Neuroscience最新文献_第10页

Formononetin attenuates LPS-induced neuroinflammation and depressive-like behaviors by regulating the Keap1/Nrf2/HO-1 pathway in the hippocampus 刺芒柄花素通过调节海马的Keap1/Nrf2/HO-1通路，减轻lps诱导的神经炎症和抑郁样行为。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2025-12-16 DOI: 10.1016/j.neuroscience.2025.12.037

Siqi Quan , Mengyuan Li , Zhouli Yue , Hui Liu , Shuaijun Peng , Roujia Guo , Xiaoyan Fang , Yucheng Li

Neuroinflammation and oxidative stress are major pathogenic drivers of depression, with the Keap1/Nrf2/HO-1 pathway serving as a key regulator of both processes. Formononetin (FMN) is a naturally occurring isoflavone with anti-inflammatory and antioxidant activities; however, its potential to exert antidepressant effects through activation of this pathway has not been investigated. In this study, lipopolysaccharide (LPS, 1 mg/kg, i.p.) was used to induce neuroinflammation and depressive-like behaviors in mice, and FMN (20 or 40 mg/kg) was administered for seven days prior to LPS challenge. FMN dose-dependently alleviated LPS-induced behavioral deficits, including reduced sucrose preference, decreased locomotor activity, and prolonged immobility in the tail suspension test. Hematoxylin-eosin (HE) and Nissl staining revealed that FMN markedly attenuated LPS-induced hippocampal neuronal damage. FMN also inhibited microglial activation, as evidenced by reduced Iba-1 expression, decreased NF-κB phosphorylation, and downregulation of both mRNA and protein levels of pro-inflammatory cytokines, including IL-1β, TNF-α, and IL-6. Furthermore, LPS-induced lipid peroxidation was significantly attenuated, as indicated by lower levels of 4-hydroxynonenal (4-HNE). Molecular docking suggested a potential direct interaction between FMN and Keap1, while Western blot analysis confirmed that FMN downregulated Keap1 and upregulated Nrf2 and HO-1 protein expression. Collectively, these findings demonstrate that FMN alleviates LPS-induced neuroinflammation and depressive-like behaviors, likely through activating the Keap1/Nrf2/HO-1 pathway, supporting its potential as a preventive candidate for inflammation-associated depression.

神经炎症和氧化应激是抑郁症的主要致病因素，而Keap1/Nrf2/HO-1通路是这两个过程的关键调节因子。芒柄花素（FMN）是一种天然存在的异黄酮，具有抗炎和抗氧化活性；然而，其通过激活该通路发挥抗抑郁作用的潜力尚未被研究。在本研究中，用脂多糖（LPS, 1 mg/kg, i.p.）诱导小鼠神经炎症和抑郁样行为，并在LPS攻击前7天给予FMN（20或40 mg/kg）。FMN剂量依赖性地减轻了lps诱导的行为缺陷，包括降低蔗糖偏好，降低运动活动，延长尾悬试验中的不动时间。苏木精-伊红（HE）和尼氏染色显示FMN明显减轻lps诱导的海马神经元损伤。FMN还能抑制小胶质细胞的激活，这可以通过降低Iba-1的表达、降低NF-κB的磷酸化以及下调IL-1β、TNF-α和IL-6等促炎细胞因子的mRNA和蛋白水平来证明。此外，通过降低4-羟基壬烯醛（4-HNE）水平，lps诱导的脂质过氧化显著减弱。分子对接提示FMN与Keap1之间可能存在直接相互作用，Western blot分析证实FMN下调Keap1，上调Nrf2和HO-1蛋白的表达。总的来说，这些发现表明，FMN可能通过激活Keap1/Nrf2/HO-1通路，减轻了lps诱导的神经炎症和抑郁样行为，支持其作为炎症相关抑郁的预防性候选药物的潜力。

