demonstrate that only the mutant SOD1 protein (i.e., not wild-type SOD1) is degraded by selective autophagy. Furthermore, we found that both wild-type and mutant SOD1 are secreted directly from microglia. These findings provide an opportunity to elucidate the precise mechanism through which microglia manage mutant SOD1 proteins during the pathological process of ALS and are likely to lead to improvements in ALS treatment strategies.

家族性肌萎缩性侧索硬化症（ALS）相关突变体zn -超氧化物歧化酶1 （SOD1）蛋白的获得性毒性与运动神经元死亡有关，在运动神经元、星形胶质细胞和神经元轴突的细胞质中观察到胞质聚集体或包涵体，但在小胶质细胞中没有观察到。这项研究阐明了突变SOD1不聚集在小胶质细胞中并被小胶质细胞清除的机制。我们生成了pcdna3 - venus标记的SOD1构建体：野生型SOD1和突变型SOD1作为对照，A4V、D90A和G93A SOD1突变体作为疾病相关构建体；这些质粒被引入Ra2小胶质细胞系进行后续评价。在症状后的G93A小鼠脊髓中，在小胶质细胞中检测到很少的SOD1突变蛋白聚集，与先前的报道一致。我们的新发现，基于免疫组织化学，Western blot和酶免疫分析，显示突变型SOD1在小胶质细胞中的蛋白表达明显低于野生型SOD1。此外，我们在自噬抑制实验中观察到突变体SOD1蛋白水平的恢复及其与选择性自噬相关蛋白WDFY3的共定位。这些体外实验结果表明，只有突变型SOD1蛋白（即，不是野生型SOD1）被选择性自噬降解。此外，我们发现野生型和突变型SOD1都直接从小胶质细胞分泌。这些发现为阐明小胶质细胞在ALS病理过程中管理突变SOD1蛋白的确切机制提供了机会，并可能导致ALS治疗策略的改进。

{"title":"An ALS-associated mutant SOD1 protein can be eliminated in microglia culture by selective autophagy.","authors":"Kumiko Murakami, Norihiro Sudou, Atushi Kurata, Motoko Kawaguchi-Niida","doi":"10.1016/j.neuroscience.2026.01.017","DOIUrl":"10.1016/j.neuroscience.2026.01.017","url":null,"abstract":"<p><p>The acquired toxicity of the familial amyotrophic lateral sclerosis (ALS)-associated mutant Zn-superoxide dismutase 1 (SOD1) protein has been implicated in motoneuron death, and cytosolic aggregates or inclusions have been observed in the cytoplasm of motoneurons, astrocytes, and neuronal axons but not in that of microglia. This study elucidates the mechanisms by which mutant SOD1 does not aggregate in and is cleared by microglia. We generated pcDNA3-Venus-tagged SOD1 constructs: wild-type SOD1 and mutant SOD1 were used as controls, and the A4V, D90A, and G93A SOD1 mutants were used as disease-related constructs; these plasmids were introduced into the Ra2 microglia line for subsequent evaluation. In spinal cords collected from postsymptomatic G93A mice, very little aggregation of the mutant SOD1 protein was detected in microglia, consistent with previous reports. Our new findings, which were based on immunohistochemical, Western blot, and enzyme immunoassay analyses, revealed that the protein expression of mutant SOD1 in microglia is significantly lower than that of wild-type SOD1. Furthermore, we observed the recovery of mutant SOD1 protein levels in autophagy suppression experiments and its colocalization with WDFY3, a selective autophagy-related protein. These in vitro results demonstrate that only the mutant SOD1 protein (i.e., not wild-type SOD1) is degraded by selective autophagy. Furthermore, we found that both wild-type and mutant SOD1 are secreted directly from microglia. These findings provide an opportunity to elucidate the precise mechanism through which microglia manage mutant SOD1 proteins during the pathological process of ALS and are likely to lead to improvements in ALS treatment strategies.</p>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":" ","pages":"47-58"},"PeriodicalIF":2.8,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146044102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Bibliometric analysis of neuroinflammation in Alzheimer’s Disease: Insights from APP/PS1 mouse model research in the past two decades 阿尔茨海默病神经炎症的文献计量学分析：过去二十年APP/PS1小鼠模型研究的见解

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2026-01-20 DOI: 10.1016/j.neuroscience.2026.01.020

Li Yan , Haibin Wang , Jianrong Shi , Hongsheng Tan , Qing Liu

Background: The APP/PS1 transgenic mouse is a foundational model in Alzheimer’s disease (AD) research, particularly for investigating the pivotal role of neuroinflammation in disease pathogenesis. Although substantial experimental work has explored inflammatory mechanisms in AD, the field still lacks a comprehensive overview of how research hotspots have evolved, which key scientific questions remain unresolved, and how global research efforts align with existing mechanistic gaps. Therefore, this investigation systematically evaluated scholarly trends, geographic contributions, institutional productivity, and thematic evolution to synthesize actionable insights that will guide subsequent experimental designs.

Methods: Bibliometric analysis was conducted on peer-reviewed articles indexed in the Web of Science Core Collection (2005–2024). Analytical tools, including VOSviewer, CiteSpace, and Bibliometrix, were employed to quantify research output, collaborative networks, citation metrics, and keyword co-occurrence patterns.

Results: Annual publication numbers exhibited exponential growth post-2015, reflecting an intensified focus on neuroinflammatory mechanisms in AD. China and the United States contributed 83.4 % of total publications, with the University of Barcelona as the most productive institution. High-impact journals such as Nature, Nature Neuroscience, and Brain Behavior Immunity. The analysis identified key scientific issues and evolving research fronts, with current hot topics focusing on oxidative stress, activated microglia releasing inflammatory cytokines, and abnormal autophagy-lysosome pathways.

