Neuroscience最新文献_第9页

Misfolding protein pathology detected in a chronic mouse model of multiple sclerosis 多发性硬化症慢性小鼠模型中错误折叠蛋白的病理检测。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2026-02-16 Epub Date: 2025-12-25 DOI: 10.1016/j.neuroscience.2025.12.063

Tatiana P. MacKeigan , Megan L. Morgan , Sierra Mitchell, Peter K. Stys

Multiple sclerosis (MS) is one of the most common causes of neurological disability in young adults. The pathobiology of MS includes both autoimmune inflammation and underlying degeneration, with the current challenge being to better understand and treat MS progression. The cuprizone (CPZ) mouse model is commonly used to study de- and remyelination. Despite initial robust myelin repair after toxin withdrawal, mice display progressive callosal atrophy, myelin loss, and gliosis. We tested the hypothesis that this delayed demyelination is due to a progressive degenerative proteopathy. Male C57BL/6 mouse brain sections harvested 8 months after a demyelinating CPZ insult followed by repair were positive for anti-oligomer and anti-fibril epitopes using the antibodies A11 and LOC (p < 0.05 and p < 0.001, respectively). Tissues were also stained with the fluorescent amyloid probes Thioflavin-S (ThS) or pFTAA. Quantitative spectral analysis of the corpus callosum (CC) indicated a subtle but widespread accumulation of ß-sheet-rich material (p < 0.001 and p < 0.0001, respectively). Taken together, our results are consistent with deposition of misfolded proteins facilitating chronic degeneration of axons and myelin in the post-CPZ CC leading to a progressive MS-like pathology. This “late post-CPZ” model could shed light on mechanisms of progressive late degeneration in the MS brain and represents a new animal model of progressive MS, allowing development of novel therapies for this phase of the disease. Our data also raise the possibility that the underlying cytodegenerative component of MS may be driven by subtle toxic amyloid accumulation as in many other traditional neurodegenerative disorders.

多发性硬化症（MS）是年轻人神经功能障碍的最常见原因之一。MS的病理生物学包括自身免疫性炎症和潜在的变性，目前的挑战是更好地理解和治疗MS的进展。铜酮（CPZ）小鼠模型通常用于研究脱髓鞘和髓鞘再生。尽管毒素戒断后最初髓磷脂修复强劲，但小鼠表现出进行性胼胝体萎缩，髓磷脂丢失和胶质瘤。我们检验了这种延迟脱髓鞘是由于进行性退行性蛋白质病的假设。雄性C57BL/6小鼠脑切片在脱髓鞘CPZ损伤和修复后8 个月采集，使用抗体A11和LOC抗低聚物和抗纤维表位阳性(p

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引用次数: 0

Reduced EEG complexity in stable coronary artery disease: an evidence of covert brain dysfunction 稳定冠状动脉疾病脑电图复杂性降低：隐性脑功能障碍的证据

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2026-02-16 Epub Date: 2025-12-26 DOI: 10.1016/j.neuroscience.2025.12.061

Bixiu Huo , Bin Wang , Hongxiao Jia

Background

Accumulating evidence indicates that coronary heart disease (CHD) is frequently accompanied by cerebral injury. Non-linear electroencephalogram (EEG) analysis is an effective method for capturing abnormal EEG signal dynamics. This study characterized the complexity of EEG in CHD patients based on non-linear indices.

Methods

Twenty-seven patients with CHD were enrolled, as well as an equal number of non-coronary controls. Five-minute, resting-state EEG recordings were obtained under standardized conditions. Non-linear dynamics were quantified using Lempel–Ziv complexity (LZC), permutation Lempel–Ziv complexity (PLZC), sample entropy (SampEn), and permutation entropy (PE). Between-group differences were assessed by independent-samples t-tests. Within the CHD cohort, Pearson correlations were calculated between each non-linear index and clinical variables—age, disease duration, left-ventricular ejection fraction (LVEF %), and number of affected coronary arteries.