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引用次数: 0

Corrigendum to “A review of the TGF-β1 pathway in Alzheimer’s disease and depression: Possible restoration potential of antidepressants” [Neuroscience 585 (2025) 429–440] “TGF-β1通路在阿尔茨海默病和抑郁症中的回顾：抗抑郁药的可能恢复潜力”[Neuroscience] 585(2025) 429-440]的更正。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2025-12-16 DOI: 10.1016/j.neuroscience.2025.12.006

Eleni Ioannidou , Theofanis Vavilis , Zisis Bourtzos , Eleni Stamoula

引用次数: 0

Breaking boundaries: Dopamine’s role in prediction error, salient novelty, and memory reconsolidation 打破界限：多巴胺在预测错误、显著新奇性和记忆再巩固中的作用。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2025-12-16 DOI: 10.1016/j.neuroscience.2025.12.038

Olivia S. O’Neill, Boyer D. Winters

For memories to remain relevant and adaptive over the lifespan, modifications under specific conditions are required. Memory reconsolidation theory suggests that when a memory is reactivated, it can become labile, a state known as destabilization. This process is regulated by complex and dynamic neurobiological changes representing biological boundary conditions, which likely protect important memories from undergoing unnecessary or potentially maladaptive modifications. External cues, such as prediction error or other forms of salient novel information, can promote destabilization of these resistant memory traces. Accordingly, various neurobiological mechanisms related to the signaling of prediction errors and salient novelty have been implicated in overcoming boundary conditions, permitting memory modification. Here, we review the existing literature regarding the mechanisms for overcoming biological boundary conditions, with specific focus on the role of the neurotransmitter dopamine and its well documented functions related to prediction error, novelty detection, and memory reconsolidation. We aim to describe the nuanced role of dopamine in these processes as it pertains to destabilizing modification-resistant memories, highlight potential interactions with alternate neurotransmitter systems for this process, and bridge findings from reward learning and novelty processing to convey a holistic view of dopamine’s role in memory reconsolidation more broadly.

为了使记忆在整个生命周期中保持相关性和适应性，需要在特定条件下进行修改。记忆再巩固理论认为，当记忆被重新激活时，它会变得不稳定，这种状态被称为不稳定。这一过程受到复杂和动态的神经生物学变化的调节，这些变化代表了生物边界条件，可能保护重要的记忆免受不必要的或潜在的不适应的修改。外部线索，如预测错误或其他形式的显著新信息，可以促进这些抵抗记忆痕迹的不稳定。因此，与预测错误和显著新颖性信号相关的各种神经生物学机制涉及克服边界条件，允许记忆修改。在此，我们回顾了关于克服生物边界条件机制的现有文献，特别关注神经递质多巴胺的作用及其与预测误差、新颖性检测和记忆再巩固相关的功能。我们的目标是描述多巴胺在这些过程中的微妙作用，因为它与不稳定的修改抵抗记忆有关，强调与替代神经递质系统在这一过程中的潜在相互作用，并将奖励学习和新奇处理的发现联系起来，以更广泛地传达多巴胺在记忆再巩固中的作用的整体观点。

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引用次数: 0

The brain signs of wear and tear: Chronic stress associated alpha oscillations in the pregenual anterior cingulate cortex lead to fatigue 大脑磨损的迹象：慢性应激相关的前扣带皮层α振荡导致疲劳。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2025-12-16 DOI: 10.1016/j.neuroscience.2025.12.020

Sven Vanneste , Jan Ost , Dirk De Ridder

Chronic stress or distress exerts profound effects on brain function, particularly in regions involved in emotion regulation and cognitive control. Here, we investigate the relationship between chronic stress, alpha oscillatory activity in the pregenual anterior cingulate cortex (pgACC), and fatigue in a large cohort (n = 589) comprising both healthy individuals and patients with neurological or psychiatric disorders. Using resting-state EEG, we identify a negative correlation between stress-related increases in pgACC alpha oscillations and the severity of fatigue. These findings suggest that chronic stress disrupts normal inhibitory control within the pgACC, potentially leading to heightened energy demands and fatigue. Our results advance the understanding of the neural mechanisms underlying stress-related fatigue and highlight pgACC alpha oscillations as a potential biomarker for assessing chronic stress effects on brain function.

