Neuroscience最新文献_第7页

Contemporary strategies in glioblastoma therapy: Recent developments and innovations 胶质母细胞瘤治疗的当代策略：最新进展与创新。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-10-03 DOI: 10.1016/j.neuroscience.2024.09.022

Glioblastoma multiforme (GBM) represents one of the most prevailing and aggressive primary brain tumors among adults. Despite advances in therapeutic approaches, the complex microenvironment of GBM poses significant challenges in its optimal therapy, which are attributed to immune evasion, tumor repopulation by stem cells, and limited drug penetration across the blood–brain barrier (BBB). Nanotechnology has emerged as a promising avenue for GBM treatment, offering biosafety, sustained drug release, enhanced solubility, and improved BBB penetrability. In this review, a comprehensive overview of recent advancements in nanocarrier-based drug delivery systems for GBM therapy is emphasized. The conventional and novel treatment modalities for GBM and the potential of nanocarriers to overcome existing limitations are comprehensively covered. Furthermore, the updates in the clinical landscape of GBM therapeutics are presented in addition to the current status of drugs and patents in the same context. Through a critical evaluation of existing literature, the therapeutic prospect and limitations of nanocarrier-based drug delivery strategies are highlighted offering insights into future research directions and clinical translation.

多形性胶质母细胞瘤（GBM）是成人中最常见、侵袭性最强的原发性脑肿瘤之一。尽管治疗方法不断进步，但 GBM 复杂的微环境给其最佳治疗带来了巨大挑战，这主要归因于免疫逃避、干细胞重新填充肿瘤以及药物通过血脑屏障（BBB）的穿透力有限。纳米技术提供了生物安全性、药物持续释放、溶解性增强和血脑屏障穿透性改善等优势，已成为治疗 GBM 的一条大有可为的途径。在这篇综述中，我们将全面概述基于纳米载体的 GBM 治疗药物递送系统的最新进展。文中全面介绍了 GBM 的传统和新型治疗方法，以及纳米载体在克服现有局限性方面的潜力。此外，还介绍了 GBM 疗法的最新临床情况，以及相关药物和专利的现状。通过对现有文献的批判性评估，强调了基于纳米载体的给药策略的治疗前景和局限性，为未来的研究方向和临床转化提供了见解。

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引用次数: 0

Posture-dependent modulation of marmoset cortical motor maps detected via rapid multichannel epidural stimulation 通过快速多通道硬膜外刺激检测狨猴皮层运动图谱的姿势依赖性调制。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-10-03 DOI: 10.1016/j.neuroscience.2024.09.047

Recent neuroimaging and electrophysiological studies have suggested substantial short-term plasticity in the topographic maps of the primary motor cortex (M1). However, previous methods lack the temporal resolution to detect rapid modulation of these maps, particularly in naturalistic conditions. To address this limitation, we previously developed a rapid stimulation mapping procedure with implanted cortical surface electrodes. In this study, employing our previously established procedure, we examined rapid topographical changes in forelimb M1 motor maps in three awake male marmoset monkeys. The results revealed that although the hotspot (the location in M1 that elicited a forelimb muscle twitch with the lowest stimulus intensity) remained constant across postures, the stimulus intensity required to elicit the forelimb muscle twitch in the perihotspot region and the size of motor representations were posture-dependent. Hindlimb posture was particularly effective in inducing these modulations. The angle of the body axis relative to the gravitational vertical line did not alter the motor maps. These results provide a proof of concept that a rapid stimulation mapping system with chronically implanted cortical electrodes can capture the dynamic regulation of forelimb motor maps in natural conditions. Moreover, they suggest that posture is a crucial variable to be controlled in future studies of motor control and cortical plasticity. Further exploration is warranted into the neural mechanisms regulating forelimb muscle representations in M1 by the hindlimb sensorimotor state.

