Neurotherapeutics最新文献

Nervonic acid supplementation mitigates disease severity biomarkers in adrenoleukodystrophy. 补充神经酸可减轻肾上腺脑白质营养不良患者的疾病严重程度生物标志物。

IF 6.9 2区医学

Neurotherapeutics Pub Date : 2026-04-07 DOI: 10.1016/j.neurot.2026.e00890

Chenxu Li, Kai Braaten, Ann B Moser, Wedad Fallatah, Maggie Lorentson, Suzette Huguenin, Anna Torrey, Marcia R Terluk, Willa Durose, Erin Nolan, Christopher Staley, Subbaya Subramanian, Troy C Lund, Reena V Kartha

{"title":"Nervonic acid supplementation mitigates disease severity biomarkers in adrenoleukodystrophy.","authors":"Chenxu Li, Kai Braaten, Ann B Moser, Wedad Fallatah, Maggie Lorentson, Suzette Huguenin, Anna Torrey, Marcia R Terluk, Willa Durose, Erin Nolan, Christopher Staley, Subbaya Subramanian, Troy C Lund, Reena V Kartha","doi":"10.1016/j.neurot.2026.e00890","DOIUrl":"https://doi.org/10.1016/j.neurot.2026.e00890","url":null,"abstract":"<p><p>X-linked adrenoleukodystrophy (ALD) is a severe neurometabolic disorder caused by mutations in the ABCD1 gene, leading to impaired peroxisomal β-oxidation of very long-chain fatty acids (VLCFAs). The accumulation of saturated VLCFAs, predominantly C26:0, in plasma and across all tissues, contributes to adrenal dysfunction and progressive neurodegeneration. No approved therapy addresses the diverse spectrum of ALD manifestations, underscoring the urgent need for safe, accessible, and preventive treatments. Nervonic acid (NA), a monounsaturated fatty acid, is potentially beneficial for ALD through its neuroprotective effects. Here, we report the safety and therapeutic efficacy of NA in a 4-week dietary intervention study using a mouse model of ALD. NA treatment significantly decreased plasma C26:0-lysophosphatidylcholine, a diagnostic and disease-severity biomarker of ALD, by about 60% as early as one week after intervention. After 4-week treatment, NA markedly reduced free C26:0 and total saturated VLCFA levels in plasma and tissues. Moreover, we observed approximately 56% reduction in brain C26:0-lysophosphatidylcholine levels in NA-fed mice, an effect not reported with other drug intervention. Through comparative microbiome analysis, we show for the first time distinct baseline differences between ALD and wild-type mice, with dietary fatty acid supplementation preventing further dysbiosis. No adverse effects on body weight or food intake were observed throughout the study. Overall, this is the first report demonstrating that an oral dietary fatty acid can ameliorate the hallmark biochemical abnormalities of ALD in plasma and brain, highlighting its potential as a safe and effective therapy, particularly for presymptomatic individuals carrying this genetic defect.</p>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":" ","pages":"e00890"},"PeriodicalIF":6.9,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147639473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The wearing-off effect with natalizumab: Back to the drawing board 纳塔利珠单抗的药效消退：从头开始。

IF 6.9 2区医学

Neurotherapeutics Pub Date : 2026-04-01 Epub Date: 2026-04-10 DOI: 10.1016/j.neurot.2026.e00903

Saira Afzal, Devon S. Conway

引用次数: 0

Neuromodulation of the central nervous system for facial pain 中枢神经系统对面部疼痛的神经调节。

IF 6.9 2区医学

Neurotherapeutics Pub Date : 2026-04-01 Epub Date: 2026-04-11 DOI: 10.1016/j.neurot.2026.e00902

Jason Yuen , Aaron Loh , Ghazaleh Darmani , Can Sarica , Nikunj Patel , Andres M. Lozano , Mojgan Hodaie