长期的压力或痛苦会对大脑功能产生深远的影响，特别是在涉及情绪调节和认知控制的区域。在这里，我们研究了慢性应激、出生前前扣带皮层(pgACC) α振荡活动和疲劳之间的关系，研究对象包括健康个体和神经或精神疾病患者（n = 589）。通过静息状态脑电图，我们发现压力相关的pgACC α振荡增加与疲劳程度之间存在负相关。这些发现表明，慢性压力破坏了pgACC内正常的抑制控制，可能导致能量需求增加和疲劳。我们的研究结果促进了对应激相关疲劳的神经机制的理解，并强调了pgACC α振荡作为评估慢性应激对脑功能影响的潜在生物标志物。

引用次数: 0

Neuroanatomical-based machine learning prediction of Alzheimer’s Disease across sex and age 基于神经解剖学的机器学习预测阿尔茨海默病的性别和年龄。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2025-12-14 DOI: 10.1016/j.neuroscience.2025.12.030

Bhaavin K. Jogeshwar, Senbao Lu, Benjamin C. Nephew

Alzheimer’s Disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and memory loss. In 2024 it affected approximately 1 in 9 people aged 65 and older in the U.S., 6.9 million individuals. Early detection and accurate AD diagnosis are crucial for improving patient outcomes. Magnetic resonance imaging (MRI) has emerged as a valuable tool for examining brain structure and identifying potential AD biomarkers. This study performs predictive analyses by employing machine learning techniques to identify key brain regions associated with AD using numerical data derived from anatomical MRI scans, going beyond standard statistical methods. Using the Random Forest Algorithm, we achieved 92.87 % accuracy in detecting AD from Mild Cognitive Impairment and Cognitive Normals. Subgroup analyses across nine sex- and age-based cohorts (69–76 years, 77–84 years, and unified 69–84 years) revealed the hippocampus, amygdala, and entorhinal cortex as con– sistent top-rank predictors. These regions showed distinct volume reductions across age and sex groups, reflecting distinct age- and sex-related neuroanatomical patterns. Younger males and females (aged 69–76) exhibited volume decreases in the right hippocampus, suggesting its importance in the early stages of AD. Older males (77–84) showed substantial volume decreases in the left inferior temporal cortex. The left middle temporal cortex showed decreased volume in females, suggesting a potential female-specific influence, while the right entorhinal cortex may have a male-specific impact. These age-specific sex differences could inform clinical research and treatment strategies, aiding in identifying neuroanatomical markers and therapeutic targets for future clinical interventions.

阿尔茨海默病（AD）是一种以认知能力下降和记忆丧失为特征的进行性神经退行性疾病。2024年，在美国65岁及以上的人中，大约有九分之一的人患有此病，共有690万人。早期发现和准确诊断阿尔茨海默病对改善患者预后至关重要。磁共振成像（MRI）已成为检查大脑结构和识别潜在AD生物标志物的有价值的工具。本研究采用机器学习技术进行预测分析，利用解剖学MRI扫描得出的数值数据识别与AD相关的关键大脑区域，超越了标准的统计方法。使用随机森林算法，我们在轻度认知障碍和认知正常人群中检测AD的准确率达到92.87 %。九个基于性别和年龄的队列（69-76 岁，77-84 岁和统一的69-84 岁）的亚组分析显示，海马体，杏仁核和内嗅皮层是一致的顶级预测因子。这些区域在不同的年龄和性别群体中显示出明显的体积减少，反映了不同的年龄和性别相关的神经解剖模式。年轻男性和女性（69-76岁）表现出右侧海马体体积减少，表明其在阿尔茨海默病早期的重要性。老年男性（77-84岁）左侧下颞叶皮层体积明显减少。女性左侧中颞叶皮层体积减小，表明可能有女性特有的影响，而右侧内嗅皮层可能有男性特有的影响。这些年龄特异性的性别差异可以为临床研究和治疗策略提供信息，有助于确定神经解剖学标记和未来临床干预的治疗靶点。

