Translational Stroke Research最新文献

{"title":"Transcarotid Artery Revascularization for Asymptomatic Carotid Stenosis: A Systematic Review and Meta-Analysis.","authors":"Zhi-Cheng Jiang, Qi-Fei Hu, Jia-Ming Huang, Xian-Wei Wang, Tong Lin, Xi-Lin Gao, Jia-Wen Cui, Jing-Lin Zhao, Dong Chen, Shu-Peng Li","doi":"10.1007/s12975-026-01457-2","DOIUrl":"10.1007/s12975-026-01457-2","url":null,"abstract":"<p><p>Management of asymptomatic carotid stenosis remains controversial despite advances in contemporary best medical therapy. Transcarotid artery revascularization (TCAR) has been introduced as an alternative revascularization option alongside carotid endarterectomy (CEA) and transfemoral carotid artery stenting (TF-CAS). Evidence focused specifically on asymptomatic carotid disease, however, remains limited and is derived mainly from observational analyses of clinical databases, with only a small amount of single-center retrospective evidence. The present study therefore examined the available comparative evidence on TCAR for asymptomatic carotid stenosis. A systematic review and meta-analysis was performed of studies reporting outcomes of TCAR in asymptomatic carotid stenosis. Eligible studies included asymptomatic cohorts or mixed populations with extractable asymptomatic subgroup data and reported outcomes after TCAR with comparison against CEA and/or TF-CAS. The primary pooled outcomes were stroke, death, stroke or death, and myocardial infarction at 30 days, together with the corresponding stroke, death, and stroke or death outcomes at approximately 1 year. For TCAR versus CEA, no significant between-group differences were identified in the pooled 30-day risks of stroke (risk ratio (RR), 1.25; 95% CI, 0.98-1.59; I²=82%), death (RR, 0.94; 95% CI, 0.64-1.38; I²=57%), or stroke or death (RR, 1.10; 95% CI, 0.95-1.26; I²=75%). In contrast, myocardial infarction within 30 days occurred less frequently after TCAR (RR, 0.68; 95% CI, 0.48-0.96; I²=71%). At approximately 1 year, pooled estimates likewise showed no significant difference in stroke (RR, 1.27; 95% CI, 0.70-2.29; I²=0%) or death (RR, 1.14; 95% CI, 0.97-1.35; I²=0%), whereas the pooled estimate for stroke or death favored CEA (RR, 1.25; 95% CI, 1.15-1.36; I²=31%). A different pattern emerged in the TCAR versus TF-CAS comparison. TCAR was associated with significantly lower pooled 30-day risks of stroke (RR, 0.60; 95% CI, 0.48-0.73; I²=0%), death (RR, 0.55; 95% CI, 0.38-0.81; I²=20%), and stroke or death (RR, 0.60; 95% CI, 0.52-0.70; I²=6%), while no significant difference was observed for 30-day myocardial infarction (RR, 0.91; 95% CI, 0.65-1.29; I²=44%). At approximately 1 year, stroke remained comparable between the 2 groups (RR, 0.75; 95% CI, 0.46-1.23; I²=26%), whereas death (RR, 1.09; 95% CI, 1.00-1.20; I²=66%) and stroke or death (RR, 0.79; 95% CI, 0.71-0.87; I²=45%) differed, with the pooled stroke-or-death estimate favoring TCAR. Current observational evidence suggests that TCAR compares favorably with TF-CAS in asymptomatic carotid stenosis. When compared with CEA, TCAR does not appear to provide a clear benefit in pooled perioperative neurologic outcomes, although myocardial infarction may occur less frequently after TCAR.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":"17 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13249911/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148206201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Remote Ischemic Postconditioning Attenuates Neuroinflammation and Suggests a Potential Benefit for Early Neurological Recovery after Subarachnoid Hemorrhage via the IL-9/JAK2-STAT5 Signaling Pathway.","authors":"Yajun Zhu, Bo Zeng, Zichao Huang, Daochen Wen, Xiaoguo Li, Fuming Liang, Zongduo Guo","doi":"10.1007/s12975-026-01455-4","DOIUrl":"10.1007/s12975-026-01455-4","url":null,"abstract":"<p><p>Subarachnoid hemorrhage (SAH) often leads to cognitive impairment, in which neuroinflammation plays a pivotal role. While remote ischemic postconditioning (RIPostC) has demonstrated neuroprotective