Conclusion: The APP/PS1 mice have a significantly enhanced mechanistic understanding of neuroimmune interactions in AD pathogenesis. Future research should explore microglia-mediated neuroinflammation and brain-gut microbiome interactions to uncover novel diagnostic and therapeutic strategies for AD. This study offers an evidence-based framework to guide researchers using APP/PS1 mice model.

背景：APP/PS1转基因小鼠是阿尔茨海默病（AD）研究的基础模型，特别是研究神经炎症在疾病发病机制中的关键作用。尽管大量的实验工作已经探索了阿尔茨海默病的炎症机制，但该领域仍然缺乏对研究热点如何演变的全面概述，哪些关键科学问题尚未解决，以及全球研究工作如何与现有的机制差距保持一致。因此，本研究系统地评估了学术趋势、地理贡献、制度生产力和专题演变，以综合可操作的见解，指导后续的实验设计。方法：对Web of Science Core Collection（2005-2024）收录的同行评议文章进行文献计量分析。利用VOSviewer、CiteSpace和Bibliometrix等分析工具对研究产出、合作网络、引文指标和关键词共现模式进行量化。结果：2015年后，年度出版物数量呈指数级增长，反映了对阿尔茨海默病神经炎症机制的加强关注。中国和美国贡献了83.4 %的总出版物，其中巴塞罗那大学是最多产的机构。高影响力期刊，如《自然》、《自然神经科学》和《脑行为免疫》。分析确定了关键的科学问题和不断发展的研究前沿，目前的热门话题集中在氧化应激、激活的小胶质细胞释放炎症细胞因子和异常的自噬-溶酶体途径。结论：APP/PS1小鼠对阿尔茨海默病发病过程中神经免疫相互作用机制的认识显著增强。未来的研究应该探索小胶质细胞介导的神经炎症和脑-肠微生物组的相互作用，以发现新的AD诊断和治疗策略。本研究为APP/PS1小鼠模型的研究提供了一个循证框架。

{"title":"Bibliometric analysis of neuroinflammation in Alzheimer’s Disease: Insights from APP/PS1 mouse model research in the past two decades","authors":"Li Yan , Haibin Wang , Jianrong Shi , Hongsheng Tan , Qing Liu","doi":"10.1016/j.neuroscience.2026.01.020","DOIUrl":"10.1016/j.neuroscience.2026.01.020","url":null,"abstract":"<div><div>Background: The APP/PS1 transgenic mouse is a foundational model in Alzheimer’s disease (AD) research, particularly for investigating the pivotal role of neuroinflammation in disease pathogenesis. Although substantial experimental work has explored inflammatory mechanisms in AD, the field still lacks a comprehensive overview of how research hotspots have evolved, which key scientific questions remain unresolved, and how global research efforts align with existing mechanistic gaps. Therefore, this investigation systematically evaluated scholarly trends, geographic contributions, institutional productivity, and thematic evolution to synthesize actionable insights that will guide subsequent experimental designs.</div><div>Methods: Bibliometric analysis was conducted on peer-reviewed articles indexed in the Web of Science Core Collection (2005–2024). Analytical tools, including VOSviewer, CiteSpace, and Bibliometrix, were employed to quantify research output, collaborative networks, citation metrics, and keyword co-occurrence patterns.</div><div>Results: Annual publication numbers exhibited exponential growth post-2015, reflecting an intensified focus on neuroinflammatory mechanisms in AD. China and the United States contributed 83.4 % of total publications, with the University of Barcelona as the most productive institution. High-impact journals such as <em>Nature</em>, <em>Nature Neuroscience</em>, and <em>Brain Behavior Immunity</em>. The analysis identified key scientific issues and evolving research fronts, with current hot topics focusing on oxidative stress, activated microglia releasing inflammatory cytokines, and abnormal autophagy-lysosome pathways.</div><div>Conclusion: The APP/PS1 mice have a significantly enhanced mechanistic understanding of neuroimmune interactions in AD pathogenesis. Future research should explore microglia-mediated neuroinflammation and brain-gut microbiome interactions to uncover novel diagnostic and therapeutic strategies for AD. This study offers an evidence-based framework to guide researchers using APP/PS1 mice model.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"597 ","pages":"Pages 76-85"},"PeriodicalIF":2.8,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146030396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

A multi-view DTI feature fusion framework for enhanced diagnosis of Alzheimer’s disease 一种用于阿尔茨海默病增强诊断的多视图DTI特征融合框架

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2026-01-20 DOI: 10.1016/j.neuroscience.2026.01.024

Jianping Qiao , Guangchao Zhou , Shaoqi Wu , Hao Shang , Qi Yuan , Jiande Sun

Alzheimer’s disease (AD) is an irreversible neurodegenerative disorder. Diffusion tensor imaging (DTI) is widely used to detect brain alterations for diagnosis, but most methods rely on single-scale information. Therefore, this study proposes the multi-view feature learning framework incorporating residual block-based 3D convolutional neural network (3D-CNN) for AD diagnosis. First, tract-based spatial statistics were applied to extract voxel-based features from fractional anisotropy (FA) and mean diffusivity (MD) maps. Second, the residual block-based 3D-CNN model was employed to extract high-level deep features, enhancing model ability to capture global contextual information. Third, fiber tracking was used to construct structural connectivity networks, which served as connectivity-based features. Fourth, radiomics was applied to extract texture and shape features from FA and MD images. These four types of features were linearly combined and subsequently reduced in dimensionality using the ReliefF algorithm. Finally, an ensemble learning strategy was employed to perform three binary classification tasks among the AD, mild cognitive impairment (MCI), and normal control (NC) groups. Additionally, layer-wise relevance propagation (LRP) was utilized to improve the interpretability of the 3D-CNN model. Evaluated on 427 subjects from the Alzheimer’s Disease Neuroimaging Initiative database, the framework integrates complementary multi-scale information, achieving superior performance. For the AD vs. NC classification, it attained an accuracy of 97.6%, a sensitivity of 98.0%, and an area under the curve of 0.964, outperforming several state-of-the-art methods. These results demonstrate that our approach enhances diagnostic accuracy and contributes to understanding disease mechanisms by identifying multi-scale biomarkers associated with known AD pathology.