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引用次数: 0

A review of deep learning techniques in Alzheimer’s disease with emphasis on data tools and transfer learning 深度学习技术在阿尔茨海默病中的应用综述，重点是数据工具和迁移学习。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2025-12-14 DOI: 10.1016/j.neuroscience.2025.12.032

Atif Mehmood , Farah Shahid , Rizwan Khan , Hamzah AlZu’bi

Alzheimer’s disease (AD) is a significant neurological condition that is marked by the gradual decline of memory and cognitive function, with a higher incidence observed in older individuals. The mental deterioration associated with this condition is irreversible, resulting in substantial consequences for both affected individuals and society as a whole. Despite relentless research efforts, a definitive cure for AD remains elusive. However, interventions targeting the early stages of the disease have shown promise in slowing its progression. Deep learning-based approaches introduced better results for the early identification of AD stages, which can be curable. Due to less annotated data, those models have many problems regarding model over-fitting and class imbalance issues, directly impacting the model’s performance. Researchers developed transfer learning-based approaches to overcome those issues, which can produce improved results on fewer annotated data samples. The primary motivation behind this article is to provide a review of the article, which is directly based on the transfer learning techniques for classifying AD stages using MRI and PET modalities. This article also provides a complete review of pre-processing tools for data extraction. It discusses the challenges that affect the performance of the models, as well as generalization challenges and biases in transfer learning.

阿尔茨海默病（AD）是一种显著的神经系统疾病，其特征是记忆和认知功能逐渐下降，在老年人中发病率较高。与这种情况有关的精神退化是不可逆转的，对受影响的个人和整个社会都造成严重后果。尽管进行了不懈的研究，但阿尔茨海默病的最终治疗方法仍然难以捉摸。然而，针对该疾病早期阶段的干预措施已显示出减缓其进展的希望。基于深度学习的方法为早期识别AD阶段带来了更好的结果，这是可以治愈的。由于标注数据较少，这些模型存在许多模型过拟合和类不平衡问题，直接影响了模型的性能。研究人员开发了基于迁移学习的方法来克服这些问题，这可以在更少的注释数据样本上产生更好的结果。这篇文章背后的主要动机是对这篇文章进行回顾，这篇文章直接基于使用MRI和PET模式对AD阶段进行分类的迁移学习技术。本文还全面介绍了用于数据提取的预处理工具。它讨论了影响模型性能的挑战，以及迁移学习中的泛化挑战和偏见。

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引用次数: 0

Early postsynaptic potentiation in hippocampal somatostatin interneurons is mTORC1-dependent and disrupted in Fmr1−/y mice 在Fmr1-/y小鼠中，海马生长抑素中间神经元的早期突触后增强依赖于mtorc1并被破坏。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2025-12-14 DOI: 10.1016/j.neuroscience.2025.12.033