potential, its clinical efficacy and underlying mechanisms remain incompletely defined. This study identified interleukin-9 (IL-9) as a key mediator of RIPostC's effects through an integrated clinical and basic research approach. In a prospective proof-of-concept clinical trial, RIPostC was associated with improved early neurological recovery and significantly upregulated serum IL-9 levels in SAH patients. It suggests a potential clinical benefit that warrants further validation. Using a murine SAH model, results showed RIPostC improved cognitive function, suppressed pro-inflammatory cytokines (IL-1β, IL-6), and elevated anti-inflammatory cytokines (IL-9, IL-10). Mechanistically, RIPostC activated the JAK2/STAT5 signaling pathway. Immunofluorescence revealed specific expression of the IL-9 receptor (IL-9R) on microglia. In vitro experiments using BV2 microglial cells confirmed that IL-9 directly promotes microglial polarization towards an anti-inflammatory M2 phenotype and enhances IL-10 production via the JAK2/STAT5 pathway. Collectively, these preliminary findings suggest that RIPostC alleviates neuroinflammation and cognitive impairment after SAH, a process mechanistically linked to the upregulation of IL-9 and subsequent activation of the JAK2/STAT5 pathway in microglia. This study positions IL-9 as a promising therapeutic target for SAH.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":"17 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148206196","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}

{"title":"Impaired Glymphatic Function and Post-stroke Cognitive Decline after Intracerebral Hemorrhage: A Serial Neuroimaging Study.","authors":"Nina H Nariman, Md Faruk Hossain, Khader M Hasan, Vahed Maroufy, Seth B Boren, Spencer Solberg, Robert Suchting, Clark Sitton, Sean I Savitz, Muhammad E Haque","doi":"10.1007/s12975-026-01453-6","DOIUrl":"10.1007/s12975-026-01453-6","url":null,"abstract":"<p><p>After an intracerebral hemorrhage (ICH), impaired glymphatic function (GF) can result in neurotoxin buildup in the brain. In this serial MRI imaging study, we investigated the association between impaired GF and post-stroke cognitive impairment (PSCI). The glymphatic system is a waste clearance mechanism in the brain, consisting of the perivascular space (PVS) formed by astroglial end-feet surrounding arteries and veins. Glymphatic dysfunction has been associated with cognitive decline in patients with neurodegenerative diseases. The diffusion tensor imaging along the perivascular space (DTI-ALPS) index is a non-invasive imaging biomarker to monitor GF. The progression of PSCI in patients after ICH has not been well reported. Here, we serially evaluated GF via measuring the DTI-ALPS index and its association with PSCI after ICH. We serially imaged 18 patients with deep ICH at 9.3 ± 9.1 (V1) and 109 ± 28 (V2) days after stroke on a 3T MRI system. Cognitive assessment and stroke severity were obtained via the Montreal Cognitive Assessment (MoCA) and NIHSS, respectively. The DTI-ALPS index was calculated by measuring diffusivity in three regions of interest (ROI) orthogonal to the PVS surrounding the medullary veins. Hematoma (HV) and edema (EV) volumes were measured. The ipsilesional DTI-ALPS index was correlated with MoCA, HV, and NIHSS. The contralesional DTI-ALPS index was used as a control. Normality of all continuous variables was assessed using the Shapiro-Wilk test. As several key variables were non-normally distributed, non-parametric analyses were used, including Wilcoxon signed-rank tests for paired comparisons, Mann-Whitney U tests for group comparisons, and partial Spearman rank correlations (rS) to examine associations between the DTI-ALPS index and clinical or volumetric measures while adjusting for age and hematoma volume. We enrolled 12 M/6F with an average age of 49 ± 13y. The ipsilesional DTI-ALPS index was significantly lower than the contralesional DTI-ALPS index (p = 0.041) at V2. Temporally, NIHSS (median [IQR] 8.5 [1.0-13.8] to 2.5 [1.0-4.0], p = 