阿尔茨海默病（AD）是一种不可逆的神经退行性疾病。弥散张量成像（Diffusion tensor imaging， DTI）被广泛用于检测大脑病变的诊断，但大多数方法依赖于单尺度信息。因此，本研究提出了基于残差块的3D卷积神经网络（3D- cnn）的多视图特征学习框架，用于AD诊断。首先，应用基于束的空间统计方法从分数各向异性（FA）和平均扩散率（MD）地图中提取基于体素的特征；其次，采用基于残差分块的3D-CNN模型提取高级深度特征，增强模型捕捉全局上下文信息的能力；第三，利用光纤跟踪构建结构连接网络，作为基于连接的特征。第四，应用放射组学技术提取FA和MD图像的纹理和形状特征。这四种类型的特征线性组合，随后使用ReliefF算法降维。最后，采用集成学习策略在AD组、轻度认知障碍组（MCI）和正常对照组（NC）中执行三个二元分类任务。此外，利用分层相关传播（LRP）来提高3D-CNN模型的可解释性。对来自阿尔茨海默病神经影像学倡议数据库的427名受试者进行评估，该框架整合了互补的多尺度信息，取得了卓越的性能。对于AD和NC分类，它的准确率为97.6%，灵敏度为98.0%，曲线下面积为0.964，优于几种最先进的方法。这些结果表明，我们的方法提高了诊断准确性，并有助于通过识别与已知AD病理相关的多尺度生物标志物来理解疾病机制。

{"title":"A multi-view DTI feature fusion framework for enhanced diagnosis of Alzheimer’s disease","authors":"Jianping Qiao , Guangchao Zhou , Shaoqi Wu , Hao Shang , Qi Yuan , Jiande Sun","doi":"10.1016/j.neuroscience.2026.01.024","DOIUrl":"10.1016/j.neuroscience.2026.01.024","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is an irreversible neurodegenerative disorder. Diffusion tensor imaging (DTI) is widely used to detect brain alterations for diagnosis, but most methods rely on single-scale information. Therefore, this study proposes the multi-view feature learning framework incorporating residual block-based 3D convolutional neural network (3D-CNN) for AD diagnosis. First, tract-based spatial statistics were applied to extract voxel-based features from fractional anisotropy (FA) and mean diffusivity (MD) maps. Second, the residual block-based 3D-CNN model was employed to extract high-level deep features, enhancing model ability to capture global contextual information. Third, fiber tracking was used to construct structural connectivity networks, which served as connectivity-based features. Fourth, radiomics was applied to extract texture and shape features from FA and MD images. These four types of features were linearly combined and subsequently reduced in dimensionality using the ReliefF algorithm. Finally, an ensemble learning strategy was employed to perform three binary classification tasks among the AD, mild cognitive impairment (MCI), and normal control (NC) groups. Additionally, layer-wise relevance propagation (LRP) was utilized to improve the interpretability of the 3D-CNN model. Evaluated on 427 subjects from the Alzheimer’s Disease Neuroimaging Initiative database, the framework integrates complementary multi-scale information, achieving superior performance. For the AD vs. NC classification, it attained an accuracy of 97.6%, a sensitivity of 98.0%, and an area under the curve of 0.964, outperforming several state-of-the-art methods. These results demonstrate that our approach enhances diagnostic accuracy and contributes to understanding disease mechanisms by identifying multi-scale biomarkers associated with known AD pathology.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"597 ","pages":"Pages 1-12"},"PeriodicalIF":2.8,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146015895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Neonatal quercetin exposure reduces motor impairments and cerebellar damage in cerebral palsy rats, with different effects on males and females 新生儿接触槲皮素可减少脑瘫大鼠的运动损伤和小脑损伤，但对雄性和雌性的影响不同。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2026-01-19 DOI: 10.1016/j.neuroscience.2026.01.023

Glayciele Leandro de Albuquerque , Raul Manhães-de-Castro , Isla Ariadny Amaral De Souza Gonzaga Paz , Eulália Rebeca da Silva-Araújo , Henrique José Cavalcanti Bezerra Gouveia , Maria Letícia Farias Tenório , Marcos Antônio da Silva Araújo , Ana Elisa Toscano

Cerebral palsy (CP) comprises a group of neuromusculoskeletal disorders resulting from fetal or infant brain injury. Quercetin has demonstrated antioxidant, anti-inflammatory and neuroprotective properties in neurological diseases. This study aimed to evaluate the effects of neonatal treatment with quercetin on motor development, neuronal loss, and inflammation in the cerebellum of rats subjected to CP. CP model was induced by postnatal anoxia (P0 and P1) and hindlimbs sensorimotor restriction (P2 to P28). Quercetin (10 mg/kg) was administered intraperitoneally from P2 to P22. Animals were analyzed for somatic growth; reflex ontogenesis; muscle strength; motor coordination; locomotor activity and gait in CatWalk; neuronal loss and inflammation in the cerebellum. Experimental CP, regardless of sex, restricted body weight gain, somatic growth, soleus muscle weight, muscle strength, motor coordination, locomotor activity and gait development, and promoted increased neuroinflammation in the cerebellum. Neonatal quercetin exposure was positive in the model of CP in males, favoring body weight gain, reducing the presence of primitive reflexes, increasing muscle strength, improving exploratory capacity in the open field, decreasing the time in the swing phase during gait, and reducing the expression of TNF in the cerebellum. In females, quercetin had a protective effect by stimulating somatic growth, favoring the regularity of steps during gait, and preventing neuronal loss in the cerebellum of CP animals. This study suggests a greater responsiveness in males compared to females, and indicates a possible protective role of quercetin in both sexes in motor development and neuroinflammation in CP models.