Mohammad J. Eslamizade , Fatemeh Saffarzadeh , Argel Aguilar-Valles

The synaptic plasticity in hippocampal pyramidal neurons is expressed without a need for activation of gene transcription and protein synthesis during the first hour of induction. The mammalian/mechanistic target of rapamycin complex 1 (mTORC1) regulates gene expression at the mRNA translation level and is required for the development of several forms of long-lasting hippocampal synaptic plasticity. However, it is unknown whether this temporal pattern is also present in other cell types, such as interneurons. We stimulated the Oriens-Alveus border to induce synaptic potentiation (SP) in somatostatin-expressing interneurons (SOM-INs). Pre-incubating slices with rapamycin prevented the development of SP during 40 min post-stimulation. To determine the specific role of mTORC1 in SOM-INs, we used a conditional SOM-Raptor^−/− (cKO) mouse line and found that early SP did not develop in SOM-Raptor cKO mice. Moreover, we used Fmr1^−/y mice, an animal model of Fragile X syndrome in which dysregulation of mTOR-dependent signaling pathway is a hallmark of its pathophysiology. Interestingly, SP did not develop in SOM-INs of Fmr1^−/y mice either. We also found a reduction of excitatory synaptic currents in these interneurons in Fmr1^−/y mice, while their membrane intrinsic excitability is comparable to that of wild-type mice. Taken together, we found that the earliest minutes of developing synaptic plasticity in SOM-INs are mTORC1-dependent. Furthermore, we found that this synaptic plasticity is lost in SOM-INs in Fmr1^−/y mice. In sum, the definition of early-phase synaptic plasticity based on its dependency on mTORC1 and its impact on autism pathophysiology should be considered in a synapse-type-specific manner.

海马锥体神经元的突触可塑性在诱导的第一个小时内不需要激活基因转录和蛋白质合成。雷帕霉素复合体1 （mTORC1）的哺乳动物/机制靶点在mRNA翻译水平调控基因表达，是几种形式的海马突触持久可塑性发展所必需的。然而，目前尚不清楚这种时间模式是否也存在于其他类型的细胞中，如中间神经元。我们刺激了东侧-肺泡边界，在表达生长抑素的中间神经元（SOM-INs）中诱导突触增强（SP）。在刺激后40 min，用雷帕霉素预孵育切片可阻止SP的发展。为了确定mTORC1在SOM-INs中的具体作用，我们使用了条件型SOM-Raptor-/- (cKO)小鼠系，发现早期SP在SOM-Raptor cKO小鼠中没有发生。此外，我们使用了Fmr1-/y小鼠，这是一种脆性 X 综合征的动物模型，其中mtor依赖的信号通路失调是其病理生理的标志。有趣的是，SP在Fmr1-/y小鼠的SOM-INs中也没有发生。我们还发现Fmr1-/y小鼠中这些中间神经元的兴奋性突触电流减少，而它们的膜固有兴奋性与野生型小鼠相当。综上所述，我们发现SOM-INs中突触可塑性发展的最早几分钟依赖于mtorc1。此外，我们发现Fmr1-/y小鼠的SOM-INs失去了这种突触可塑性。总之，基于mTORC1依赖性的早期突触可塑性的定义及其对自闭症病理生理的影响应以突触类型特异性的方式考虑。

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引用次数: 0

Super-resolution localization microscopy visualizes ischemia-related cytoskeletal and vascular alterations at the nanoscale level in a mouse model of stroke 超分辨率定位显微镜在纳米水平上观察脑卒中小鼠模型中与缺血相关的细胞骨骼和血管改变。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2025-12-14 DOI: 10.1016/j.neuroscience.2025.12.027

Achmed Mrestani , Corinna Höfling , Dominik Michalski

Ischemic stroke results in acute and long-lasting brain damage with consecutive neuronal death. Advancements in visualizing ischemia-related structural alterations at the cellular level are crucial for understanding pathophysiological processes in more detail. Considering the already established concept of the neurovascular unit, both neuronal components and the vasculature are of particular interest. This study combined conventional fluorescence and super-resolution localization microscopy, specifically direct stochastic optical reconstruction microscopy (dSTORM), to visualize cell-stabilizing neuronal and vascular elements in the setting of stroke. For this approach, neurofilament light chain (NFL), microtubule-associated protein 2 (MAP2), and collagen IV (CollIV) were detected in non-altered and ischemic brain regions of mice following 24 h of focal cerebral ischemia. Super-resolution localization microscopy enabled the visualization of the cytoskeletal elements NFL and MAP2 as filamentous structures with varying diameters and CollIV associated with the vessel wall. Due to ischemia, gradually enlarged filament diameters and higher molecular densities were observed for NFL, while the number of localizations was largely reduced for MAP2 and gradually increased for CollIV. Although these observations do not allow for conclusions regarding the functional characteristics of targeted structures, ischemia-related structural alterations at the nanoscale, i.e., the molecular level, became visible by dSTORM. Super-resolution localization microscopy thus appears to be a valuable method for investigating the ischemic consequences on cytoskeletal elements and the vasculature. The emerging insights could help elucidate the mechanisms underlying stroke-related tissue damage in more detail and identify novel neuroprotective targets.