0.002), HV (5.03 [3.31-12.62] to 1.28 [0.80-2.73] mL, p < 0.001), and EV (20.34 [9.62-35.44] to 1.09 [0.41-4.79] mL, p < 0.001) were significantly decreased. After adjustment for age and hematoma volume using partial Spearman correlation, the ipsilesional DTI-ALPS index showed a near-significant negative association with NIHSS (partial rS = - 0.48, p = 0.057) and a positive but non-significant association with MoCA (partial rS = 0.28, p = 0.301) at V2. Our finding demonstrated that the DTI-ALPS index is a feasible imaging biomarker for assessing glymphatic dysfunction and it is positively associated with cognitive impairment following intracerebral hemorrhage.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":"17 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148200126","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}

{"title":"Lysophosphatidic Acid Reduces Ischemic Brain Injury by Attenuating Vascular Permeability Through LPA4 Receptor Signaling.","authors":"Shintaro Yamada, Kazuhiro Takara, Naoi Hosoe, Anna Shimizu, Yumiko Hayashi, Lamri Lynda, Takayuki Sonoda, Kenichiro Kikuta, Hiroyasu Kidoya","doi":"10.1007/s12975-026-01451-8","DOIUrl":"10.1007/s12975-026-01451-8","url":null,"abstract":"<p><p>Blood-brain barrier (BBB) disruption significantly exacerbates secondary injury following ischemic stroke. Although lysophosphatidic acid (LPA) is known to regulate vascular stability, its specific role in preserving BBB integrity during cerebral ischemia remains unclear. Here, we investigated the neuroprotective effects of LPA using a mouse model of distal middle cerebral artery occlusion (dMCAO). Eight- to ten-week-old female C57BL/6 mice received 10 mg/kg LPA intraperitoneally immediately after ischemia, and outcomes were assessed at 48 h after dMCAO via infarct volumetry, edema quantification, BBB permeability assays (Evans blue and FITC-dextran), and transcriptomic analyses. We demonstrate that LPA treatment significantly reduced infarct volume by approximately 60% and attenuated cerebral edema at 48 h post-ischemia; This protection was accompanied by preserved BBB integrity and maintained endothelial claudin-5 expression in the ischemic territory. Single-cell analysis identified selective and sustained expression of the LPA4 receptor in ischemic vascular endothelial cells. Crucially, the protective effects of LPA on infarct size and BBB permeability were abolished in LPA4 receptor-knockout mice. These findings indicate that LPA preserves BBB integrity and mitigates ischemic brain injury via an endothelial LPA4 receptor-dependent mechanism, identifying the LPA-LPA4 signaling axis as a promising therapeutic target for reducing secondary brain injury in ischemic stroke.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":"17 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13230236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148144928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intercellular Mitochondrial Transfer as Endogenous Neuroprotection: Mechanisms and Therapeutic Implications in Ischemic Stroke.","authors":"Yun-Fan Zhang, Di Zhao, Jing-Jing Wei, Xiao Liang, Liu-Ding Wang, Jia-Wei Wang, Li-Bin Jiang, Ju-Ying Chen, Yun-Ling Zhang, Yue Liu","doi":"10.1007/s12975-026-01446-5","DOIUrl":"10.1007/s12975-026-01446-5","url":null,"abstract":"<p><p>Ischemic stroke remains a leading cause of mortality and disability worldwide. Current reperfusion therapies are limited by narrow therapeutic time windows and the risk of secondary reperfusion injury, underscoring the urgent need for novel translatable neuroprotective targets. Mitochondrial dysfunction serves as a central hub in the ischemic cascade, contributing to energy failure, oxidative stress, calcium dysregulation, and various forms of programmed cell death. Recently, intercellular mitochondrial transfer has emerged as a crucial form of metabolic communication within the neurovascular unit (NVU). In the context of ischemia-reperfusion, donor cells can transfer functional mitochondria to compromised cells, facilitating