Restoration of Glymphatic Influx After Photothrombotic Stroke Using Low-Intensity Focused Ultrasound

使用低强度聚焦超声恢复光栓性中风后类淋巴系统流入

This study aimed to investigate the regional modulation effect of low-intensity focused ultrasound (LIFU) on cerebrospinal fluid (CSF) influx dynamics, focusing on the differential changes between hemispheres in a mouse model of unilateral ischemic stroke. Daily contralesional LIFU stimulation restores impaired CSF influx bilaterally after stroke, suggesting potential therapeutic implications for stroke-related pathophysiology.

本研究旨在探讨低强度聚焦超声（LIFU）对脑脊液（CSF）流入动力学的局部调节作用，重点关注单侧缺血性中风小鼠模型中两侧大脑半球的差异变化。每日对健侧进行低强度聚焦超声刺激可使中风后双侧受损的脑脊液流入得到恢复，这提示其对中风相关病理生理机制可能具有潜在治疗意义。

REF: Hsiao MY, Lin YL, Lin MT, Liao WH, Chen WS, Wu CH. Restoration of Glymphatic Influx After Photothrombotic Stroke Using Low-Intensity Focused Ultrasound. CNS Neurosci Ther. 2025;31(6):e70451. doi:10.1111/cns.70451 PMID: 40457518

Intra-Arterial Deoxyribonuclease Therapy Improves Stroke Outcomes in Aged Mice

动脉内脱氧核糖核酸酶治疗可改善老年小鼠的中风预后

Futile recanalization affects more than half of acute ischemic stroke (AIS) patients. Neutrophil extracellular traps (NETs) are a major factor of microvascular hypoperfusion after stroke. Deoxyribonuclease I (DNase) targeting NETs exhibited a neuroprotective effect in young mice with AIS. This study explored a novel direct intra-arterial administration of DNase therapy and its effect in aged mice with AIS. Our data is the first to demonstrate that successful, direct intra-arterial DNase therapy provides more efficient cerebral reperfusion and better outcomes after recanalization during the treatment of large vessel occlusion in aged mice. This study provides evidence for the potential clinical application of catheter-delivered intra-arterial DNase therapy post-recanalization.

无效再通影响超过半数的急性缺血性脑卒中（AIS）患者。中性粒细胞胞外诱捕网（NETs）是脑卒中后微血管低灌注的主要因素。靶向NETs的脱氧核糖核酸酶I（DNase）在年轻AIS小鼠中显示出神经保护作用。本研究探索了一种新型的直接动脉内注射DNase疗法及其在老年AIS小鼠中的疗效。我们的数据首次证明，在老年小鼠大血管闭塞治疗中，成功的直接动脉内注射DNase疗法可在再通后实现更有效的脑再灌注并带来更好的预后。本研究为导管输送的动脉内注射DNase疗法在再通后的潜在临床应用提供了证据。

REF: Yin J, Wu M, White J, StClair E, Mocco J, Waters MF. Intra-Arterial Deoxyribonuclease Therapy Improves Stroke Outcomes in Aged Mice. CNS Neurosci Ther. 2025;31(6):e70461. doi:10.1111/cns.70461 PMID: 40457526

CXCL10highTNFαhighKi67+ Microglia Recruit and Activate CD8+ T Cells in the Brainstem During Experimental Cerebral Malaria

实验性脑型疟疾期间，CXCL10高表达、TNFα高表达、Ki67阳性的小胶质细胞在脑干中招募并激活CD8 + T细胞

This study aimed to investigate the heterogeneity of microglia and their role in recruiting and activating CD8+ T cells in experimental cerebral malaria (ECM). Our study identified an ECM-associated microglia subtype and explored its interaction with CD8+ T cells, which deepened the understanding of the multifaceted role of microglia in the pathogenesis of CM neuroinflammation.

本研究旨在探究实验性脑型疟疾（ECM）中微胶质细胞的异质性及其在招募和激活CD8+ T细胞中的作用。我们的研究鉴定出一种与ECM相关的微胶质细胞亚型，并探索了其与CD8+ T细胞的相互作用，这加深了对微胶质细胞在脑型疟疾神经炎症发病机制中多方面作用的理解。

REF: Wang Y, Liang J, Yang C, et al. CXCL10highTNFαhighKi67+ Microglia Recruit and Activate CD8+ T Cells in the Brainstem During Experimental Cerebral Malaria. CNS Neurosci Ther. 2025;31(6):e70425. doi:10.1111/cns.70425 PMID: 40457525

Autoantibodies Against Collapsin Response Mediator Proteins Associated With Encephalopathy/Myelopathy: A Single-Center Retrospective Study