脑瘫（CP）包括一组由胎儿或婴儿脑损伤引起的神经肌肉骨骼疾病。槲皮素在神经系统疾病中具有抗氧化、抗炎和神经保护作用。本研究旨在探讨新生儿期槲皮素对CP大鼠运动发育、神经元丢失和小脑炎症的影响。采用产后缺氧（P0和P1）和后肢感觉运动受限（P2 ~ P28）诱导CP模型。从P2至P22腹腔注射槲皮素（10 mg/kg）。对动物进行体生长分析；反射个体发育;肌肉力量;运动协调;猫步的运动活动和步态；小脑的神经元丢失和炎症。实验CP，不分性别，限制体重增加、体生长、比目鱼肌重量、肌肉力量、运动协调、运动活动和步态发育，并促进小脑神经炎症增加。新生儿槲皮素暴露在雄性CP模型中呈阳性，有利于体重增加，减少原始反射的存在，增加肌肉力量，提高开阔区域的探索能力，减少步态中摇摆阶段的时间，降低小脑中TNF的表达。在雌性CP动物中，槲皮素通过刺激体细胞生长、促进步态的规律性和防止小脑的神经元丢失而具有保护作用。这项研究表明，与女性相比，男性的反应性更强，并表明槲皮素在CP模型的运动发育和神经炎症中可能具有保护作用。

{"title":"Neonatal quercetin exposure reduces motor impairments and cerebellar damage in cerebral palsy rats, with different effects on males and females","authors":"Glayciele Leandro de Albuquerque , Raul Manhães-de-Castro , Isla Ariadny Amaral De Souza Gonzaga Paz , Eulália Rebeca da Silva-Araújo , Henrique José Cavalcanti Bezerra Gouveia , Maria Letícia Farias Tenório , Marcos Antônio da Silva Araújo , Ana Elisa Toscano","doi":"10.1016/j.neuroscience.2026.01.023","DOIUrl":"10.1016/j.neuroscience.2026.01.023","url":null,"abstract":"<div><div>Cerebral palsy (CP) comprises a group of neuromusculoskeletal disorders resulting from fetal or infant brain injury. Quercetin has demonstrated antioxidant, anti-inflammatory and neuroprotective properties in neurological diseases. This study aimed to evaluate the effects of neonatal treatment with quercetin on motor development, neuronal loss, and inflammation in the cerebellum of rats subjected to CP. CP model was induced by postnatal anoxia (P0 and P1) and hindlimbs sensorimotor restriction (P2 to P28). Quercetin (10 mg/kg) was administered intraperitoneally from P2 to P22. Animals were analyzed for somatic growth; reflex ontogenesis; muscle strength; motor coordination; locomotor activity and gait in CatWalk; neuronal loss and inflammation in the cerebellum. Experimental CP, regardless of sex, restricted body weight gain, somatic growth, soleus muscle weight, muscle strength, motor coordination, locomotor activity and gait development, and promoted increased neuroinflammation in the cerebellum. Neonatal quercetin exposure was positive in the model of CP in males, favoring body weight gain, reducing the presence of primitive reflexes, increasing muscle strength, improving exploratory capacity in the open field, decreasing the time in the swing phase during gait, and reducing the expression of TNF in the cerebellum. In females, quercetin had a protective effect by stimulating somatic growth, favoring the regularity of steps during gait, and preventing neuronal loss in the cerebellum of CP animals. This study suggests a greater responsiveness in males compared to females, and indicates a possible protective role of quercetin in both sexes in motor development and neuroinflammation in CP models.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"597 ","pages":"Pages 86-99"},"PeriodicalIF":2.8,"publicationDate":"2026-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146019188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Fiber-type-specific architecture and pathophysiology of the neuromuscular junction 神经肌肉连接处的纤维类型特异性结构和病理生理学。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2026-01-16 DOI: 10.1016/j.neuroscience.2026.01.015

Rizwan Qaisar

The neuromuscular junction (NMJ) is a specialized synapse essential for translating neuronal signals into muscle contraction. This review examines the complex structural, functional, and molecular differences in NMJs that innervate fast- and slow-twitch skeletal muscle fibers. Fast-twitch fibers, optimized for rapid and powerful contractions, possess elaborate NMJs with deep folds, high neurotransmitter turnover, and greater vulnerability to synaptic fatigue and degeneration. In contrast, slow-twitch fiber NMJs exhibit simpler but more stable architectures that support sustained, fatigue-resistant activity.

These differences are not fixed but subject to activity-dependent plasticity and pathological remodeling. Chronic stimulation, injury, and aging influence NMJ morphology, with fast-twitch junctions more prone to degeneration in conditions such as ALS, myasthenia gravis, and diabetic neuropathy. Slow-twitch NMJs often resist early deterioration due to superior trophic support, metabolic stability, and more robust expression of synaptic organizers, such as agrin and PGC-1α.

Several key signaling pathways, including agrin–MuSK–LRP4, Wnt/β-catenin, and neuregulin/ErbB, govern NMJ maintenance with fiber-type-specific nuances. These insights underscore the importance of tailoring therapeutic strategies to the muscle fiber phenotype. Gene therapies, neuromuscular electrical stimulation, and biomaterial scaffolds are emerging as promising modalities for preserving or restoring NMJ integrity, especially in fast-twitch fibers at higher risk of degeneration.

Understanding fiber-type-specific NMJ biology enhances our understanding of motor control, muscle aging, and neuromuscular disease progression, and it opens pathways for precision therapeutics that target vulnerable synapses with structural and functional specificity. This review introduces a novel perspective by emphasizing fiber-type-specific NMJ differences and their implications for targeted therapies.