最近的神经影像学和电生理学研究表明，初级运动皮层（M1）的地形图具有很大的短期可塑性。然而，以前的方法缺乏时间分辨率，无法检测这些图谱的快速调制，尤其是在自然条件下。为了解决这一局限性，我们之前开发了一种植入皮层表面电极的快速刺激绘图程序。在本研究中，我们利用之前建立的程序，检测了三只清醒雄性狨猴前肢 M1 运动图谱的快速地形变化。结果发现，虽然不同姿势下的热点（M1 中以最低刺激强度引起前肢肌肉抽搐的位置）保持不变，但在热点周围区域引起前肢肌肉抽搐所需的刺激强度和运动表征的大小与姿势有关。后肢姿势在诱发这些调节方面尤为有效。身体轴线相对于重力垂直线的角度不会改变运动图谱。这些结果提供了一个概念证明，即通过长期植入皮层电极的快速刺激绘图系统可以捕捉自然条件下前肢运动图谱的动态调节。此外，这些结果还表明，在未来的运动控制和皮层可塑性研究中，姿势是一个需要控制的关键变量。后肢感觉运动状态调节前肢肌肉在M1中表征的神经机制值得进一步探索。

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引用次数: 0

Continuous theta burst stimulation ameliorates cognitive deficits in microinfarcts mice via inhibiting glial activation and promoting paravascular CSF-ISF exchange 持续θ脉冲刺激通过抑制神经胶质激活和促进血管旁CSF-ISF交换，改善微梗死小鼠的认知缺陷。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-10-02 DOI: 10.1016/j.neuroscience.2024.09.046

Microinfarcts are widespread in the elderly, accompanied by varying degrees of cognitive decline. Continuous theta burst stimulation (cTBS) has been demonstrated to be neuroprotective on cognitive dysfunction, but the underlying cellular mechanism has been still not clear. In the present study, we evaluated the effects of cTBS on cognitive function and brain pathological changes in mice model of microinfarcts. The spatial learning and memory was assessed by Morris water maze (MWM), Glymphatic clearance efficiency was evaluated using in vivo two-photon imaging. The loss of neurons, activation of astrocytes and microglia, the expression and polarity distribution of the astrocytic aquaporin-4 (AQP4) were assessed by immunofluorescence staining. Our results showed that cTBS treatment significantly improved the spatial learning and memory, accelerated the efficiency of glymphatic clearance, up-regulated the AQP4 expression and improved the polarity distribution of AQP4 in microinfarcts mice. Besides, cTBS treatment increased the number of surviving neurons, whereas decreased the activated astrocytes and microglia. Our study suggested that cTBS accelerated glymphatic clearance and inhibited the excessive gliogenesis, which ultimately exerted neuroprotective effects on microinfarcts mice.

微梗塞在老年人中很普遍，并伴有不同程度的认知功能下降。连续θ脉冲刺激（cTBS）已被证实对认知功能障碍有神经保护作用，但其潜在的细胞机制仍不清楚。在本研究中，我们评估了 cTBS 对微梗死小鼠模型认知功能和脑病理变化的影响。我们用莫里斯水迷宫（MWM）评估了小鼠的空间学习和记忆能力，并用体内双光子成像技术评估了小鼠的幽门清除率。通过免疫荧光染色评估了神经元的损失、星形胶质细胞和小胶质细胞的活化、星形胶质细胞水通道蛋白-4（AQP4）的表达和极性分布。结果表明，cTBS能明显改善微梗死小鼠的空间学习和记忆能力，加快血糖清除效率，上调AQP4的表达，改善AQP4的极性分布。此外，cTBS 还能增加存活神经元的数量，减少激活的星形胶质细胞和小胶质细胞。我们的研究表明，cTBS能加速甘油清除，抑制神经胶质细胞的过度生成，最终对微梗死小鼠发挥神经保护作用。

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引用次数: 0

Sex differences in fear expression and persistence in an animal model of Post-Traumatic Stress Disorder 创伤后应激障碍动物模型中恐惧表达和持续性的性别差异。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-10-02 DOI: 10.1016/j.neuroscience.2024.09.045

Post-Traumatic Stress Disorder (PTSD) is a complex psychiatric condition arising from traumatic experiences, marked by abnormal fear memories. Despite women are twice as likely as men to develop PTSD, the biological mechanisms underlying this disparity remain inadequately explored, particularly in preclinical studies involving female subjects.

Previous research shows that female rats exhibit active fear responses, while males display passive behaviors. Additionally, sex differences in ultrasonic vocalizations (USVs) during fear conditioning have been observed, indicating varying emotional responses.