Results

Compared with controls, the CHD cohort exhibited significantly reduced LZC_mean, LZC_midp, SampEn, PLZC, and PE at multiple electrodes distributed across the entire scalp. A representative finding showed that: at electrode T8, LZC_mean was lower in CHD patients than in controls (0.73 ± 0.09 vs 0.79 ± 0.08; t = −2.683, p = 0.010). Age and disease duration were negatively correlated with several non-linear indices; for example, disease duration inversely predicted LZC_midp at FPz (r = −0.573, adjusted p = 0.004). LVEF% was positively associated with selected measures. No significant correlations were found between the number of affected coronary arteries and any EEG complexity metrics.

Conclusion

CHD patients demonstrated significantly lower total spectrum EEG complexity compared to non-CHD controls, offering novel electrophysiological evidence of central nervous system impairment in cardiovascular disease and suggesting potential functional brain alterations.

背景：越来越多的证据表明，冠心病（CHD）经常伴有脑损伤。非线性脑电图分析是捕捉异常脑电图动态信号的有效方法。本研究基于非线性指标表征冠心病患者脑电图的复杂性。方法：纳入27例冠心病患者，以及同等数量的非冠状动脉对照组。在标准化条件下获得5分钟静息状态脑电图记录。采用Lempel-Ziv复杂度（LZC）、置换Lempel-Ziv复杂度（PLZC）、样本熵（SampEn）和置换熵（PE）对非线性动力学进行量化。采用独立样本t检验评估组间差异。在冠心病队列中，计算每个非线性指数与临床变量（年龄、病程、左室射血分数（LVEF %）和受影响冠状动脉数量）之间的Pearson相关性。结果：与对照组相比，冠心病组在分布于整个头皮的多个电极上的LZCmean、LZCmidp、SampEn、PLZC和PE均显著降低。一项具有代表性的研究结果显示：在电极T8，冠心病患者的LZCmean低于对照组（0.73 ± 0.09 vs 0.79 ± 0.08;t = -2.683,p = 0.010）。年龄、病程与多个非线性指标呈负相关；例如，疾病持续时间与LZCmidp在FPz呈负相关（r = -0.573，调整后p = 0.004）。LVEF%与所选措施呈正相关。受影响的冠状动脉数目与脑电图复杂性指标之间无显著相关性。结论：与非冠心病对照组相比，冠心病患者脑电图总谱复杂性明显降低，为心血管疾病中枢神经系统损伤提供了新的电生理证据，提示潜在的脑功能改变。

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引用次数: 0

Comprehensive analysis of spinal cord inflammatory factors in HIV Tat-induced neuropathy in mice HIV - tat诱导小鼠神经病变脊髓炎症因子的综合分析。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2026-02-16 Epub Date: 2026-01-06 DOI: 10.1016/j.neuroscience.2026.01.005

Ahmad Kohsar , Peter Wilson-Braun , Elizabeth N. Bean , Madison Philhower , Benjamin J. Harrison , Ling Cao

Despite advancements in HIV treatment, HIV neuropathy, caused by nerve damage following HIV infection, continues to be a major cause of morbidity. Inflammatory responses both in the central and peripheral nervous systems have been implicated as contributing mechanisms, but the role of the HIV protein Trans-Activator of Transcription (Tat) in HIV neuropathy is not well understood. In this study, we report the development of neuropathy-like behavioral changes in doxycycline-inducible HIV Tat transgenic (iTat) mice using comprehensive behavioral assessments. These changes include increased hind paw mechanical sensory sensitivities in both sexes, and increased cold sensitivity and reduced hind paw grip strength predominantly in females. Hind paw skin intra-epidermal nerve fiber (IENF) density showed a small but significant transient increase in the density of CGRP+ fibers at day 21 post-Tat induction in both sexes, while the recovery was faster in females. As Tat is induced primarily in the central nervous system in iTat mice, we therefore focused on elucidating central mechanisms by performing inflammation-targeted RNA profiling in lumbar spinal cord via NanoString assay followed by bioinformatic analysis to identify signaling pathways that may be responsible for the observed symptomatic changes. Three key signaling pathways − apoptosis, inflammation mediated by chemokine and cytokine, and Toll-like receptor signaling pathways − were identified. Subsequent qRT-PCR assays confirmed Tat-induced changes of selected genes. Altogether, we demonstrated that Tat induction is associated with sex-dependent neuropathy-like changes. The concurrent changes in selected inflammation-related signaling pathways within lumbar spinal cord shed light on potential underlying central mechanisms.