神经肌肉连接（NMJ）是一种特殊的突触，是将神经元信号转化为肌肉收缩所必需的。本文综述了支配快缩和慢缩骨骼肌纤维的NMJs的复杂结构、功能和分子差异。快速抽搐纤维，优化为快速和强大的收缩，具有复杂的NMJs深褶皱，高神经递质周转率，更容易受到突触疲劳和退化。相比之下，慢肌纤维NMJs表现出更简单但更稳定的结构，支持持续的抗疲劳活动。这些差异不是固定的，而是受活动依赖性可塑性和病理性重塑的影响。慢性刺激、损伤和衰老影响NMJ形态，在ALS、重症肌无力和糖尿病神经病变等情况下，快速抽搐连接更容易发生变性。由于优越的营养支持、代谢稳定性和更强的突触组织者（如agrin和PGC-1α）表达，慢抽搐NMJs通常能够抵抗早期退化。几种关键的信号通路，包括agrin-MuSK-LRP4、Wnt/β-catenin和neuregulin/ErbB，通过纤维类型特异性的细微差别控制NMJ的维持。这些见解强调了针对肌纤维表型定制治疗策略的重要性。基因疗法、神经肌肉电刺激和生物材料支架正在成为保存或恢复NMJ完整性的有希望的方式，特别是在变性风险较高的快肌纤维中。了解纤维类型特异性的NMJ生物学增强了我们对运动控制、肌肉老化和神经肌肉疾病进展的理解，并为针对结构和功能特异性的易损突触的精确治疗开辟了途径。这篇综述通过强调纤维类型特异性NMJ差异及其对靶向治疗的影响，介绍了一个新的观点。

{"title":"Fiber-type-specific architecture and pathophysiology of the neuromuscular junction","authors":"Rizwan Qaisar","doi":"10.1016/j.neuroscience.2026.01.015","DOIUrl":"10.1016/j.neuroscience.2026.01.015","url":null,"abstract":"<div><div>The neuromuscular junction (NMJ) is a specialized synapse essential for translating neuronal signals into muscle contraction. This review examines the complex structural, functional, and molecular differences in NMJs that innervate fast- and slow-twitch skeletal muscle fibers. Fast-twitch fibers, optimized for rapid and powerful contractions, possess elaborate NMJs with deep folds, high neurotransmitter turnover, and greater vulnerability to synaptic fatigue and degeneration. In contrast, slow-twitch fiber NMJs exhibit simpler but more stable architectures that support sustained, fatigue-resistant activity.</div><div>These differences are not fixed but subject to activity-dependent plasticity and pathological remodeling. Chronic stimulation, injury, and aging influence NMJ morphology, with fast-twitch junctions more prone to degeneration in conditions such as ALS, myasthenia gravis, and diabetic neuropathy. Slow-twitch NMJs often resist early deterioration due to superior trophic support, metabolic stability, and more robust expression of synaptic organizers, such as agrin and PGC-1α.</div><div>Several key signaling pathways, including agrin–MuSK–LRP4, Wnt/β-catenin, and neuregulin/ErbB, govern NMJ maintenance with fiber-type-specific nuances. These insights underscore the importance of tailoring therapeutic strategies to the muscle fiber phenotype. Gene therapies, neuromuscular electrical stimulation, and biomaterial scaffolds are emerging as promising modalities for preserving or restoring NMJ integrity, especially in fast-twitch fibers at higher risk of degeneration.</div><div>Understanding fiber-type-specific NMJ biology enhances our understanding of motor control, muscle aging, and neuromuscular disease progression, and it opens pathways for precision therapeutics that target vulnerable synapses with structural and functional specificity. This review introduces a novel perspective by emphasizing fiber-type-specific NMJ differences and their implications for targeted therapies.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"597 ","pages":"Pages 13-26"},"PeriodicalIF":2.8,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145998616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Gray-white matter contrast as an index of neurobiological alterations in anorexia nervosa 灰质对比作为神经性厌食症神经生物学改变的指标。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2026-01-14 DOI: 10.1016/j.neuroscience.2026.01.012

Sanberk Ugur , Christopher R. Madan , Valentina Meregalli , Sofia Gentili , Serena Giovannini , Marco Romanelli , Renzo Manara , Angela Favaro , Enrico Collantoni

This neuroimaging study sought to characterize differences in cortical gray-white matter contrast (GWC) between individuals with anorexia nervosa (AN) and age-matched healthy controls (HC) and compare these findings with conventional cortical thickness (CT) measures. The study included 58 female participants (29 AN, 29 HC). T1-weighted images were acquired using a 3 T scanner and processed with FreeSurfer. GWC maps were calculated at each cortical vertex. Vertex-wise general linear models assessed group differences in GWC controlling for age only, and controlling for age and vertex-wise CT. A separate model tested CT differences. Models were corrected for multiple comparisons using cluster-wise correction. Spearman correlations related mean GWC in significant clusters to BMI at scan, age at onset, and illness duration. The age-only model revealed two clusters in the left hemisphere with higher GWC in patients with AN, namely the inferior temporal cortex and medial orbitofrontal cortex. No clusters survived in the model controlling for age and CT. The CT analysis revealed no significant group differences. Mean GWC in clusters did not correlate with clinical severity indices in AN. Patients with AN exhibit focal increases in GWC despite the absence of detectable cortical thinning, suggesting that the GWC can provide complementary information in understanding the neurobiology of AN. The elimination of GWC differences when adjusting for CT likely reflects shared variance rather than true absence of effect. Lack of correlations with clinical indices may be due to limited sample size. Future longitudinal and multimodal studies are warranted to determine the underpinnings of GWC alterations.