Here, we validated a traumatic stress model consisting of footshock exposure paired with social isolation − originally developed in male rats − on females for the first time, focusing on sex differences in fear memory expression, retention and extinction. Our findings reveal that only during trauma exposure, males predominantly exhibited passive responses, whereas females demonstrated more active responses, despite both sexes emitting similar numbers of alarm USVs. Females also showed lower levels of freezing and USV emissions throughout extinction sessions and displayed a higher extinction rate compared to males. Notably, only males displayed a conditioned fear response when triggered by a single mild stressor.

These findings highlight sex differences in trauma responses and fear memory processes. The study emphasizes the importance of incorporating 22-kHz USV evaluations along with other behavioral metrics for a comprehensive understanding of fear memory. This research contributes to the existing literature on traumatic stress models as well as underscores the necessity of including female subjects in preclinical studies to better inform treatment and prevention strategies tailored to both sexes.

创伤后应激障碍（PTSD）是一种复杂的精神疾病，由创伤经历引起，以异常恐惧记忆为特征。尽管女性罹患创伤后应激障碍的几率是男性的两倍，但这种差异背后的生物机制仍未得到充分探究，尤其是在涉及女性受试者的临床前研究中。先前的研究表明，雌性大鼠表现出主动的恐惧反应，而雄性大鼠则表现出被动行为。此外，还观察到恐惧条件反射过程中超声波发声（USVs）的性别差异，这表明了不同的情绪反应。在这里，我们首次在雌性大鼠身上验证了一种创伤应激模型，该模型包括脚震暴露和社会隔离（最初是在雄性大鼠身上开发的），重点研究了恐惧记忆表达、保持和消退的性别差异。我们的研究结果表明，只有在受到创伤时，雄性大鼠才会主要表现出被动反应，而雌性大鼠则表现出更多的主动反应，尽管雌雄大鼠发出的警报USV数量相似。与雄性相比，雌性在整个熄灭过程中表现出较低水平的冻结和USV发射，并显示出更高的熄灭率。值得注意的是，只有雄性在单个轻微应激源触发时表现出条件性恐惧反应。这些发现凸显了创伤反应和恐惧记忆过程中的性别差异。该研究强调了将 22 千赫 USV 评估与其他行为指标结合起来以全面了解恐惧记忆的重要性。这项研究为现有的创伤应激模型文献做出了贡献，同时也强调了将女性受试者纳入临床前研究的必要性，以便更好地为适合两性的治疗和预防策略提供信息。

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引用次数: 0

Proteomic insights into early-stage Alzheimer’s disease: Identifying key neuronal proteins impacted by amyloid beta oligomers in an in vitro model 早期阿尔茨海默病的蛋白质组学研究：在体外模型中识别受淀粉样β寡聚体影响的关键神经元蛋白

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-10-01 DOI: 10.1016/j.neuroscience.2024.09.050

Alzheimer’s disease (AD) remains a pressing global health concern, necessitating comprehensive investigations into its underlying molecular mechanisms. While the late-stage pathophysiology of this disease is well understood, it is crucial to examine the role of amyloid beta oligomers (Aβo), which form in the brain during the early stages of disease development. These toxic oligomers could affect neuronal viability and generate oxidative stress in the brain. In this study, we exposed SHSY-5Y cells to Aβo. The increase in intracellular reactive oxygen species and apoptosis observed in Aβo-treated cells mimics the early stages of AD. Comprehensive proteomic profiling identified 2966 differentially expressed proteins, with 123 significantly modulated. Utilizing the NeuroPro database, we identified 80 confirmed AD-related proteins and 43 novel candidates. Seven AD-related proteins with a NeuroPro score ≥ 5 were shortlisted. Furthermore, these proteins are found to be associated with Aβ plaques in AD brains. VGF, LTF, PARP1, and MAOA have been implicated in various mechanisms underlying AD, including synaptic plasticity, iron homeostasis, DNA repair, and neurotransmitter degradation. Our study also revealed the involvement of less-explored proteins like MYH9, CISD1, and SNRNP70, which play critical roles in cytoskeletal dynamics, mitochondrial function, and RNA splicing, respectively. These findings underscore the complex pathophysiology of AD, highlighting potential biomarkers and therapeutic targets for early intervention. The present study advances the understanding of Aβo-induced oxidative stress and neuronal damage, providing a foundation for future research into early-stage AD diagnosis and subsequent treatment strategies.