尽管艾滋病毒治疗取得了进展，但由艾滋病毒感染后神经损伤引起的艾滋病毒神经病变仍然是发病率的主要原因。中枢和外周神经系统的炎症反应被认为是促成机制，但HIV蛋白反式转录激活因子（Tat）在HIV神经病变中的作用尚不清楚。在这项研究中，我们使用综合行为评估报告了多西环素诱导的HIV Tat转基因（iTat）小鼠神经病变样行为变化的发展。这些变化包括两性后爪机械感觉敏感性的增加，以及冷敏感性的增加和后爪握力的减少，主要发生在雌性。后爪皮肤表皮内神经纤维（IENF）密度在诱导后第21天两性CGRP+纤维密度均有短暂性的小幅但显著的增加，雌性恢复较快。由于Tat主要在iTat小鼠的中枢神经系统中诱导，因此，我们将重点放在阐明中枢机制上，通过纳米串测定在腰椎脊髓中进行炎症靶向RNA分析，然后进行生物信息学分析，以确定可能导致观察到的症状变化的信号通路。三个关键的信号通路-细胞凋亡，炎症介导的趋化因子和细胞因子，和toll样受体信号通路-确定。随后的qRT-PCR分析证实了tat诱导的选定基因的变化。总之，我们证明了Tat诱导与性别依赖性神经性病变样改变有关。腰椎内炎症相关信号通路的同步变化揭示了潜在的中枢机制。

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引用次数: 0

Persons with cerebral palsy display improved occipital cortical entrainment after gait training 脑瘫患者在步态训练后表现出改善的枕皮质夹带。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2026-02-16 Epub Date: 2025-12-17 DOI: 10.1016/j.neuroscience.2025.12.043

Max J. Kurz , Elizabeth Dao , Morgan T. Busboom , Elizabeth Heinrichs-Graham , Brad Corr , Katie L. Bemis , Logan White , Kimberley S. Scott , Tony W. Wilson

Prior neuroimaging work has shown that people with cerebral palsy (CP) often have visual processing impairments that impact their motor actions. We evaluated if a physical therapy gait training paradigm that incorporated visuomotor tasks has the potential to improve mobility and result in training-related changes in the entrainment of the occipital cortices of people with CP. People with CP (N = 29; Age = 19.9 ± 7.3 years; Gross Motor Classification Score Levels I-III) underwent 24 gait training sessions and completed a comprehensive battery of clinical assessments to quantify their mobility improvements. Magnetoencephalography (MEG) was used to image the cortical activity induced by viewing a 15 Hz flashing stimulus before and after therapy. Neurotypical controls (N = 34; Age = 23.1 ± 3.7 years) were used to gauge the extent of the cortical aberrations and the direction of treatment effects. The group with CP exhibited significantly weaker neural activity in the occipital cortices relative to the neurotypical controls prior to therapy. However, the strength of this event-related synchronization (ERS) increased following therapy. Furthermore, those with a larger change in the strength of the ERS tended to have the greatest improvements in preferred walking speed after therapy. Gait training paradigms that incorporate visuomotor tasks might have the potential to improve mobility, as well as occipital cortical activity in people with CP.