本神经影像学研究旨在描述神经性厌食症（AN）患者和年龄匹配的健康对照（HC）之间皮层灰质对比（GWC）的差异，并将这些结果与常规皮层厚度（CT）测量结果进行比较。该研究包括58名女性参与者（29名男性，29名男性）。使用3 T扫描仪获取t1加权图像，并使用FreeSurfer进行处理。在每个皮质顶点处计算GWC图。顶点方向的一般线性模型评估了仅控制年龄的GWC和控制年龄和顶点方向CT的组间差异。一个单独的模型测试CT差异。使用聚类校正对模型进行多次比较校正。Spearman相关性与扫描时BMI、发病年龄和病程相关。仅年龄模型显示，AN患者的左半球有两个GWC较高的簇，即下颞叶皮质和内侧眶额皮质。在控制年龄和CT的模型中，没有集群存活。CT分析显示各组间无明显差异。群集的平均GWC与AN的临床严重程度指数无关。尽管没有可检测到的皮质变薄，但AN患者的GWC表现出局灶性增加，这表明GWC可以为理解AN的神经生物学提供补充信息。当调整CT时，GWC差异的消除可能反映了共同的方差，而不是真正的没有影响。与临床指标缺乏相关性可能是由于样本量有限。未来的纵向和多模态研究有必要确定GWC变化的基础。

{"title":"Gray-white matter contrast as an index of neurobiological alterations in anorexia nervosa","authors":"Sanberk Ugur , Christopher R. Madan , Valentina Meregalli , Sofia Gentili , Serena Giovannini , Marco Romanelli , Renzo Manara , Angela Favaro , Enrico Collantoni","doi":"10.1016/j.neuroscience.2026.01.012","DOIUrl":"10.1016/j.neuroscience.2026.01.012","url":null,"abstract":"<div><div>This neuroimaging study sought to characterize differences in cortical gray-white matter contrast (GWC) between individuals with anorexia nervosa (AN) and age-matched healthy controls (HC) and compare these findings with conventional cortical thickness (CT) measures. The study included 58 female participants (29 AN, 29 HC). T1-weighted images were acquired using a 3 T scanner and processed with FreeSurfer. GWC maps were calculated at each cortical vertex. Vertex-wise general linear models assessed group differences in GWC controlling for age only, and controlling for age and vertex-wise CT. A separate model tested CT differences. Models were corrected for multiple comparisons using cluster-wise correction. Spearman correlations related mean GWC in significant clusters to BMI at scan, age at onset, and illness duration. The age-only model revealed two clusters in the left hemisphere with higher GWC in patients with AN, namely the inferior temporal cortex and medial orbitofrontal cortex. No clusters survived in the model controlling for age and CT. The CT analysis revealed no significant group differences. Mean GWC in clusters did not correlate with clinical severity indices in AN. Patients with AN exhibit focal increases in GWC despite the absence of detectable cortical thinning, suggesting that the GWC can provide complementary information in understanding the neurobiology of AN. The elimination of GWC differences when adjusting for CT likely reflects shared variance rather than true absence of effect. Lack of correlations with clinical indices may be due to limited sample size. Future longitudinal and multimodal studies are warranted to determine the underpinnings of GWC alterations.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"596 ","pages":"Pages 68-74"},"PeriodicalIF":2.8,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145990135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Differential modulation of cognitive control by approach and avoidance motivation. 接近动机和回避动机对认知控制的差异调节。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2026-01-14 DOI: 10.1016/j.neuroscience.2026.01.006

Yan Fei Ma, Rong Cao, Jian Wang, Song Xue

The trade-off between proactive and reactive cognitive control refers to the dynamic regulation process by which individuals flexibly allocate cognitive resources according to task demands-representing a core feature of cognitive control flexibility. Previous research has shown that emotion can significantly affect this trade-off, but most studies have focused on emotional valence and arousal, lacking a systematic investigation into how emotional motivation influences the trade-off in cognitive control. Using the AX-Continuous Performance Task paradigm, the present study systematically examined the mechanisms by which different emotional motivations impact the trade-off between proactive and reactive control. Results showed that proactive control increased under both approach and avoidance motivation, as indicated by higher Proactive Control Index scores and larger CNV amplitudes than baseline. In contrast, reactive control improved only under avoidance motivation: behaviorally, avoidance enhanced BX performance, and electrophysiologically it produced a larger P3a amplitude than both approach and baseline. Approach motivation did not produce a reliable change in reactive control. These findings suggest that approach and avoidance motivation differentially modulate proactive and reactive control, thereby influencing the dynamic trade-off between cognitive control modes and revealing a regulatory process through which emotion may shape cognitive control strategy selection.

主动认知控制与被动认知控制的权衡是指个体根据任务需求灵活分配认知资源的动态调节过程，是认知控制灵活性的核心特征。先前的研究表明，情绪可以显著影响这种权衡，但大多数研究都集中在情绪效价和情绪唤醒上，缺乏对情绪动机如何影响认知控制中的权衡的系统研究。本研究采用ax -连续绩效任务范式，系统考察了不同情绪动机影响主动控制与反应控制取舍的机制。结果表明，在接近和回避动机下，主动控制指数得分和CNV振幅均高于基线。相比之下，反应性控制仅在回避动机下得到改善：行为上，回避增强了BX表现，电生理上，它比接近和基线产生更大的P3a振幅。接近动机并没有在反应性控制中产生可靠的改变。研究结果表明，趋近动机和回避动机对主动控制和反应控制的调节存在差异，从而影响认知控制模式之间的动态权衡，揭示了情绪影响认知控制策略选择的调节过程。