阿尔茨海默病（AD）仍然是一个紧迫的全球健康问题，需要对其潜在的分子机制进行全面研究。虽然这种疾病的晚期病理生理学已经非常清楚，但研究淀粉样β低聚物（Aβo）的作用至关重要，这种低聚物是在疾病发展的早期阶段在大脑中形成的。这些有毒的低聚物会影响神经元的活力，并在大脑中产生氧化应激。在这项研究中，我们将SHSY-5Y细胞暴露于Aβo。在Aβo处理的细胞中观察到的细胞内活性氧增加和细胞凋亡模拟了AD的早期阶段。全面的蛋白质组分析确定了 2966 种不同表达的蛋白质，其中 123 种受到显著调控。利用 NeuroPro 数据库，我们确定了 80 个已证实的 AD 相关蛋白和 43 个新的候选蛋白。7个NeuroPro评分≥5的AD相关蛋白入围。此外，我们还发现这些蛋白与 AD 大脑中的 Aβ 斑块有关。VGF、LTF、PARP1和MAOA与AD的多种机制有关，包括突触可塑性、铁稳态、DNA修复和神经递质降解。我们的研究还揭示了 MYH9、CISD1 和 SNRNP70 等鲜为人知的蛋白质的参与，它们分别在细胞骨架动力学、线粒体功能和 RNA 剪接中发挥着关键作用。这些发现强调了AD复杂的病理生理学，突出了早期干预的潜在生物标志物和治疗靶点。本研究加深了人们对Aβ-诱导的氧化应激和神经元损伤的理解，为今后研究早期AD诊断和后续治疗策略奠定了基础。

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引用次数: 0

Mild traumatic brain injury gives rise to chronic depression-like behavior and associated alterations in glutamatergic protein expression 轻度脑外伤会导致慢性抑郁样行为以及相关的谷氨酸蛋白表达改变。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-09-30 DOI: 10.1016/j.neuroscience.2024.09.039

Mild traumatic brain injury (mTBI) is known to result in chronic somatic, cognitive, and emotional symptoms. Depression is commonly reported among individuals suffering from persistent concussion symptoms; however, the underlying mechanisms are not understood. The glutamatergic system has recently been linked with mTBI and depression due to reports of similar changes in expression of glutamatergic proteins. Using a closed-head controlled cortical impact (cCCI) model in adult male rats (n = 8/group), this study investigated the emergence of self-care deficits and changes in social interaction behaviors at four, eight and twelve weeks post-injury. Western blotting was used to assess associated changes in expression of glutamate transporters and N-methyl-D-aspartate (NMDA) receptor subunits at twelve weeks. Splash test results revealed deficits in self-care behaviors beginning at eight weeks, which continued through twelve weeks in the injury group. Injured animals also exhibited decreased preference for social novelty at four weeks and loss of desire for social interaction as a whole by twelve weeks. GluN1 was increased in injured animals compared to shams in the frontal cortex and amygdala, while decreased GLT-1 was observed in the hippocampus. Linear regression was performed to evaluate relationships between behavioral and molecular variables; the results suggested that injury affects these relationships in a region-dependent manner. Together, these results suggest that the development of chronic depression-like behavior was associated with changes in glutamatergic protein expression. Deeper investigations into how injury influences glutamatergic synaptic protein expression are needed, as this has the potential to affect circuit-level neurotransmission that drives depression-like behavior following mTBI.