先前的神经影像学研究表明，脑瘫患者通常有影响其运动行为的视觉处理障碍。我们评估了结合视觉运动任务的物理疗法步态训练模式是否有可能改善CP患者的活动能力，并导致枕皮质运动相关的训练变化。CP患者（N = 29；年龄 = 19.9 ± 7.3 岁；大运动分类评分水平I-III）接受了24次步态训练，并完成了一组全面的临床评估，以量化他们的活动能力改善。使用脑磁图（MEG）对治疗前后观看15 Hz闪烁刺激引起的皮质活动进行成像。神经正常对照组（N = 34；年龄 = 23.1 ± 3.7 岁）用于测量皮质畸变的程度和治疗效果的方向。与治疗前的神经正常对照组相比，CP组枕皮质的神经活动明显减弱。然而，这种事件相关同步（ERS）的强度在治疗后增加。此外，ERS强度变化较大的患者在治疗后首选步行速度的改善最大。结合视觉运动任务的步态训练范式可能有潜力改善CP患者的移动性和枕皮质活动。

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引用次数: 0

Spinal dorsal horn GABAergic neuron activation underlies electroacupuncture analgesia in inflammatory pain 脊髓背角gaba能神经元激活是电针镇痛炎症性疼痛的基础。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2026-02-16 Epub Date: 2025-12-24 DOI: 10.1016/j.neuroscience.2025.12.060

Hao Zheng, Xiaoyue Sun, Junkang Chen, Liaoyuxian Deng, Yani Li, Xiaoyu Wang, Yangshuai Su, Xianghong Jing, Zhiyun Zhang

While acupuncture is known to alleviate pain by activating local low-threshold afferents and engaging gate control mechanisms in the spinal cord dorsal horn, the specific role of spinal inhibitory neurons in this process remains unclear. The present study aimed to identify whether A-fiber intensity electroacupuncture (EA) enhances spinal inhibitory tone by recruiting gamma-aminobutyric acidergic (GABAergic) neurons to suppress spinal nociceptive transmission in inflammatory pain. We employed single-fiber recordings on sciatic nerve to determine the A-fiber activation threshold for EA intervention. Behavioral tests confirmed that EA at A-fiber intensity significantly alleviated mechanical hyperalgesia, weight-bearing imbalance, and gait abnormalities in mice with complete Freund’s adjuvant (CFA)-induced inflammatory pain. Transgenic mice with Cre recombinase expression driven by the vesicular GABA transporter promoter (VGAT-Cre) combined with in vivo fiber photometry revealed that this analgesia was associated with enhanced activity of dorsal horn GABAergic neurons. Crucially, chemogenetic activation of GABAergic dorsal horn neurons produced robust analgesic effects, whereas their inhibition increased mechanical sensitivity and enhanced neuronal activation in the superficial laminae of dorsal horn. Furthermore, EA at A-fiber intensity significantly attenuated noxious stimulus-induced neuronal c-Fos expression in the superficial dorsal horn. Notably, optogenetic inhibition of GABAergic neurons reversed EA-induced analgesia. Our results demonstrate that EA at A-fiber intensity alleviates inflammatory pain by recruiting GABAergic neurons in the spinal dorsal horn, thereby enhancing inhibitory tone on spinal nociceptive transmission.

虽然已知针灸通过激活局部低阈值传入神经和参与脊髓背角的门控机制来减轻疼痛，但脊髓抑制神经元在这一过程中的具体作用尚不清楚。本研究旨在确定a纤维强度电针（EA）是否通过募集γ -氨基丁酸能（GABAergic）神经元来抑制炎症性疼痛的脊髓伤害性传递，从而增强脊髓抑制性张力。我们采用坐骨神经单纤维记录来确定EA干预的a -纤维激活阈值。行为学实验证实，a -纤维强度的EA显著缓解了完全性弗氏佐剂（CFA）诱导的炎症性疼痛小鼠的机械性痛觉过敏、负重失衡和步态异常。由囊泡GABA转运子启动子（VGAT-Cre）驱动的Cre重组酶转基因小鼠结合体内纤维光度法显示，这种镇痛与背角GABA能神经元活性增强有关。至关重要的是，对gaba能背角神经元的化学发生操作表明，这些神经元的激活产生镇痛作用，而对它们的抑制增加了机械敏感性以及背角浅层的神经元激活。与此一致的是，a纤维强度的EA显著减弱了有害刺激诱导的浅背角神经元c-Fos的表达。我们的研究结果表明，a纤维强度的EA通过募集脊髓背角的gaba能神经元来减轻炎症性疼痛，从而增强脊髓伤害性传递的抑制性张力。