{"title":"Neuromodulation of the central nervous system for facial pain","authors":"Jason Yuen , Aaron Loh , Ghazaleh Darmani , Can Sarica , Nikunj Patel , Andres M. Lozano , Mojgan Hodaie","doi":"10.1016/j.neurot.2026.e00902","DOIUrl":"10.1016/j.neurot.2026.e00902","url":null,"abstract":"<div><div>Chronic craniofacial pain can lead to significant morbidity and reduced quality-of-life. Refractory pain subsequently leads to maladaptive changes within the central nervous system (CNS). It is logical to consider modulation of implicated neural networks to mitigate or reverse these changes in order to alleviate suffering. In this report, we reviewed the current literature in neuromodulation of CNS in facial pain treatment. We conducted PRISMA-compliant systematic review using MEDLINE and EMBASE databases. We included studies applying stimulation to the CNS to treat facial pain. Demographic data, design, duration, participants, clinical details, outcomes, adverse effects were extracted. Out of 1005 unique publications, 57 were included for analysis. Main techniques included were transcranial direct current stimulation (tDCS), repetitive transcranial magnetic stimulation (rTMS), motor cortex stimulation (MCS), deep brain stimulation (DBS), and spinal cord stimulation (SCS). For tDCS, rTMS, and MCS, the main stimulation target was primary motor cortex; while several different DBS targets (e.g., thalamic nuclei, anterior cingulate cortex, periaqueductal grey matter) were studied. While most studies showed improvement in Numeric Rating Scale for pain, values range widely from 11.1% in one MCS study to 90% in one rTMS study, with majority within 20–60%. There is heterogeneity across research designs, including patient selection, outcome measures, and follow-up. Standardized reporting framework is required to allow direct comparison between different modalities within subgroups of facial pain patients.</div></div>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":"23 3","pages":"Article e00902"},"PeriodicalIF":6.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147675350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Involvement of trimethylamine N-oxide in major depressive disorder via astrocytic d-Serine dysregulation 三甲胺n -氧化物通过星形细胞d-丝氨酸失调参与重度抑郁症。

IF 6.9 2区医学

Neurotherapeutics Pub Date : 2026-04-01 Epub Date: 2026-04-15 DOI: 10.1016/j.neurot.2026.e00909

Liwang Lin , Longyu Li , Shiao Ren , Liping Liu , Ying Liu , Wenlei Zhang , Zengliang Gao , Xiaoting Ni , Haoxuan Li , Xinsheng Duan , Sijing Tao , Tianyu Zhao , Xin Hai

{"title":"Involvement of trimethylamine N-oxide in major depressive disorder via astrocytic d-Serine dysregulation","authors":"Liwang Lin , Longyu Li , Shiao Ren , Liping Liu , Ying Liu , Wenlei Zhang , Zengliang Gao , Xiaoting Ni , Haoxuan Li , Xinsheng Duan , Sijing Tao , Tianyu Zhao , Xin Hai","doi":"10.1016/j.neurot.2026.e00909","DOIUrl":"10.1016/j.neurot.2026.e00909","url":null,"abstract":"<div><div>Trimethylamine N-oxide (TMAO), a co-metabolite of the gut microbiota and host, has been implicated in the pathogenesis of various neuropsychiatric disorders. However, its role in major depressive disorder (MDD) remains poorly understood. This study aims to verify the relationship between TMAO and MDD and elucidate the underlying mechanisms. Plasma TMAO concentrations were quantified by HPLC-MS/MS and compared between MDD patients and healthy controls. To explore the effects of TMAO on depressive-like behavior and cerebral <span>d</span>-serine metabolism, mice were administered TMAO via dietary supplementation. Finally, astrocytes were treated with TMAO to examine its impact on <span>d</span>-serine metabolism at the cellular level. Here, we found that plasma TMAO levels were significantly elevated in MDD patients and positively correlated with both HAMD-17 and HAMA-14 scores. Consistently, mice fed TMAO for seven weeks exhibited pronounced depressive-like behaviors. While TMAO exposure did not induce apparent astrocytic damage, it markedly promoted <span>d</span>-serine secretion and caused notable neuronal injury. Mechanistically, TMAO activated the AMPK/SIRT-1 signaling pathway in astrocytes, resulting in upregulated serine racemase expression. Furthermore, both exogenous <span>d</span>-serine and conditioned medium from TMAO-treated astrocytes triggered neuronal apoptosis. Collectively, these findings demonstrate that TMAO contributes to MDD pathogenesis by activating astrocytic AMPK/SIRT-1 signaling to enhance <span>d</span>-serine production, subsequently inducing neuronal apoptosis. TMAO may thus represent a promising therapeutic target for MDD.</div></div>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":"23 3","pages":"Article e00909"},"PeriodicalIF":6.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147698547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Leptin antagonism improves Rett syndrome phenotype in symptomatic Mecp2-deficient mice 瘦素拮抗剂改善症状性mecp2缺陷小鼠Rett综合征表型

IF 6.9 2区医学

Neurotherapeutics Pub Date : 2026-04-01 Epub Date: 2026-04-18 DOI: 10.1016/j.neurot.2026.e00910

Yasmine Belaïdouni , Diabe Diabira , Pascal Salin , Mélanie Brosset-Heckel , Victoria Valsamides , Jean-Charles Graziano , Catarina Santos , Clément Menuet , Gary A. Wayman , Jean-Luc Gaiarsa