{"title":"Differential modulation of cognitive control by approach and avoidance motivation.","authors":"Yan Fei Ma, Rong Cao, Jian Wang, Song Xue","doi":"10.1016/j.neuroscience.2026.01.006","DOIUrl":"10.1016/j.neuroscience.2026.01.006","url":null,"abstract":"<p><p>The trade-off between proactive and reactive cognitive control refers to the dynamic regulation process by which individuals flexibly allocate cognitive resources according to task demands-representing a core feature of cognitive control flexibility. Previous research has shown that emotion can significantly affect this trade-off, but most studies have focused on emotional valence and arousal, lacking a systematic investigation into how emotional motivation influences the trade-off in cognitive control. Using the AX-Continuous Performance Task paradigm, the present study systematically examined the mechanisms by which different emotional motivations impact the trade-off between proactive and reactive control. Results showed that proactive control increased under both approach and avoidance motivation, as indicated by higher Proactive Control Index scores and larger CNV amplitudes than baseline. In contrast, reactive control improved only under avoidance motivation: behaviorally, avoidance enhanced BX performance, and electrophysiologically it produced a larger P3a amplitude than both approach and baseline. Approach motivation did not produce a reliable change in reactive control. These findings suggest that approach and avoidance motivation differentially modulate proactive and reactive control, thereby influencing the dynamic trade-off between cognitive control modes and revealing a regulatory process through which emotion may shape cognitive control strategy selection.</p>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":" ","pages":"29-37"},"PeriodicalIF":2.8,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145990197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Alterations of brain activity in noise-exposed rats after transcutaneous auricular vagus nerve stimulation evaluated via fMRI fMRI评估噪声暴露大鼠经皮耳迷走神经刺激后脑活动的变化。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2026-01-14 DOI: 10.1016/j.neuroscience.2026.01.014

Nian Li , Liqin Zhang , Xu Tian , Yang Zhao , Guodong Feng , Zhiqiang Gao

This study aims to explore the role of the central nervous system network outside the auditory system in the development process of noise − induced central injury. A noise-exposed rat model was established with unilateral narrow-band noise. Auditory brainstem response (ABR) measured hearing thresholds at Click and 8, 16, 24, 32 kHz pre- and post-noise exposure. Experimental rats were split into transcutaneous auricular vagus nerve stimulation (ta-VNS) and sham subgroups for 2-week intervention. Resting-state fMRI (rs-fMRI) was performed on all groups (ta-VNS, sham, control) post-noise exposure and 2 weeks post-intervention. After noise exposure, 22 rats had elevated hearing thresholds at 8, 24, 32 kHz. fMRI revealed increased ALFF/ReHo in the entorhinal cortex, amygdalar cortex, and hippocampus, decreased values in the prelimbic cortex, basal forebrain, striatum, and cingulate cortex, and enhanced cingulate cortex-basal forebrain functional connectivity. The rats were divided into ta-VNS (n = 10) and sham (n = 12) subgroups for 2-week intervention. Compared with the control group (n = 9), both subgroups showed similar brain activation/inhibition in regions like the entorhinal cortex pre- vs. post-intervention. However, the ta-VNS group reversed noise-induced reduced neural activity in the prelimbic cortex and basal forebrain, and significantly enhanced their functional connectivity. Noise exposure increased entorhinal cortex, hippocampus, and amygdala activity in rats, potentially linked to aversive emotions and abnormal auditory memory. The prelimbic cortex-centered network may gate noise-induced aversive perception, with cingulate cortex activity/connectivity disrupted. ta-VNS may alleviate such perception by reversing reduced neural activity in gating-related regions and enhancing their connectivity, plus strengthening brainstem-limbic and brainstem-cerebellum functional links.

本研究旨在探讨听觉系统外的中枢神经系统网络在噪声性中枢损伤发生发展过程中的作用。采用单侧窄带噪声建立噪声暴露大鼠模型。听觉脑干反应（ABR）测量了噪声暴露前后在咔哒声和8、16、24、32 kHz时的听力阈值。实验大鼠分为经皮耳迷走神经刺激组（ta-VNS）和假手术组，干预2周。在噪声暴露后和干预后2 周，对各组（ta-VNS、假手术、对照组）进行静息状态功能磁共振成像（rs-fMRI）检查。噪声暴露后，22只大鼠在8、24、32 kHz时听力阈值升高。fMRI显示ALFF/ReHo在内嗅皮质、杏仁核皮质和海马中升高，在前边缘皮质、基底前脑、纹状体和扣带皮质中降低，扣带皮质-基底前脑功能连通性增强。将大鼠分为ta-VNS组（n = 10）和sham组（n = 12），干预2周。与对照组相比（n = 9），两个亚组在干预前后的内嗅皮质等区域表现出相似的大脑激活/抑制。然而，ta-VNS组逆转了噪声引起的边缘皮层和基底前脑神经活动的减少，并显著增强了它们的功能连通性。噪音暴露增加了大鼠的内嗅皮层、海马体和杏仁核的活动，这可能与厌恶情绪和异常的听觉记忆有关。以边缘皮层为中心的网络可能会抑制噪声诱导的厌恶感知，导致扣带皮层活动/连接中断。ta-VNS可能通过逆转门控相关区域减少的神经活动，增强它们的连通性，以及加强脑干-边缘和脑干-小脑的功能联系来减轻这种感觉。