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引用次数: 0

Reliable and dynamic monitoring changes in cortical excitation and inhibition balance using aperiodic 1/f slope: functions, diseases and drug effects 利用非周期性1/f斜率可靠和动态监测皮层兴奋和抑制平衡的变化：功能、疾病和药物效应。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2026-02-16 Epub Date: 2025-12-20 DOI: 10.1016/j.neuroscience.2025.12.050

Zeyi Wang , Sungchil Yang , Jianping Lu , Qiang Zhou

Understanding the excitation/inhibition (E/I) balance is fundamental to deciphering cortical circuit dynamics, supporting cognition, and elucidating the pathophysiology of brain disorders, yet methods for assessing E/I balance in vivo remain limited. While recent studies have proposed the aperiodic component (1/f slope) of the local field potentials (LFPs) power spectrum as a potential indicator of E/I balance, this hypothesis has lacked systematic, multi-level in vivo validation. Here, we systematically tested the hypothesis that the aperiodic 1/f slope can serve as a reliable proxy for dynamically monitoring change in E/I balance. In freely moving male mice, we first optimized the analytical parameters for the 1/f slope. We then demonstrated that the slope quantitatively tracks shifts in inhibition induced by pharmacological manipulations in a dose-dependent manner, captures the rapid dynamic shift to inhibition induced by cell-type-specific optogenetic manipulation, and shows generality across drugs altering E/I with diverse mechanisms. On an applied level, we show that the 1/f slope tracks performance-related neural dynamics during a working memory task and indicates the direction of E/I balance in mouse models of epilepsy and depression. Collectively, our findings establish the 1/f slope as a reliable, rapid and sensitive proxy for monitoring E/I balance shift, offering a potential, practical tool for monitoring brain dynamics and as a biomarker for translational research.

了解兴奋/抑制（E/I）平衡是解读皮质电路动力学、支持认知和阐明脑疾病病理生理学的基础，但评估体内E/I平衡的方法仍然有限。虽然最近的研究提出了局部场电位（LFPs）功率谱的非周期分量（1/f斜率）作为E/I平衡的潜在指标，但这一假设缺乏系统的、多层次的体内验证。在这里，我们系统地检验了假设，即非周期性的1/f斜率可以作为动态监测E/I平衡变化的可靠代理。在自由运动的雄性小鼠中，我们首先优化了1/f斜率的分析参数。然后，我们证明了斜率以剂量依赖的方式定量跟踪药理学操作诱导的抑制变化，捕获了细胞类型特异性光遗传学操作诱导的抑制的快速动态变化，并显示了药物以不同机制改变E/I的普遍性。在应用层面上，我们发现1/f斜率跟踪工作记忆任务期间与表现相关的神经动力学，并指示癫痫和抑郁小鼠模型中E/I平衡的方向。总的来说，我们的研究结果确立了1/f斜率作为监测E/I平衡转移的可靠、快速和敏感的代理，为监测脑动力学提供了一个潜在的、实用的工具，并作为转化研究的生物标志物。

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引用次数: 0

Modulation of cofilin 1 phosphorylation induces juvenile-like plasticity in the adult mouse visual cortex 调节cofilin 1磷酸化诱导成年小鼠视觉皮层的青少年样可塑性。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2026-02-16 Epub Date: 2026-01-06 DOI: 10.1016/j.neuroscience.2026.01.003

Agustina Dapueto , Emilia Hayek , Alejo Acuña , Bruno Pannunzio , Leonel Gomez , Francesco M. Rossi

Cofilin 1 is an actin-depolymerizing protein that plays a fundamental role in actin dynamics, particularly within dendritic spines, where it has been implicated in both structural and functional plasticity. We recently demonstrated, using a combination of differential proteomics, western blot and immunohistochemistry, that the expression of cofilin 1 and its inactive phosphorylated form is dynamically regulated in the mouse visual cortex. Expression levels change across critical periods of postnatal development and are modulated by visual experience, suggesting that cofilin 1 plays a dynamic role in synaptic remodeling during windows of heightened cortical plasticity.