metabolic rescue and remodeling the local microenvironment. Extensive in vivo and in vitro studies have shown that astrocytes, mesenchymal stem cells (MSCs), and pericytes can deliver mitochondria to neurons or brain microvascular endothelial cells (BMECs) through mechanisms such as tunneling nanotubes (TNTs), extracellular vesicles (EVs), and gap junctions. This transfer helps maintain blood-brain barrier (BBB) integrity and promotes neurological recovery. The process is finely regulated by inflammatory signaling, metabolic reprogramming, and epigenetic modulation, all of which influence the directionality and functional outcomes of the transfer. As a result, pharmacotherapies, non-pharmacological interventions, and direct mitochondrial transplantation have demonstrated considerable neuroprotective potential in experimental models and early-stage clinical research. However, challenges related to transfer selectivity, the durability of effects, delivery efficiency, and immune safety still hinder clinical translation. Future efforts must prioritize elucidating the underlying mechanisms, standardizing protocols, and developing precise stratification strategies to advance mitochondrial transfer-based interventions from proof-of-concept to a controllable and evaluable therapeutic option for stroke treatment.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":"17 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13216090/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148043952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: Implication of MicroRNA503 in Brain Endothelial Cell Function and Ischemic Stroke.","authors":"Huiting Zhang, Qunwen Pan, Zi Xie, Yanyu Chen, Jinju Wang, Ji Bihl, Wangtao Zhong, Yanfang Chen, Bin Zhao, Xiaotang Ma","doi":"10.1007/s12975-026-01449-2","DOIUrl":"10.1007/s12975-026-01449-2","url":null,"abstract":"","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":"17 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148044008","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}

{"title":"Neuroinflammation in Ischemic Stroke: Mechanisms, Systemic Interactions, and Therapeutic Targets.","authors":"Eduardo Soares, Willeke F Westendorp, Jonathan M Coutinho, Matthijs C Brouwer, Diederik van de Beek","doi":"10.1007/s12975-026-01442-9","DOIUrl":"10.1007/s12975-026-01442-9","url":null,"abstract":"<p><p>Ischemic stroke is the second leading cause of death worldwide and its global burden is predicted to increase over the upcoming decades. Acute therapies primarily focus on recanalization of the occluded blood vessels by intravenous thrombolysis and endovascular thrombectomy, but these therapies are not suitable for all patients. Also, in case of successful reperfusion, there remains a risk of secondary tissue damage known as ischemia-reperfusion injury. Inflammation plays a crucial role in both the infarcted tissue and ischemia-reperfusion injury after stroke. Innate and adaptive immune systems may drive an exacerbated inflammatory response after stroke, impacting patients' outcome. Research in stroke pathophysiology and the role of the immune system after stroke suggests that outcome may be improved by using immune-based therapies preventing this secondary tissue damage. Here we display a comprehensive description of chronological immune events at the cellular and molecular levels in different compartments after stroke and discuss the potential neuroprotective role of regulatory T cells (T_regs). We connect both anti and pro-inflammatory cascades in parallel within different body compartments over time and explore the potential for manipulation of specific immune events to develop new therapies.