抗塌陷反应调节蛋白自身抗体与脑病/脊髓病的相关性：一项单中心回顾性研究

Collapsin response mediator protein (CRMP) consists of five subtypes (CRMP1-5), which share high homology and are expressed in the nervous system. Anti-CRMP2 and anti-CRMP5 antibodies (Abs) have been reported in autoimmune encephalitis (AE). This study retrospectively evaluated the diagnostic value of CRMP auto-Abs in patients with suspected immune-mediated encephalopathy/myelopathy. Anti-CRMPs Abs may indicate immune-mediated neuronal damage in encephalopathy, including encephalitis, and may serve as potential biomarkers for neuronal injury.

塌陷反应调节蛋白（CRMP）由五种亚型（CRMP1 - 5）组成，它们具有高度同源性，且在神经系统中表达。已有报道称，自身免疫性脑炎（AE）患者体内存在抗CRMP2和抗CRMP5抗体（Abs）。本研究回顾性评估了CRMP自身抗体在疑似免疫介导性脑病/脊髓病患者中的诊断价值。抗CRMP抗体可能提示包括脑炎在内的脑病中存在免疫介导的神经元损伤，并且有望成为神经元损伤的潜在生物标志物。

REF: Wang D, Wang Q, Jie S, et al. Autoantibodies Against Collapsin Response Mediator Proteins Associated With Encephalopathy/Myelopathy: A Single-Center Retrospective Study. CNS Neurosci Ther. 2025;31(6):e70423. doi:10.1111/cns.70423 PMID: 40583162

Differentiation Defect Into GABAergic Neurons in Cerebral Organoids From Autism Patients

自闭症患者脑类器官中γ-氨基丁酸能神经元分化缺陷

Autism spectrum disorder (ASD) is a neurodevelopmental condition that affects social communication and behaviors. While previous studies using animal models have substantially expanded our knowledge about ASD, the lack of an appropriate human model system that accurately recapitulates the human-specific pathophysiology of ASD hinders the precise understanding of its etiology and the development of effective therapies. This study aims to replicate pathological phenotypes in cerebral organoids derived from idiopathic ASD patients and to conduct proof-of-concept research for the development of ASD therapeutics. Our findings provide a framework for utilizing patient-derived cerebral organoids in the development of personalized pharmaceutical treatment for ASD.

自闭症谱系障碍（ASD）是一种影响社交沟通和行为的神经发育性疾病。尽管此前利用动物模型开展的研究极大地拓展了我们对自闭症谱系障碍的认识，但缺乏能准确重现自闭症谱系障碍人类特异性病理生理学特征的合适人类模型系统，阻碍了我们对其病因的精准理解以及有效疗法的开发。本研究旨在在源自特发性自闭症谱系障碍患者的类脑器官中重现病理表型，并为自闭症谱系障碍治疗方法的开发开展概念验证研究。我们的研究结果为利用患者来源的类脑器官开发自闭症谱系障碍个性化药物治疗方案提供了框架。

REF: Hali S, Yao X, Hao G, et al. Differentiation Defect Into GABAergic Neurons in Cerebral Organoids From Autism Patients. CNS Neurosci Ther. 2025;31(6):e70449. doi:10.1111/cns.70449 PMID: 40457513

Network Topography Alterations in Alzheimer's Disease: Insights From Motif Changes via Multisite Datasets (N = 3262)

阿尔茨海默病中的网络拓扑改变：基于多中心数据集（N = 3262）的 motifs 变化见解

Convergent studies have demonstrated that the topological structure of the brain network undergoes significant alterations in Alzheimer's Disease (AD). However, the underlying mechanisms driving these topological changes remain unclear. Network motifs, as fundamental components of brain networks, provide valuable insights into how disconnections may lead to alterations in the macroscale topological structure. These findings provide novel insights into the relationship between disconnection and the topological structure of the brain network in AD.

多项研究一致表明，阿尔茨海默病（AD）患者的脑网络拓扑结构会发生显著改变。然而，驱动这些拓扑变化的潜在机制仍不清楚。网络模体作为脑网络的基本组成部分，为理解连接中断如何导致宏观尺度拓扑结构改变提供了有价值的见解。这些发现为AD患者脑网络连接中断与拓扑结构之间的关系提供了新的认识。

REF: Zhao J, Duan Y, Zhao K, et al. Network Topography Alterations in Alzheimer's Disease: Insights From Motif Changes via Multisite Datasets (N = 3262). CNS Neurosci Ther. 2025;31(6):e70428. doi:10.1111/cns.70428 PMID: 40537925