缺血性中风导致急性和持久的脑损伤，并伴有连续的神经元死亡。在细胞水平上可视化缺血相关结构改变的进展对于更详细地理解病理生理过程至关重要。考虑到已经建立的神经血管单位的概念，神经元成分和脉管系统都是特别感兴趣的。这项研究结合了传统的荧光和超分辨率定位显微镜，特别是直接随机光学重建显微镜（dSTORM），在中风的背景下观察细胞稳定的神经元和血管成分。该方法在小鼠局灶性脑缺血24 h后，在未改变和缺血脑区检测神经丝轻链（NFL）、微管相关蛋白2 （MAP2）和胶原IV （CollIV）。超分辨率定位显微镜能够将细胞骨架元件NFL和MAP2可视化为不同直径的丝状结构，而CollIV与血管壁相关。由于缺血，NFL的纤维直径逐渐增大，分子密度逐渐升高，而MAP2的定位数量大量减少，CollIV的定位数量逐渐增加。虽然这些观察结果不能得出关于目标结构的功能特征的结论，但在纳米尺度上，即分子水平上，缺血相关的结构改变可以通过dSTORM看到。因此，超分辨率定位显微镜似乎是一种有价值的方法来研究缺血对细胞骨架元件和脉管系统的影响。这些新发现有助于更详细地阐明中风相关组织损伤的机制，并确定新的神经保护靶点。

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引用次数: 0

Monoacylglycerol lipase inhibition improves motor function and reduces oxidative stress in hemiparkinsonian mice 单酰基甘油脂肪酶抑制可改善半帕金森小鼠的运动功能并减少氧化应激

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2025-12-13 DOI: 10.1016/j.neuroscience.2025.12.025

Delia Maciel Mendoza-Camacho , Juan Manuel Viveros-Paredes , Mario Eduardo Flores-Soto , Alma Hortensia Martínez-Preciado , Aldo Rafael Tejeda-Martínez

Parkinson’s Disease (PD) is characterized by motor symptoms, loss of dopaminergic neurons, and oxidative stress in the Substantia Nigra pars compacta (SNpc) and striatum of patients, as well as in models of parkinsonism. Recent studies show that the endocannabinoid system present in the basal ganglia has a strong influence on the progression of PD, with the inhibition of the enzyme Monoacylglycerol Lipase (MAGL) being a promising therapeutic strategy. Therefore, the aim of this study was to evaluate the effect of MAGL inhibition on locomotion and oxidative stress in a murine model of hemiparkinsonism. For this study, male C57BL/6J mice were divided into four groups: 1) Control group, 2) 6-OHDA group, which received the hemiparkinsonism model, 3) JZL184 group, which received a dose of 8 mg/kg/day for 7 days of the JZL184 inhibitor, and 4) 6-OHDA + JZL184 group, which had the hemiparkinsonism model and, 14 days later, began administration with JZL184. It was found that the hemiparkinsonism mice showed significant improvements both in locomotor performance and in levels of lipoperoxidation, total antioxidant capacity, superoxide dismutase activity, and in quantity and activity of mitochondrial complex I, once the MAGL inhibitor was administered to this group. Treatment with the JZL184 inhibitor demonstrated improved locomotor ability and reduced oxidative stress levels in the SNpc and striatum of mice with hemiparkinsonism. This suggests that MAGL inhibition could be a therapeutic alternative for PD in the future.