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":"17 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13212741/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148035228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intra-Arterial Selective Hypothermic Human Serum Albumin Perfusion Attenuates Cerebral Ischemia-Reperfusion Injury.","authors":"Yue Wang, Yingying Ding, Yuhai Wang, Tao Xin, Xunming Ji","doi":"10.1007/s12975-026-01450-9","DOIUrl":"10.1007/s12975-026-01450-9","url":null,"abstract":"<p><p>Alleviating cerebral ischemia-reperfusion injury (CIRI) is a crucial link in improving the prognosis of patients with acute ischemic stroke (AIS). Currently, although intra-arterial selective cooling saline infusion (IA-SCSI) can mitigate this injury to a certain extent, its therapeutic effect is limited and difficult to meet clinical needs. Our previous studies have confirmed that human serum albumin (HSA) exerts definite neuroprotective effects. However, as a macromolecular colloidal solution, elderly patients with cardiopulmonary insufficiency can only tolerate low-dose administration, a limitation that directly hinders its efficacy and clinical translation. Intra-arterial selective drug delivery enables targeted delivery of drugs to injured sites, with an effective dose significantly lower than conventional intravenous administration, which can enhance local drug concentration while reducing the risk of systemic adverse reactions. Based on this, the present study focuses on the intra-arterial selective cooling HSA infusion (IA-SCAI) regimen, aiming to systematically explore its neuroprotective effects and provide new ideas for optimizing the treatment strategy of AIS. Using the rat middle cerebral artery occlusion (MCAO) model as the research object, an IA-SCAI intervention regimen was established to systematically investigate the effects of this regimen on neurological function and related mechanisms in rats after cerebral ischemia-reperfusion. Compared with IA-SCSI, intra-arterial selective saline infusion (IA-SSI) and intra-arterial selective albumin infusion (IA-SAI), IA-SCAI exhibited superior neuroprotective effects: it not only significantly alleviated the neuroinflammatory response induced by cerebral ischemia-reperfusion injury but also effectively improved the long-term neurological function recovery of rats. Further mechanistic studies revealed that this intervention regimen can reduce blood-brain barrier (BBB) injury by inhibiting the abnormal activation of the ROCK1/MLC pathway and decreasing the expression of F-actin, which may be one of the core mechanisms underlying its neuroprotective effects. HSA represents an ideal perfusate for intra-arterial selective cooling infusion, as it alleviates CIRI by inhibiting the activation of the ROCK1/MLC pathway, reducing F-actin expression to mitigate BBB damage, and suppressing neuroinflammatory responses, thereby providing a new and effective strategy for the clinical treatment of AIS.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":"17 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147975577","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}

{"title":"Associations of Blood Soluble Fas and IGF-I with Risk of Hemorrhagic Stroke: The Circulatory Risk Communities Study (CIRCS).","authors":"Kenichi Ariyada, Tomoko Sankai, Kazumasa Yamagishi, Isao Muraki, Yuji Shimizu, Hironori Imano, Takeshi Tanigawa, Hiroyasu Iso","doi":"10.1007/s12975-026-01447-4","DOIUrl":"10.1007/s12975-026-01447-4","url":null,"abstract":"<p><strong>Background: </strong>Although several studies have examined the associations between apoptosis-related factors or growth factors and cardiovascular diseases, evidence on their prospective association with hemorrhagic stroke remains limited.</p><p><strong>Methods: </strong>We conducted a nested case-control study within the large cohort of the Circulatory Risk in Communities Study in Japan. A total of 98 cases (60 intracerebral hemorrhage and 38 subarachnoid hemorrhage; 34 men and 64 women, aged 35 to 83 years at baseline) were included, along with 196 controls matched by age, sex, community, and year of sample collection. We measured serum levels of the soluble form of Fas and insulin-like growth factor-I among cases and controls. The odds ratios of total hemorrhagic stroke and its subtypes were calculated using conditional logistic regression analyses.