In this study, we sought to determine whether cofilin 1 influences experience-dependent plasticity in the adult visual cortex, a stage where plasticity is more restricted but still inducible under specific conditions. Specifically, we administered a synthetic peptide inhibitor of cofilin 1 activity in vivo (PCOF). Following monocular deprivation, adult mice received either the PCOF peptide or a control peptide. Structural plasticity was assessed by quantifying dendritic spine density using Golgi-like staining, while visual plasticity was evaluated by measuring visual acuity through the optomotor response test.

Our results show that, in adult mice treated with the PCOF peptide − but not in controls − monocular deprivation led to a significant reduction in dendritic spine density in the contralateral visual cortex, as well as a decrease in visual acuity of the previously deprived eye. These findings indicate that cofilin 1 activity is crucial for the regulation of experience-dependent plasticity in the adult mouse visual cortex.

Cofilin 1是一种肌动蛋白解聚蛋白，在肌动蛋白动力学中起着重要作用，特别是在树突棘中，它与结构和功能可塑性都有关系。我们最近通过结合差异蛋白质组学、western blot和免疫组织化学证明，cofilin 1及其无活性磷酸化形式的表达在小鼠视觉皮层中受到动态调节。在出生后发育的关键时期，cofilin 1的表达水平会发生变化，并受到视觉经验的调节，这表明在皮层可塑性增强的窗口期，cofilin 1在突触重塑中起着动态作用。在本研究中，我们试图确定cofilin 1是否会影响成人视觉皮层的经验依赖性可塑性，在这个阶段，可塑性受到更多限制，但在特定条件下仍可诱导。具体来说，我们在体内使用了合成的cofilin 1活性肽抑制剂（PCOF）。在单眼剥夺后，成年小鼠接受PCOF肽或对照肽。通过高尔基样染色定量树突棘密度评估结构可塑性，通过视动反应测试测量视力评估视觉可塑性。我们的研究结果表明，在接受PCOF肽治疗的成年小鼠（而不是对照组）中，单眼剥夺导致对侧视觉皮层树突棘密度显著降低，同时先前被剥夺的眼睛的视力也有所下降。这些发现表明，cofilin 1的活性对成年小鼠视觉皮层经验依赖性可塑性的调节至关重要。

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引用次数: 0

Alterations of functional connectivity between hyperdirect pathway regions and outside regions in Parkinson’s disease patients with freezing of gait 帕金森病患者步态冻结时超直接通路区域与外部区域功能连通性的改变

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2026-02-16 Epub Date: 2025-12-23 DOI: 10.1016/j.neuroscience.2025.12.058

Yuting Li , Shuwen Bo , Jian-Feng Qu , Xiuhang Ruan , Bin Chen , Mengyan Li , Yujian Zou , Changzheng Shi , Xinhua Wei

Emerging neuroimaging evidence has propelled the formulation of the hypothesis that freezing of gait (FOG) in Parkinson’s disease (PD) arises from dysfunction within the locomotor network. However, to date, there has been a lack of functional connectivity analyses targeting the hyperdirect pathway (HDP) to explore this hypothesis. In this study, we investigate impaired communication within the HDP neural circuitry in FOG patients. Fifty-nine PD patients (33 PD-nFOG and 26 PD-FOG) and thirty matched healthy controls underwent resting-state functional magnetic resonance imaging. Both ROI-wise and voxel-wise based resting-state functional connectivity were calculated in this study. No group differences were observed in the ROI-wise functional connectivity among the regions within the HDP. However, significant reduced functional connectivity based on voxel-wise analysis were observed between the HDP and several brain regions, including the default mode network (DMN), sensorimotor cortex, limbic system and cerebellum in PD, which were associated with psychiatric symptoms, emotional decline, and motor dysfunction. Of note, compared to PD-nFOG, PD-FOG showed increased functional connectivity between the HDP and the cerebellum and the middle occipital gyrus, which was associated with motor impairment in the contralateral limbs. These data extend neuroimaging evidence on that compensatory increased functional connectivity in HDP in FOG patients may indicate a failure compensate for clinical manifestations of limb akinesia, and may represent a loss of low-level automatic control of gait regulation by the basal ganglia.