Dual Roles of Autophagy in Radiation-Induced Brain Injury: Mechanistic Insights and Therapeutic Implications

自噬在放射性脑损伤中的双重作用：机制见解与治疗意义

Cranial radiotherapy, while essential for treating brain tumors, often leads to radiation-induced brain injury, a debilitating condition marked by cognitive decline and neuronal damage. Autophagy, a key cellular process for recycling damaged organelles and proteins, has emerged as both a protective and detrimental player in radiation-induced brain injury. By elucidating the mechanistic underpinnings of autophagy in radiation-induced brain injury, this review underscores its dual roles and therapeutic relevance, offering a foundation for targeted interventions that optimize autophagic balance to protect brain function postradiotherapy.

尽管颅脑放疗对于治疗脑肿瘤至关重要，但它常常会导致放射性脑损伤，这是一种以认知能力下降和神经元损伤为特征的使人衰弱的病症。自噬是细胞回收受损细胞器和蛋白质的关键过程，它在放射性脑损伤中既起到保护作用，也有有害影响。通过阐明自噬在放射性脑损伤中的机制基础，本综述强调了其双重作用和治疗意义，为进行靶向干预提供了基础，旨在优化自噬平衡，以保护放疗后脑功能。

REF: Tian J, Mao Y, Liu D, et al. Dual Roles of Autophagy in Radiation-Induced Brain Injury: Mechanistic Insights and Therapeutic Implications. CNS Neurosci Ther. 2025;31(6):e70464. doi:10.1111/cns.70464 PMID: 40491058

Functional MRI Analysis of Brain Activity in Rats With Diabetic Bladder Dysfunction

糖尿病膀胱功能障碍大鼠脑活动的功能磁共振成像分析

This study aimed to investigate brain activity using functional magnetic resonance imaging (fMRI) in rats with 12-week diabetic bladder dysfunction (DBD). Furthermore, as prior research has suggested that NLX-112, a 5-HT1A receptor agonist, may alleviate DBD, we sought to explore its effects on brain activity in DBD rats. DBD rats exhibit heightened thalamic and PAG activity during micturition, potentially due to enlarged bladder capacity, with cortical activity serving as a compensatory mechanism. These findings highlight potential neural targets for DBD treatment.

本研究旨在利用功能磁共振成像（fMRI）研究患有12周糖尿病膀胱功能障碍（DBD）的大鼠的大脑活动。此外，由于先前的研究表明5 - HT1A受体激动剂NLX - 112可能缓解DBD，我们试图探究其对DBD大鼠大脑活动的影响。DBD大鼠在排尿时丘脑和导水管周围灰质（PAG）活动增强，这可能是由于膀胱容量增大所致，而皮质活动起到补偿机制的作用。这些发现凸显了DBD治疗的潜在神经靶点。

REF: Li M, Chen X, Ye J, et al. Functional MRI Analysis of Brain Activity in Rats With Diabetic Bladder Dysfunction. CNS Neurosci Ther. 2025;31(6):e70466. doi:10.1111/cns.70466 PMID: 40458921

Whole Brain Monosynaptic Input of Distinct Neurons in the Globus Pallidus Externa

苍白球外侧部不同神经元的全脑单突触输入

The globus pallidus externa (GPe) is involved in mediating physiological functions and contains two types of neurons: Forkhead box protein P2-expressing (GPeFoxP2) neurons which inhibit motor, and parvalbumin-expressing (GPePV) neurons which improve motor. The functional complexity of the GPe, directly linked to its neuronal heterogeneity, necessitates exploring the neuroanatomical circuits of its distinct neuron types as a foundation for functional research. Collectively, our results reveal the similarities and differences in the input projections to the two types of neurons in the GPe and lay the neuroanatomic groundwork for further studies to explore the critical physiological functions of GPe.

苍白球外侧部（GPe）参与介导生理功能，包含两种类型的神经元：表达叉头框蛋白P2的（GPeFoxP2）神经元，其抑制运动；以及表达小白蛋白的（GPePV）神经元，其改善运动。GPe的功能复杂性与它的神经元异质性直接相关，这就需要探索其不同神经元类型的神经解剖学回路，以此作为功能研究的基础。总体而言，我们的研究结果揭示了GPe中这两种类型神经元输入投射的异同，并为进一步探索GPe关键生理功能的研究奠定了神经解剖学基础。

REF: Ma MF, Hu J, Hao YX, et al. Whole Brain Monosynaptic Input of Distinct Neurons in the Globus Pallidus Externa. CNS Neurosci Ther. 2025;31(6):e70459. doi:10.1111/cns.70459 PMID: 40464272