众所周知，轻度创伤性脑损伤（mTBI）会导致慢性躯体、认知和情绪症状。据报道，在患有持续性脑震荡症状的人中，抑郁症患者很常见；然而，其潜在机制尚不清楚。谷氨酸能系统最近与 mTBI 和抑郁症联系在一起，因为有报告称谷氨酸能蛋白的表达发生了类似的变化。本研究使用成年雄性大鼠（n = 8只/组）的闭头控制性皮层撞击（cCCI）模型，调查了受伤后4周、8周和12周出现的自理障碍和社会互动行为的变化。研究人员使用 Western 印迹法评估了十二周时谷氨酸转运体和 N 甲基-D-天冬氨酸（NMDA）受体亚单位表达的相关变化。泼溅试验结果显示，受伤组动物从八周开始出现自理行为障碍，并一直持续到十二周。受伤动物在四周时还表现出对社会新奇事物的偏好下降，到十二周时则表现出对社会互动的整体丧失。在额叶皮层和杏仁核中，受伤动物的 GluN1 比假体动物有所增加，而在海马中则观察到 GLT-1 的减少。对行为和分子变量之间的关系进行了线性回归评估；结果表明，损伤以区域依赖的方式影响这些关系。这些结果表明，慢性抑郁样行为的发生与谷氨酸能蛋白表达的变化有关。我们需要对损伤如何影响谷氨酸能突触蛋白表达进行更深入的研究，因为这有可能影响电路级神经递质，而电路级神经递质是 mTBI 后抑郁样行为的驱动因素。

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引用次数: 0

Maintained volitional activation of the muscle alters the cortical processing of proprioceptive afference from the ankle joint 肌肉的持续自主激活会改变大脑皮层对来自踝关节的本体感觉的处理。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-09-30 DOI: 10.1016/j.neuroscience.2024.09.049

Cortical proprioceptive processing of intermittent, passive movements can be assessed by extracting evoked and induced electroencephalographic (EEG) responses to somatosensory stimuli. Although the existent prior research on somatosensory stimulations, it remains unknown to what extent ongoing volitional muscle activation modulates the proprioceptive cortical processing of passive ankle-joint rotations.

Twenty-five healthy volunteers (28.8 ± 7 yr, 14 males) underwent a total of 100 right ankle-joint passive rotations (4° dorsiflexions, 4 ± 0.25 s inter-stimulus interval, 30°/s peak angular velocity) evoked by a movement actuator during passive condition with relaxed ankle and active condition with a constant plantarflexion torque of 5 ± 2.5 Nm. Simultaneously, EEG, electromyographic (EMG) and kinematic signals were collected. Spatiotemporal features of evoked and induced EEG responses to the stimuli were extracted to estimate the modulation of the cortical proprioceptive processing between the active and passive conditions.

Proprioceptive stimuli during the active condition elicited robustly ∼26 % larger evoked response and ∼38 % larger beta suppression amplitudes, but ∼42 % weaker beta rebound amplitude over the primary sensorimotor cortex than the passive condition, with no differences in terms of response latencies.

These findings indicate that the active volitional motor task during naturalistic proprioceptive stimulation of the ankle joint enhances related cortical activation and reduces related cortical inhibition with respect to the passive condition. Possible factors explaining these results include mechanisms occurring at several levels of the proprioceptive processing from the peripheral muscle (i.e. mechanical, muscle spindle status, etc.) to the different central (i.e. spinal, sub-cortical and cortical) levels.

通过提取对躯体感觉刺激的诱发和诱导脑电图（EEG）反应，可以评估间歇性被动运动的大脑皮层本体感觉处理过程。尽管之前已有关于躯体感觉刺激的研究，但持续的肌肉意志激活在多大程度上调节了被动踝关节旋转的本体感觉皮层处理仍是未知数。25 名健康志愿者（28.8 ± 7 岁，14 名男性）在踝关节放松的被动状态和 5 ± 2.5 牛米恒定跖屈扭矩的主动状态下，接受了运动致动器诱发的总共 100 次右踝关节被动旋转（背屈 4°，刺激间隔 4 ± 0.25 秒，峰值角速度 30°/秒）。同时收集脑电图、肌电图（EMG）和运动学信号。提取脑电图对刺激的诱发和诱导反应的时空特征，以估计主动和被动条件下大脑皮层本体感觉处理的调节情况。与被动条件相比，主动条件下的本体感觉刺激在初级感觉运动皮层引起的诱发反应和β抑制振幅分别增加了26%和38%，但β反弹振幅却减弱了42%，而反应潜伏期则没有差异。这些研究结果表明，与被动状态相比，在对踝关节进行自然本体感觉刺激时，主动的意志运动任务会增强相关的皮层激活，并减少相关的皮层抑制。解释这些结果的可能因素包括从外周肌肉（即机械、肌纺锤状态等）到不同中枢（即脊髓、皮层下和皮层）水平的本体感觉处理的多个层次的机制。