新出现的神经影像学证据推动了帕金森病（PD）中步态冻结（FOG）由运动网络功能障碍引起的假设的形成。然而，迄今为止，还缺乏针对超直接通路（HDP）的功能连接分析来探索这一假设。在这项研究中，我们研究了FOG患者HDP神经回路中的沟通障碍。59名PD患者（33名PD- nfog和26名PD- fog）和30名匹配的健康对照进行静息状态功能磁共振成像。本研究计算了基于roi和基于体素的静息状态功能连接。在HDP内各区域之间的roi功能连通性方面没有观察到组间差异。然而，基于体素分析，观察到HDP与PD患者的几个脑区（包括默认模式网络（DMN）、感觉运动皮层、边缘系统和小脑）之间的功能连通性显著降低，这些脑区与精神症状、情绪下降和运动功能障碍有关。值得注意的是，与PD-nFOG相比，PD-FOG显示HDP与小脑和枕中回之间的功能连通性增加，这与对侧肢体的运动障碍有关。这些数据扩展了神经影像学证据，证明FOG患者HDP代偿性功能连接增加可能表明肢体运动障碍临床表现的代偿失败，并可能代表基底神经节对步态调节的低水平自动控制的丧失。

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引用次数: 0

EEG theta dynamics for error processing during online movement control 在线运动控制中误差处理的EEG θ动态。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2026-02-16 Epub Date: 2025-12-28 DOI: 10.1016/j.neuroscience.2025.12.065

Sarah Kessouri , Frederic R Danion , Jean-François Lepage , Pierre-Michel Bernier

To ensure optimal visuomotor feedback control during manual tracking, the brain must continuously monitor the error between the hand and the target. Modulations in the theta band (3–8 Hz) are related to error processing, but this has been mainly shown in cognitive control contexts. Hence, their relationship with hand-target errors during online control remains unclear. Here we assessed the impact of motor error processing on EEG theta-band activity in 29 healthy participants while they performed continuous tracking of a moving target with their dominant (right) hand. Two conditions were used to manipulate error processing demands: 1) in the Repeated condition, the same target trajectory was presented 80 times, allowing participants to implicitly learn the pattern and reduce tracking errors; 2) in the Random condition, 80 different trajectories were used, inducing persistent high tracking errors. Behavioral analyses confirmed that tracking errors were significantly higher in the Random than in the Repeated condition. Importantly, EEG theta power was also significantly higher in the Random condition, with a peak difference occurring at electrodes overlaying the left sensorimotor regions. This effect was selective to theta activity, as there was no modulation in alpha- (8–12 Hz) and beta-band (15–30 Hz) activity. Overall, this study extends the role of theta oscillations to online error processing in the context of motor control. It is possible that theta modulations reflected cortical activity mediating the communication and integration of information within sensorimotor circuits including the motor, premotor and parietal cortex, which are known to mediate online movement control.

在手动跟踪过程中，为了保证最佳的视觉运动反馈控制，大脑必须持续监测手与目标之间的误差。θ波段（3-8 Hz）的调制与错误处理有关，但这主要表现在认知控制环境中。因此，它们与在线控制中手靶误差的关系尚不清楚。在这里，我们评估了运动错误处理对29名健康参与者的脑电图θ波段活动的影响，当他们用左手（右手）连续跟踪运动目标时。实验采用两种条件来操纵错误处理需求：1)重复条件下，同一目标轨迹被呈现80次，使被试内隐学习模式，减少跟踪误差；2)在随机条件下，使用了80种不同的轨迹，导致持续的高跟踪误差。行为分析证实，随机条件下的跟踪误差明显高于重复条件。重要的是，随机条件下的EEG θ波功率也明显更高，在左侧感觉运动区域的电极上出现峰值差异。这种效应对θ活动是选择性的，因为α -（8-12 Hz）和β波段（15-30 Hz）活动没有调制。总的来说，本研究将θ振荡的作用扩展到运动控制中的在线错误处理。θ波调制可能反映了在感觉运动回路（包括运动、前运动和顶叶皮层）中介导信息交流和整合的皮质活动，这些回路已知介导在线运动控制。