帕金森病（PD）的特征是运动症状，多巴胺能神经元的丧失，以及患者和帕金森模型中黑质致密部（SNpc）和纹状体的氧化应激。最近的研究表明，存在于基底节区的内源性大麻素系统对PD的进展有很强的影响，抑制单酰基甘油脂肪酶（MAGL）是一种很有前途的治疗策略。因此，本研究的目的是评估MAGL抑制对半帕金森模型小鼠运动和氧化应激的影响。本研究将雄性C57BL/6J小鼠分为四组：1)对照组，2)6-OHDA组，给予半帕金森病模型，3)JZL184组，给予JZL184抑制剂8 mg/kg/d，连续7天，4)6-OHDA + JZL184组，建立半帕金森病模型，14天后开始给药。研究发现，给半帕金森小鼠注射MAGL抑制剂后，其运动能力、脂质过氧化水平、总抗氧化能力、超氧化物歧化酶活性以及线粒体复合体I的数量和活性均有显著改善。JZL184抑制剂改善了半帕金森小鼠SNpc和纹状体的运动能力，降低了氧化应激水平。这表明MAGL抑制可能是未来PD的一种治疗选择。

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引用次数: 0

Temporal interference non-invasive deep brainstimulation: bibliometric, clinical translation and potential for neurorestoratology 时间干扰非侵入性脑深部刺激：文献计量学、临床翻译和神经修复学潜力。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2025-12-13 DOI: 10.1016/j.neuroscience.2025.12.031

Zhanxiang Lin , Weixian Zeng , Weili Zhu , Cheng Tan , Zicai Liu

Background and objectives

Temporal interference stimulation (TIS) is a novel, non-invasive neuromodulation technique that effectively overcomes the depth and electric field dispersion issues of conventional transcranial electrical stimulation. TIS holds promise for achieving greater functional recovery than current neural repair methods. This study aims to assess the current status, trends, and hotspots in TIS development, review its evolution, explore its advanced applications in neurorestoratology, and provide theoretical and practical guidance for its future advancement.

Materials and methods

A literature search was performed using the Web of Science database to identify TIS-related studies, and CiteSpace and VOSviewer were used for analysis and visualization. Additionally, PubMed databases were searched with subject terms and keywords to explore the development, evolution, and application of TIS technology in neurorestoratology.

Results and conclusions

A total of 127 relevant publications were included in the bibliometric analysis. Since the TIS technique was introduced in 2017, the number of related studies has grown annually. The United States and China lead in TIS research output. “Deep brain stimulation” is the most common keyword, highlighting the technique’s objectives and potential. The review results indicate that TIS is a safe and effective non-invasive deep brain stimulation method. Although the technology is still in the stages of computer simulations, animal studies, and small human trials, TIS is poised to become a promising tool for neurorestoratology, as the body of literature has expanded over the past 9 years.

背景和目的：时间干扰电刺激（TIES）是一种新型的、无创的神经调节技术，它有效地克服了传统经颅电刺激的深度和电场分散问题。与目前的神经修复方法相比，TIES有望实现更大的功能恢复。本研究旨在评估TIES的发展现状、趋势和热点，回顾其发展历程，探索其在神经修复学中的先进应用，为其未来的发展提供理论和实践指导。材料和方法：使用Web of Science数据库检索相关文献，使用CiteSpace和VOSviewer进行分析和可视化。此外，检索PubMed和CNKI数据库，检索主题词和关键词，探讨TIES技术在神经修复学中的发展、演变和应用。结果与结论：文献计量学分析共纳入87篇相关文献。自2017年引入TIES技术以来，相关研究数量每年都在增加。美国和中国在TIES研究产出方面处于领先地位。“深部脑刺激”是最常见的关键词，突出了这项技术的目标和潜力。综述结果表明，TIES是一种安全有效的无创脑深部电刺激方法。虽然这项技术仍处于计算机模拟、动物研究和小型人体试验阶段，但随着过去9 年文献的不断扩展，TIES有望成为一种有前途的神经康复工具。

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引用次数: 0