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引用次数: 0

Vitamin D: The crucial neuroprotective factor for nerve cells 维生素 D：神经细胞的重要神经保护因子。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-09-27 DOI: 10.1016/j.neuroscience.2024.09.042

Vitamin D is well known for its role in regulating the absorption and utilization of calcium and phosphorus as well as bone formation, and a growing number of studies have shown that vitamin D also has important roles in the nervous system, such as maintaining neurological homeostasis and protecting normal brain function, and that neurons and glial cells may be the targets of these effects. Most reviews of vitamin D’s effects on the nervous system have focused on its overall effects, without distinguishing the contributors to these effects. In this review, we mainly focus on the cells of the central nervous system, summarizing the effects of vitamin D on them and the related pathways. With this review, we hope to elucidate the role of vitamin D in the nervous system at the cellular level and provide new insights into the prevention and treatment of neurodegenerative diseases in the direction of neuroprotection, myelin regeneration, and so on.

维生素 D 因其在调节钙和磷的吸收和利用以及骨骼形成方面的作用而广为人知，越来越多的研究表明，维生素 D 在神经系统中也有重要作用，如维持神经系统的平衡和保护大脑的正常功能，而神经元和神经胶质细胞可能是这些作用的靶点。大多数关于维生素 D 对神经系统影响的综述都集中在其整体影响上，而没有区分这些影响的促成因素。在这篇综述中，我们主要关注中枢神经系统细胞，总结维生素 D 对它们的影响以及相关途径。我们希望通过这篇综述，从细胞层面阐明维生素 D 在神经系统中的作用，并从神经保护、髓鞘再生等方向为预防和治疗神经退行性疾病提供新的见解。

引用次数: 0

Therapeutic potential of astrocyte-derived extracellular vesicles in mitigating cytotoxicity and transcriptome changes in human brain endothelial cells 星形胶质细胞衍生的细胞外囊泡在减轻细胞毒性和人脑内皮细胞转录组变化方面的治疗潜力

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-09-27 DOI: 10.1016/j.neuroscience.2024.09.040

This study investigates the therapeutic effect of astrocyte-derived extracellular vesicles (EVs) in mitigating neurotoxicity-induced transcriptome changes, mitochondrial function, and base excision repair mechanisms in human brain endothelial cells (HBECs). Neurodegenerative disorders are marked by inflammatory processes impacting the blood–brain barrier (BBB) that involve its main components- HBECs and astrocytes. Astrocytes maintain homeostasis through various mechanisms, including EV release. The effect of these EVs on mitigating neurotoxicity in HBECs has not been investigated. This study assesses the impact of astrocyte-derived EVs on global transcriptome changes, cell proliferation, cytotoxicity, oxidative DNA damage, and mitochondrial morphology in HBECs exposed to the neurotoxic reagent Na₂Cr₂O₇. Exposure to Na₂Cr₂O₇ for 5 and 16 h induced oxidative DNA damage, measured by an increase in genomic 8OHdG, while the EVs reduced the accumulation of the adduct. A neurotoxic environment caused a non-statistically significant upregulation of the DNA repair enzyme OGG1 while the addition of astrocyte-derived EVs was associated with the same level of expression. EVs caused increased cell proliferation and reduced cytotoxicity in Na₂Cr₂O₇-treated cells. Mitochondrial dysfunction associated with a reduced copy number and circular morphology induced by neurotoxic exposure was not reversed by astrocyte-derived EVs. High-throughput RNA sequencing revealed that exposure to Na₂Cr₂O₇ suppressed immune response genes. The addition of astrocyte-derived EVs resulted in the dysregulation of long noncoding RNAs impacting genes associated with brain development and angiogenesis. These findings reveal the positive impact of astrocytes-derived EVs in mitigating neurotoxicity and as potential therapeutic avenues for neurodegenerative diseases.