</p><p><strong>Results: </strong>The median follow-up period from baseline to onset was 7.0 years. The multivariable odds ratios (95% confidence intervals) of total hemorrhagic stroke associated with a 1-standard deviation increment of soluble Fas (2.3 ng/mL) and insulin-like growth factor-I (40.5 ng/mL) were 0.93 (0.66-1.32) and 0.61 (0.41-0.89), respectively. The inverse association with insulin-like growth factor-I levels was similar for subarachnoid hemorrhage and intracerebral hemorrhage: the respective multivariable odds ratios were 0.53 (0.28-0.98) and 0.62 (0.37-1.04).</p><p><strong>Conclusions: </strong>The present study identified an inverse association between insulin-like growth factor-I levels and the risk of hemorrhagic stroke.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":"17 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13186836/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147975567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Direct Versus Indirect Bypass in Early-Stage Moyamoya (Suzuki I-III): A Propensity Score-Weighted Study.","authors":"Basel Musmar, Joanna M Roy, Hammam Abdalrazeq, Victor Gabriel El-Hajj, Michael Rizzuto, Matthews Lan, Pious Patel, Michael Baldassari, Arbaz Momin, Yazan Shamli Oghli, Marissa Tucci, Joseph Schaefer, Caitlin Ritz, Keenan Piper, Marc Mounzer, Kareem El Naamani, Ching-Jen Chen, Roland Jabre, Hassan Saad, Jonathan A Grossberg, Adam A Dmytriw, Aman B Patel, Mirhojjat Khorasanizadeh, Christopher S Ogilvy, Ajith J Thomas, Andre Monteiro, Adnan Siddiqui, Gustavo M Cortez, Ricardo A Hanel, Guilherme Porto, Alejandro M Spiotta, Anthony J Piscopo, David M Hasan, Mohammad Ghorbani, Joshua Weinberg, Shahid M Nimjee, Kimon Bekelis, Mohamed M Salem, Jan-Karl Burkhardt, Akli Zetchi, Charles Matouk, Brian M Howard, Rosalind Lai, Rose Du, Stavropoula I Tjoumakaris, Michael Reid Gooch, Robert H Rosenwasser, Pascal Jabbour","doi":"10.1007/s12975-026-01448-3","DOIUrl":"10.1007/s12975-026-01448-3","url":null,"abstract":"<p><p>Moyamoya angiopathy (MMA) lacks stage-specific comparative evidence for surgical strategy. Because many studies mix Suzuki grades, potential technique effects may be obscured. We compared direct revascularization (DR) with indirect revascularization (IR) in a stage-restricted cohort (Suzuki I-III), using propensity score weighting (PSW). We conducted a multicenter retrospective cohort study across 13 academic centers. Adults with confirmed MMA (Suzuki I-III) who underwent DR or IR were included. Patients < 16 years and combined procedures were excluded. Outcomes were symptomatic stroke, overall perioperative stroke, intraoperative complications, discharge NIHSS/mRS, length of stay, and follow-up stroke. PSW used Covariate Balancing Propensity Scores (CBPS) with absolute standardized mean difference (ASMD) diagnostics. Group differences were modeled with logistic/linear regression, and stroke-free survival was compared by Kaplan-Meier/log-rank. We analyzed 208 hemispheres (IR = 104; DR = 104). Baseline demographics and comorbidities were similar. Unadjusted analyses showed no significant differences in overall perioperative stroke (10.5% IR vs. 8.6% DR; p=.63), symptomatic perioperative stroke, intraoperative complications, discharge NIHSS/mRS, length of stay, or follow-up stroke (8.6% IR vs. 5.8% DR; p=.43). Stroke-free survival did not differ (log-rank p=.40). After PSW, findings remained unchanged across endpoints (e.g., all perioperative stroke OR 1.82; 95% CI, 0.61 to 5.45; p=.27). In adults with MMA at Suzuki I-III, no significant between-group differences were detected between DR and IR in the studied clinical outcomes. Technique selection can be individualized to anatomy, hemodynamics, and center expertise. Prospective, stage-stratified studies with standardized angiographic and hemodynamic endpoints are warranted.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":"17 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147949659","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}