{"title":"Alterations of brain activity in noise-exposed rats after transcutaneous auricular vagus nerve stimulation evaluated via fMRI","authors":"Nian Li , Liqin Zhang , Xu Tian , Yang Zhao , Guodong Feng , Zhiqiang Gao","doi":"10.1016/j.neuroscience.2026.01.014","DOIUrl":"10.1016/j.neuroscience.2026.01.014","url":null,"abstract":"<div><div>This study aims to explore the role of the central nervous system network outside the auditory system in the development process of noise − induced central injury. A noise-exposed rat model was established with unilateral narrow-band noise. Auditory brainstem response (ABR) measured hearing thresholds at Click and 8, 16, 24, 32 kHz pre- and post-noise exposure. Experimental rats were split into transcutaneous auricular vagus nerve stimulation (ta-VNS) and sham subgroups for 2-week intervention. Resting-state fMRI (rs-fMRI) was performed on all groups (ta-VNS, sham, control) post-noise exposure and 2 weeks post-intervention. After noise exposure, 22 rats had elevated hearing thresholds at 8, 24, 32 kHz. fMRI revealed increased ALFF/ReHo in the entorhinal cortex, amygdalar cortex, and hippocampus, decreased values in the prelimbic cortex, basal forebrain, striatum, and cingulate cortex, and enhanced cingulate cortex-basal forebrain functional connectivity. The rats were divided into ta-VNS (n = 10) and sham (n = 12) subgroups for 2-week intervention. Compared with the control group (n = 9), both subgroups showed similar brain activation/inhibition in regions like the entorhinal cortex pre- vs. post-intervention. However, the ta-VNS group reversed noise-induced reduced neural activity in the prelimbic cortex and basal forebrain, and significantly enhanced their functional connectivity. Noise exposure increased entorhinal cortex, hippocampus, and amygdala activity in rats, potentially linked to aversive emotions and abnormal auditory memory. The prelimbic cortex-centered network may gate noise-induced aversive perception, with cingulate cortex activity/connectivity disrupted. ta-VNS may alleviate such perception by reversing reduced neural activity in gating-related regions and enhancing their connectivity, plus strengthening brainstem-limbic and brainstem-cerebellum functional links.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"596 ","pages":"Pages 54-67"},"PeriodicalIF":2.8,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145990137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Omega-3 supplementation prevents functional and neural respiratory damage present in an animal model of Parkinson’s disease 补充Omega-3可预防帕金森病动物模型中出现的功能和神经呼吸损伤。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2026-01-14 DOI: 10.1016/j.neuroscience.2026.01.016

Taina O. Macedo , Lais M. Cabral , Nicole C. Miranda , Fulvio A. Scorza , Thiago S. Moreira , Ana C. Takakura

Parkinson’s Disease (PD) is a neurodegenerative disorder primarily characterized by the progressive loss of dopaminergic neurons in the substantia nigra, leading to classical motor symptoms such as tremors, rigidity, and bradykinesia. In later stages, patients frequently develop non-classical symptoms, including respiratory dysfunctions, which may result from neurodegeneration in brainstem regions involved in respiratory control, such as the pre-Bötzinger Complex (preBötC) and the retrotrapezoid nucleus (RTN). These changes are likely driven by oxidative stress and neuroinflammation.

Given the antioxidant and anti-inflammatory properties of omega-3 polyunsaturated fatty acids, this study investigated whether omega-3 supplementation could prevent respiratory-related neuroanatomical and respiratory dysfunctional alterations in a mouse model of PD induced by bilateral injection of 6-hydroxydopamine into the striatum. Omega-3 supplementation prevented respiratory dysfunction by preventing neuronal loss in the preBötC and RTN, reducing glial reactivity and oxidative stress, and maintaining respiratory frequency. These findings support the therapeutic potential of omega-3 in mitigating respiratory dysfunction in PD.

帕金森病（PD）是一种神经退行性疾病，其主要特征是黑质中多巴胺能神经元的进行性丧失，导致典型的运动症状，如震颤、僵硬和运动迟缓。在晚期，患者经常出现非典型症状，包括呼吸功能障碍，这可能是由参与呼吸控制的脑干区域神经退行性变引起的，如pre-Bötzinger复合体（preBötC）和后梯形核（RTN）。这些变化可能是由氧化应激和神经炎症引起的。鉴于omega-3多不饱和脂肪酸的抗氧化和抗炎特性，本研究探讨了omega-3补充剂是否可以预防双侧纹状体注射6-羟多巴胺诱导的PD小鼠模型呼吸相关神经解剖学和呼吸功能障碍的改变。Omega-3补充剂通过防止preBötC和RTN中的神经元丢失，降低神经胶质反应性和氧化应激，以及维持呼吸频率来预防呼吸功能障碍。这些发现支持omega-3在缓解PD患者呼吸功能障碍方面的治疗潜力。

{"title":"Omega-3 supplementation prevents functional and neural respiratory damage present in an animal model of Parkinson’s disease","authors":"Taina O. Macedo , Lais M. Cabral , Nicole C. Miranda , Fulvio A. Scorza , Thiago S. Moreira , Ana C. Takakura","doi":"10.1016/j.neuroscience.2026.01.016","DOIUrl":"10.1016/j.neuroscience.2026.01.016","url":null,"abstract":"<div><div>Parkinson’s Disease (PD) is a neurodegenerative disorder primarily characterized by the progressive loss of dopaminergic neurons in the substantia nigra, leading to classical motor symptoms such as tremors, rigidity, and bradykinesia. In later stages, patients frequently develop non-classical symptoms, including respiratory dysfunctions, which may result from neurodegeneration in brainstem regions involved in respiratory control, such as the pre-Bötzinger Complex (preBötC) and the retrotrapezoid nucleus (RTN). These changes are likely driven by oxidative stress and neuroinflammation.</div><div>Given the antioxidant and anti-inflammatory properties of omega-3 polyunsaturated fatty acids, this study investigated whether omega-3 supplementation could prevent respiratory-related neuroanatomical and respiratory dysfunctional alterations in a mouse model of PD induced by bilateral injection of 6-hydroxydopamine into the striatum. Omega-3 supplementation prevented respiratory dysfunction by preventing neuronal loss in the preBötC and RTN, reducing glial reactivity and oxidative stress, and maintaining respiratory frequency. These findings support the therapeutic potential of omega-3 in mitigating respiratory dysfunction in PD.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"596 ","pages":"Pages 115-127"},"PeriodicalIF":2.8,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145990215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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