A Pivotal Study to Evaluate the Safety and Effectiveness of Exablate Model 4000 Using Microbubble Resonators to Temporarily Mediate Blood-Brain Barrier Disruption (BBBD) in Subjects With Suspected Infiltrating Glioma

The purpose of this study is to evaluate the safety and effectiveness of using the Exablate Type 2 system using microbubble resonators (Exablate Test Arm) to disrupt the Blood-Brain Barrier for the purpose of temporarily transforming, and thereby 'marking', regions of infiltrating gliomas prior to planned surgical resection, for the purpose of improving tumor visualization during the surgery to achieve a greater proportion of subjects who receive a Gross Total Resection (GTR) per plan compared to those not undergoing a BBBD procedure prior to resection (Control Arm).

开始日期2024-12-01

申办/合作机构

Insightec Ltd.

NCT06090955 / RecruitingN/AIIT

Modulating Surgery-Induced Blood-Brain Barrier Disruption in Elderly: Impact of Dexmedetomidine and Lidocaine, a Randomized Controlled Trial

Postoperative delirium (POD) is the most common complications (
50-60%) in elderly and major challenges to our rapidly growing aging population. Growing evidence suggests a possible role for neuroinflammation in the development of delirium, which is facilitated by a transient increase in blood-brain barrier (BBB) permeability. Lidocaine and dexmedetomidine, commonly used anesthetic adjuncts, have anti-inflammatory properties. Both drugs are reported to have modulatory effect on the intergrity of BBB and associated with a beneficial effect on postoperative neurocognitive dysfunction. In this regard, The investigators aimed to prospectively compare the modulatory effect of the intraoperative administration of dexmedetomidine or lidocaine with a sham control group (normal saline solution) on surgery-induced BBB disruption.

开始日期2023-10-25

申办/合作机构

Samsung Medical Center

NCT03322813 / SuspendedN/A

A Study to Evaluate the Safety and Feasibility of Exablate Model 4000 Type-2 to Temporarily Mediate Blood-Brain Barrier Disruption (BBBD) in Patients With Suspected Infiltrating Glioma in the Setting of Planned Surgical Interventions

This study is designed to assess the safety and feasibility of using the ExAblate, Type 2 to temporarily disrupt the blood brain barrier in non-enhancing suspected infiltrating glioma. The ExAblate Model 4000 Type-2 is intended for use as a tool to disrupt the BBB.

开始日期2023-10-01

申办/合作机构

Insightec Ltd.

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100 项与血脑屏障缺陷相关的转化医学

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2025-08-01·Neural Regeneration Research

Interaction of major facilitator superfamily domain containing 2A with the blood–brain barrier

Article

作者: Miao, Feng ; Yang, Juanjuan ; Dong, Taiwei ; Luan, Fei ; Wei, Peifeng ; Ma, Yilun

The functional and structural integrity of the blood–brain barrier is crucial in maintaining homeostasis in the brain microenvironment; however, the molecular mechanisms underlying the formation and function of the blood–brain barrier remain poorly understood. The major facilitator superfamily domain containing 2A has been identified as a key regulator of blood–brain barrier function. It plays a critical role in promoting and maintaining the formation and functional stability of the blood–brain barrier, in addition to the transport of lipids, such as docosahexaenoic acid, across the blood–brain barrier. Furthermore, an increasing number of studies have suggested that major facilitator superfamily domain containing 2A is involved in the molecular mechanisms of blood–brain barrier dysfunction in a variety of neurological diseases; however, little is known regarding the mechanisms by which major facilitator superfamily domain containing 2A affects the blood–brain barrier. This paper provides a comprehensive and systematic review of the close relationship between major facilitator superfamily domain containing 2A proteins and the blood–brain barrier, including their basic structures and functions, cross-linking between major facilitator superfamily domain containing 2A and the blood–brain barrier, and the in-depth studies on lipid transport and the regulation of blood–brain barrier permeability. This comprehensive systematic review contributes to an in-depth understanding of the important role of major facilitator superfamily domain containing 2A proteins in maintaining the structure and function of the blood–brain barrier and the research progress to date. This will not only help to elucidate the pathogenesis of neurological diseases, improve the accuracy of laboratory diagnosis, and optimize clinical treatment strategies, but it may also play an important role in prognostic monitoring. In addition, the effects of major facilitator superfamily domain containing 2A on blood–brain barrier leakage in various diseases and the research progress on cross-blood–brain barrier drug delivery are summarized. This review may contribute to the development of new approaches for the treatment of neurological diseases.