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引用次数: 0

Altered cerebral thyroid hormone, WNT and NOTCH signalling and impaired myelination following intrauterine growth restriction in rats 大鼠宫内生长受限后脑甲状腺激素、WNT和NOTCH信号改变和髓鞘形成受损。

IF 2.8 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2026-02-16 Epub Date: 2025-12-31 DOI: 10.1016/j.neuroscience.2025.12.068

Aminath Azhan , Angela L. Cumberland , Ginevra Chincarini , Mikaela Barresi , Nadia Hale , David H. Rowitch , Flora Wong , David W. Walker , Mary Tolcos

Intrauterine growth restriction (IUGR) is associated with impaired brain development, including hypomyelination. Preclinical studies suggest that reduced myelination in IUGR may result from delayed oligodendrocyte maturation, but the mechanisms remain unclear. We examined whether altered expression of positive (thyroid hormone, TH) and negative (WNT and NOTCH signalling) regulators of oligodendrocyte maturation and myelination contribute to this delay. We induced IUGR in pregnant rats via bilateral uterine vessel ligation at embryonic day 18; sham surgeries generated controls. At postnatal day (P) 7, P14, and P35, we assessed oligodendrocytes (Olig2, APC) and myelinated fibres (MBP) by immunostaining, and measured expression of TH-related and WNT/NOTCH pathway genes using RT-qPCR in the cerebral white matter (P7 and P14 only). We found that IUGR offspring exhibited reduced MBP-immunoreactivity in the corpus callosum (P7) and external capsule (P7 and P14), and decreased density of APC-positive oligodendrocytes at P14. No difference in these measures were observed at P35, nor in the density of Olig2-positive cells at any age. At P7, IUGR brains showed increased Tcf4, Delta1 and Hes5 expression (WNT/NOTCH), and reduced Mct8, Oatp1c1, Dio1, and Dio3 mRNA expression (TH signalling), which were not different between groups by P14. Reductions in Mct8 mRNA expression were confirmed by immunohistochemical analysis. Our findings suggest that alteration of TH, WNT, and NOTCH signalling may be associated with impaired oligodendrocyte maturation and myelination in IUGR, providing insight into the mechanisms underlying white matter injury in IUGR infants.

宫内生长受限（IUGR）与大脑发育受损有关，包括髓鞘发育低下。临床前研究表明IUGR中髓鞘形成减少可能是由于少突胶质细胞成熟延迟所致，但其机制尚不清楚。我们研究了少突胶质细胞成熟和髓鞘形成的阳性（甲状腺激素，TH）和阴性（WNT和NOTCH信号）调节因子的表达改变是否导致了这种延迟。我们在胚胎第18天通过双侧子宫血管结扎诱导妊娠大鼠IUGR；假手术产生对照。在出生后第7、14和35天，我们通过免疫染色评估少突胶质细胞（Olig2、APC）和髓鞘纤维（MBP），并使用RT-qPCR检测脑白质（仅P7和P14）中th相关和WNT/NOTCH通路基因的表达。我们发现IUGR后代胼胝体（P7）和外囊（P7和P14）的mbp免疫反应性降低，P14的apc阳性少突胶质细胞密度降低。在P35时，这些指标没有差异，在任何年龄，olig2阳性细胞的密度也没有差异。在P7时，IUGR脑显示Tcf4、Delta1和Hes5 （WNT/NOTCH）表达增加，Mct8、Oatp1c1、Dio1和Dio3 mRNA （TH信号）表达减少，各组间无P14差异。免疫组织化学分析证实Mct8 mRNA表达降低。我们的研究结果表明，TH、WNT和NOTCH信号的改变可能与IUGR中少突胶质细胞成熟和髓鞘形成受损有关，为IUGR婴儿白质损伤的机制提供了新的见解。

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引用次数: 0