{"title":"Leptin antagonism improves Rett syndrome phenotype in symptomatic Mecp2-deficient mice","authors":"Yasmine Belaïdouni , Diabe Diabira , Pascal Salin , Mélanie Brosset-Heckel , Victoria Valsamides , Jean-Charles Graziano , Catarina Santos , Clément Menuet , Gary A. Wayman , Jean-Luc Gaiarsa","doi":"10.1016/j.neurot.2026.e00910","DOIUrl":"10.1016/j.neurot.2026.e00910","url":null,"abstract":"<div><div>Rett syndrome (RTT) is a severe X-linked neurodevelopmental disorder caused by mutations in <em>MECP2</em>. Elevated circulating levels of the adipocyte hormone leptin are consistently observed in patients and in mouse models, yet their contribution to disease progression has remained unclear. Here, we show that reducing leptin signaling—either pharmacologically or genetically—significantly alleviates RTT-like phenotypes in <em>Mecp2</em>-deficient mice. In males, these interventions preserved general health, prevented weight loss, and improved breathing and locomotor functions. At the neuronal level, they restored excitatory/inhibitory balance in the hippocampus and somatosensory cortex and rescued hippocampal synaptic plasticity. In females, delaying the pathological rise of leptin levels postponed symptom progression. These findings uncover leptin as a key contributor to RTT pathophysiology and position leptin-targeted interventions as a promising therapeutic strategy for this currently untreatable disorder.</div></div>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":"23 3","pages":"Article e00910"},"PeriodicalIF":6.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147703254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Telomerase mRNA-Lipid nanoparticles attenuate neuroinflammation after traumatic brain injury in mice 端粒酶mrna -脂质纳米颗粒减轻小鼠创伤性脑损伤后的神经炎症

IF 6.9 2区医学

Neurotherapeutics Pub Date : 2026-04-01 Epub Date: 2026-05-08 DOI: 10.1016/j.neurot.2026.e00917

Goknur Kara , Morgan Holcomb , Anjana Tiwari , Hannah Flinn , Trinity Eimer , Austin Marshall , Marissa Burke , Peter Park , Karem A. Court , John P. Cooke , Biana Godin , Sonia Villapol

{"title":"Telomerase mRNA-Lipid nanoparticles attenuate neuroinflammation after traumatic brain injury in mice","authors":"Goknur Kara , Morgan Holcomb , Anjana Tiwari , Hannah Flinn , Trinity Eimer , Austin Marshall , Marissa Burke , Peter Park , Karem A. Court , John P. Cooke , Biana Godin , Sonia Villapol","doi":"10.1016/j.neurot.2026.e00917","DOIUrl":"10.1016/j.neurot.2026.e00917","url":null,"abstract":"<div><div>Traumatic brain injury (TBI) is a leading cause of chronic neurological disability, yet no disease-modifying therapy exists. Emerging evidence indicates that TBI activates cellular aging programs, including telomere erosion and persistent inflammation, that contribute to progressive neurodegeneration. Telomerase reverse transcriptase (TERT) maintains telomere homeostasis and provides cytoprotective effects in the central nervous system but it has not been therapeutically targeted after TBI. Here, we developed an mRNA nanotherapy consisting of mouse TERT mRNA encapsulated in lipid nanoparticles (mTERT-LNPs) and evaluated it in a mouse model of moderate TBI. We first established that TBI transiently disrupts TERT biology, with reduced cortical TERT mRNA and shortened telomeres at 3 days post-injury (dpi), followed by partial recovery by 14 dpi. mTERT-LNPs were well tolerated <em>in vitro</em> and <em>in vivo</em>. Following intravenous delivery in the acute post-injury window, LNPs localized to the injured brain and displayed expected peripheral biodistribution. A single systemic dose increased cortical TERT mRNA and protein and partially restored telomere length at 3 dpi. TERT mRNA delivery significantly reduced Iba1+ microglial activation and suppressed pro-inflammatory cytokines. Systemically, mTERT-LNPs lowered serum C-reactive protein indicating reduced peripheral inflammation, without adverse effects on peripheral organs. Several outcomes showed sex-dependent patterns. Collectively, these data provide the first <em>in vivo</em> evidence that telomerase therapy can modulate telomere biology and neuroinflammation after TBI, supporting mRNA-LNP-mediated TERT restoration as a scalable, mechanistically grounded strategy for disease modification in TBI and related disorders.</div></div>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":"23 3","pages":"Article e00917"},"PeriodicalIF":6.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147849972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Neuroprotective therapy after traumatic brain injury: does the window for treatment extend for months? 创伤性脑损伤后的神经保护治疗：治疗的窗口期是否延长数月？