2025-08-01·Neural Regeneration Research

Hypidone hydrochloride (YL-0919) ameliorates functional deficits after traumatic brain injury in mice by activating the sigma-1 receptor for antioxidation

Article

作者: Hou, Xiaojuan ; Yang, Yixin ; Bai, Yafan ; Zhang, Yue ; Li, Jinfeng ; Wang, Guyan ; Li, Yunfeng ; Ma, Hui

JOURNAL/nrgr/04.03/01300535-202508000-00023/figure1/v/2024-09-30T120553Z/r/image-tiff Traumatic brain injury involves complex pathophysiological mechanisms, among which oxidative stress significantly contributes to the occurrence of secondary injury. In this study, we evaluated hypidone hydrochloride (YL-0919), a self-developed antidepressant with selective sigma-1 receptor agonist properties, and its associated mechanisms and targets in traumatic brain injury. Behavioral experiments to assess functional deficits were followed by assessment of neuronal damage through histological analyses and examination of blood-brain barrier permeability and brain edema. Next, we investigated the antioxidative effects of YL-0919 by assessing the levels of traditional markers of oxidative stress in vivo in mice and in vitro in HT22 cells. Finally, the targeted action of YL-0919 was verified by employing a sigma-1 receptor antagonist (BD-1047). Our findings demonstrated that YL-0919 markedly improved deficits in motor function and spatial cognition on day 3 post traumatic brain injury, while also decreasing neuronal mortality and reversing blood–brain barrier disruption and brain edema. Furthermore, YL-0919 effectively combated oxidative stress both in vivo and in vitro. The protective effects of YL-0919 were partially inhibited by BD-1047. These results indicated that YL-0919 relieved impairments in motor and spatial cognition by restraining oxidative stress, a neuroprotective effect that was partially reversed by the sigma-1 receptor antagonist BD-1047. YL-0919 may have potential as a new treatment for traumatic brain injury.

2025-08-01·Neural Regeneration Research

Neuroprotective potential for mitigating ischemia-reperfusion-induced damage

Article

作者: Zuo, Aizhen ; Sun, Huiqi ; Liu, Runqing ; Ye, Zi ; Wang, Nan ; Wang, Hangxing ; Jin, Cen ; Feng, Luqian ; Yang, Hua

Reperfusion following cerebral ischemia causes both structural and functional damage to brain tissue and could aggravate a patient’s condition; this phenomenon is known as cerebral ischemia-reperfusion injury. Current studies have elucidated the neuroprotective role of the sirtuin protein family (Sirtuins) in modulating cerebral ischemia-reperfusion injury. However, the potential of utilizing it as a novel intervention target to influence the prognosis of cerebral ischemia-reperfusion injury requires additional exploration. In this review, the origin and research progress of Sirtuins are summarized, suggesting the involvement of Sirtuins in diverse mechanisms that affect cerebral ischemia-reperfusion injury, including inflammation, oxidative stress, blood–brain barrier damage, apoptosis, pyroptosis, and autophagy. The therapeutic avenues related to Sirtuins that may improve the prognosis of cerebral ischemia-reperfusion injury were also investigated by modulating Sirtuins expression and affecting representative pathways, such as nuclear factor-kappa B signaling, oxidative stress mediated by adenosine monophosphate-activated protein kinase, and the forkhead box O. This review also summarizes the potential of endogenous substances, such as RNA and hormones, drugs, dietary supplements, and emerging therapies that regulate Sirtuins expression. This review also reveals that regulating Sirtuins mitigates cerebral ischemia-reperfusion injury when combined with other risk factors. While Sirtuins show promise as a potential target for the treatment of cerebral ischemia-reperfusion injury, most recent studies are based on rodent models with circadian rhythms that are distinct from those of humans, potentially influencing the efficacy of Sirtuins-targeting drug therapies. Overall, this review provides new insights into the role of Sirtuins in the pathology and treatment of cerebral ischemia-reperfusion injury.