本研究调查了星形胶质细胞衍生的细胞外囊泡（EVs）在减轻神经毒性诱导的转录组变化、线粒体功能和人脑内皮细胞（HBECs）碱基切除修复机制方面的治疗效果。神经退行性疾病以影响血脑屏障（BBB）的炎症过程为特征，涉及其主要成分--HBECs 和星形胶质细胞。星形胶质细胞通过包括 EV 释放在内的各种机制维持体内平衡。这些 EV 对减轻 HBEC 神经毒性的影响尚未得到研究。本研究评估了星形胶质细胞衍生的 EV 对暴露于神经毒性试剂 Na2Cr2O7 的 HBECs 的全局转录组变化、细胞增殖、细胞毒性、氧化 DNA 损伤和线粒体形态的影响。暴露于Na2Cr2O7 5小时和16小时可诱导氧化DNA损伤（通过基因组8OHdG的增加来测量），而EVs可减少加合物的积累。神经毒性环境会导致DNA修复酶OGG1的上调，但无统计学意义，而加入源自星形胶质细胞的EVs则会导致相同水平的表达。在 Na2Cr2O7 处理过的细胞中，EVs 增加了细胞增殖，降低了细胞毒性。神经毒性暴露诱发的线粒体功能障碍与拷贝数减少和圆形形态有关，但星形胶质细胞衍生的EVs并不能逆转这种功能障碍。高通量 RNA 测序显示，暴露于 Na2Cr2O7 会抑制免疫反应基因。加入星形胶质细胞衍生的EVs会导致长非编码RNA失调，影响与大脑发育和血管生成相关的基因。这些发现揭示了星形胶质细胞衍生的EVs在减轻神经毒性方面的积极影响，也是治疗神经退行性疾病的潜在途径。

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引用次数: 0

Disrupted white matter structural networks in patients with acute ischemic stroke in the right basal ganglia. 急性缺血性脑卒中患者右侧基底节白质结构网络紊乱。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-09-26 DOI: 10.1016/j.neuroscience.2024.08.003

Meizhong Chen, Yuntao Wang, Zhongming Li

Widespread structural changes have been observed in patients with stroke in previous diffusion tensor imaging studies. However, the topological organization of white matter structural networks after acute ischemic stroke (AIS) in the right basal ganglia (BG) remains unknown. The aim of our study is to investigate whether the topological structure of the white matter structural network is altered in patients with AIS in the right BG, and its relationship with cognition. Graph theoretical analysis was employed to investigate the topological architecture of whole-brain white matter structural networks in 40 AIS patients in the right BG and 40 healthy controls (HC), and network-based statistics (NBS) were applied to examine structural connectivity alterations. Compared to HC, AIS patients exhibited altered global network properties characterized by increased small-worldness, normalized clustering coefficient, and shortest path length, as well as decreased clustering coefficient, local efficiency, and global efficiency. The nodes with significantly decreased nodal properties in AIS patients were primarily located in the default mode network, limbic system, sensorimotor system, salience network, and central executive network. Reduced structural connectivity detected by NBS in AIS patients were primarily located in the lesional hemisphere. Furthermore, altered nodal properties were correlated with cognitive scores. Documenting the alterations in the topological patterns of white matter structural networks will help to promote the understanding of the neural mechanisms of cognitive impairment after AIS in the right BG.

在以往的弥散张量成像研究中，已观察到中风患者出现了广泛的结构变化。然而，急性缺血性脑卒中（AIS）后右侧基底节（BG）白质结构网络的拓扑组织仍然未知。我们的研究旨在探讨急性缺血性脑卒中患者右侧基底节白质结构网络的拓扑结构是否发生改变及其与认知的关系。我们采用图论分析法研究了40名右侧BG的AIS患者和40名健康对照者（HC）的全脑白质结构网络的拓扑结构，并采用基于网络的统计学方法（NBS）研究了结构连接的改变。与健康对照组相比，AIS 患者的全局网络特性发生了改变，其特征是小世界度、归一化聚类系数和最短路径长度增加，聚类系数、局部效率和全局效率降低。AIS患者节点属性明显降低的节点主要位于默认模式网络、边缘系统、感觉运动系统、显著性网络和中央执行网络。通过 NBS 检测到的 AIS 患者结构连接性降低主要位于病变半球。此外，节点特性的改变与认知评分相关。记录白质结构网络拓扑模式的改变将有助于促进对右侧BG AIS后认知障碍神经机制的理解。

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引用次数: 0