IF 6.9 2区医学

Neurotherapeutics Pub Date : 2026-04-01 Epub Date: 2026-04-13 DOI: 10.1016/j.neurot.2026.e00908

Cillian Lynch PhD, Ramon Diaz-Arrastia MD, PhD

引用次数: 0

The EGR1/ZFP36 axis governs glycosphingolipid metabolic reprogramming in monocyte-derived macrophages in guillain-barré syndrome EGR1/ZFP36轴调控格林-巴氏综合征中单核细胞源性巨噬细胞的糖鞘脂代谢重编程。

IF 6.9 2区医学

Neurotherapeutics Pub Date : 2026-04-01 Epub Date: 2026-03-30 DOI: 10.1016/j.neurot.2026.e00895

Meng Li , Qiaoming Liu , Weixi Chen , Fangchao Jiang , Jihe Song , Xinshu Du , Feihong Jia , Xinrui Wang , Shuanghong Sun , Baichao Han , Weihe Liu , Yuan Chen , Guangyou Wang , Di Zhong

{"title":"The EGR1/ZFP36 axis governs glycosphingolipid metabolic reprogramming in monocyte-derived macrophages in guillain-barré syndrome","authors":"Meng Li , Qiaoming Liu , Weixi Chen , Fangchao Jiang , Jihe Song , Xinshu Du , Feihong Jia , Xinrui Wang , Shuanghong Sun , Baichao Han , Weihe Liu , Yuan Chen , Guangyou Wang , Di Zhong","doi":"10.1016/j.neurot.2026.e00895","DOIUrl":"10.1016/j.neurot.2026.e00895","url":null,"abstract":"<div><div>Guillain-Barré syndrome (GBS) is an immune-mediated demyelinating disorder of peripheral nerves with an unclear pathogenesis. This study integrated GBS clinical single-cell data with EAN model transcriptome data, establishing <em>in vivo</em> and <em>in vitro</em> experimental systems to reveal, for the first time, a novel mechanism involving EGR1-ZFP36 and its mediated metabolic reprogramming in GBS pathogenesis. Findings indicated that the transcription factor EGR1 and its predicted target gene ZFP36 were downregulated in both GBS patients and EAN rats. Molecular interaction validation confirmed that EGR1 directly bound to and activated the transcription of ZFP36. Transcriptomic and metabolomic analyses revealed that the EGR1/ZFP36 axis specifically drove macrophage reprogramming toward a glycosphingolipid metabolism-active state. Functionally, EGR1 overexpression promoted the expression of key glycosphingolipid metabolism genes (HEXA, HEXB) by upregulating ZFP36, thereby facilitating polarization toward the anti-inflammatory M2 phenotype. Animal experiments further demonstrated that EGR1 overexpression improved motor function and ameliorated myelin damage in the EAN model, with this protective effect being mediated by ZFP36. Collectively, this study reveals that EGR1 drives glycosphingolipid metabolic reprogramming in monocyte-derived macrophages by transcriptionally activating ZFP36, thereby regulating cellular polarization and participating in the demyelination process of GBS. This discovery not only provides a novel perspective on understanding the immunometabolic mechanisms of GBS but also lays a theoretical foundation for potential therapeutic strategies targeting the EGR1-ZFP36-glycosphingolipid metabolism axis.</div></div>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":"23 3","pages":"Article e00895"},"PeriodicalIF":6.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147593492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bilateral intermittent theta burst stimulation over the primary motor cortex improves motor and affective symptoms via thalamic network reintegration in mid-stage Parkinson's disease 初级运动皮层的双侧间歇性θ波爆发刺激通过丘脑网络重新整合改善中期帕金森病的运动和情感症状。

IF 6.9 2区医学

Neurotherapeutics Pub Date : 2026-04-01 Epub Date: 2026-04-28 DOI: 10.1016/j.neurot.2026.e00911

Paloma Macías-García , Raúl Rashid-López , Álvaro J. Cruz-Gómez , Francisco L. Sánchez-Fernández , Esteban Sarrias-Arrabal , Fátima Cano-Cano , Elena Lozano-Soto , Florencia Sanmartino , Raúl Espinosa-Rosso , Javier J. González-Rosa

{"title":"Bilateral intermittent theta burst stimulation over the primary motor cortex improves motor and affective symptoms via thalamic network reintegration in mid-stage Parkinson's disease","authors":"Paloma Macías-García , Raúl Rashid-López , Álvaro J. Cruz-Gómez , Francisco L. Sánchez-Fernández , Esteban Sarrias-Arrabal , Fátima Cano-Cano , Elena Lozano-Soto , Florencia Sanmartino , Raúl Espinosa-Rosso , Javier J. González-Rosa","doi":"10.1016/j.neurot.2026.e00911","DOIUrl":"10.1016/j.neurot.2026.e00911","url":null,"abstract":"<div><div>Bilateral intermittent theta burst stimulation (iTBS) targeting the primary motor cortex (M1) has emerged as a promising neuromodulatory approach for Parkinson's disease (PD), although evidence supporting its clinical efficacy as an adjunctive treatment remains limited. This randomized, double-blind, sham-controlled crossover study examined the therapeutic potential of bilateral M1-iTBS in fifteen patients with mid-stage PD in the on-medication state. Motor, neuropsychiatric, and cognitive outcomes were assessed through standardized clinical scales following five iTBS sessions, alongside voxelwise resting-state functional magnetic resonance imaging, to identify neural-related mechanisms. Real iTBS induced a maximum improvement of nine points on the Movement Disorder Society-Unified PD Rating Scale part III, with clinical responders (≥20% improvement) demonstrating an eleven-point enhancement. Responders exhibited strengthened cerebello-thalamic and thalamo-cortical connectivity, suggesting partial thalamic functional reintegration with associative cortices and compensatory functional reorganization, which correlated significantly with reduced bradykinesia. Additionally, real iTBS produced clinically meaningful improvement in affective symptomatology in depression and anxiety responder patients, accompanied by modulation of top-down and bottom-up emotion regulation circuits and normalization of cerebellar activity. These findings support bilateral M1-iTBS as an effective adjunctive intervention for managing motor and nonmotor manifestations in patients with mid-stage PD, with mechanistic insights provided by symptom-related functional connectivity changes.</div></div>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":"23 3","pages":"Article e00911"},"PeriodicalIF":6.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147777183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Feasibility and safety of vertebrobasilar artery cooling infusion (VACI) following thrombectomy for acute posterior circulation ischemic stroke: A pilot randomized controlled trial 急性后循环缺血性脑卒中取栓后椎基底动脉冷却输注（VACI）的可行性和安全性：一项随机对照试验

IF 6.9 2区医学

Neurotherapeutics Pub Date : 2026-04-01 Epub Date: 2026-04-02 DOI: 10.1016/j.neurot.2026.e00894

Zhe Cheng , Yuchuan Ding , Gary Rajah , Jie Gao , Fenghai Li , Linlin Ma , Jing Liu , Xiaokun Geng

{"title":"Feasibility and safety of vertebrobasilar artery cooling infusion (VACI) following thrombectomy for acute posterior circulation ischemic stroke: A pilot randomized controlled trial","authors":"Zhe Cheng , Yuchuan Ding , Gary Rajah , Jie Gao , Fenghai Li , Linlin Ma , Jing Liu , Xiaokun Geng","doi":"10.1016/j.neurot.2026.e00894","DOIUrl":"10.1016/j.neurot.2026.e00894","url":null,"abstract":"<div><div>Not all patients with acute ischemic stroke (AIS) benefit from endovascular therapy (EVT), particularly in the posterior circulation. This pilot randomized controlled trial evaluated the safety, feasibility, and preliminary efficacy of vertebrobasilar artery cooling infusion (VACI) administered after successful recanalization as a neuroprotective strategy for posterior circulation AIS. Participants were randomly assigned (1:1) to VACI or control. The VACI group received 300 mL of 4 °C saline infused into the vertebral artery at 30 mL/min after thrombectomy, whereas controls received 300 mL of 37 °C saline. All patients received standard guideline-based care. The primary endpoint was symptomatic intracranial hemorrhage (sICH). Secondary endpoints included functional outcomes, infarct volume, mortality, intracranial hemorrhage (ICH), vasospasm, coagulation abnormalities, pneumonia, and urinary tract infection. VACI following EVT appears safe and feasible in posterior circulation AIS and may offer potential neuroprotective benefit. Forty patients were enrolled and analyzed. The incidence of sICH did not differ between groups. Rates of neurological deterioration and other complications were comparable. Favorable trends were observed in the VACI group, including improved early neurological recovery (median NIHSS 6 vs. 12.5) and smaller final infarct volume (9.0 vs. 17.5 mL). Mortality was numerically lower in the VACI group at 90 days (10.0% vs. 20.0%) and at 7 days (5.0% vs. 20.0%). Although differences were not statistically significant, outcomes consistently favored VACI. VACI following EVT appears safe and feasible in posterior circulation AIS and may offer potential neuroprotective benefit.</div></div>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":"23 3","pages":"Article e00894"},"PeriodicalIF":6.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147601994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0