{"title":"EXPRESS: Letter to the Editor Regarding \"Much ado about eating: Intermittent fasting and post-stroke neuroprotection\".","authors":"Guilherme Bezerra Carneiro, Carolina Moreno Pace, Eberval Gadelha Figueiredo","doi":"10.1177/0271678X261501655","DOIUrl":"https://doi.org/10.1177/0271678X261501655","url":null,"abstract":"<p><p>Vemuganti and colleagues highlight intermittent fasting (IF)'s neuroprotective potential post-stroke via autophagy and mitochondrial biogenesis. However, clinical translation faces hurdles in metabolically vulnerable patients. This letter critiques IF's bedside applicability, emphasizing post-stroke catabolic stress, dysphagia (~50% cases), sarcopenia risk, and cardiovascular concerns. Recent evidence links short eating windows to higher mortality, countering IF benefits. The obesity paradox suggests nutritional reserves aid survival. Strategies: protein-prioritized planning, dysphagia screening, dietitian monitoring, and supplements. Until RCTs confirm safety/efficacy, prioritize nutritional adequacy. Preclinical insights warrant study.Keywords: dysphagia, intermittent fasting, neuroprotection, obesity paradox, sarcopenia.</p>","PeriodicalId":520660,"journal":{"name":"Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism","volume":" ","pages":"271678X261501655"},"PeriodicalIF":4.5,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149229831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Audrey Drapeau, Mathilde Paré, Marc-Antoine Roy, Lawrence Labrecque, Nassif Chamoun, Mahmoudreza Taghizadeh, Joel Stephen Burma, Saqib Saleem, Catherine Fortier, Mohsen Agharazii, Patrice Brassard
{"title":"EXPRESS: Comprehensive assessment of the cerebral pressure-flow relationship in chronic kidney disease.","authors":"Audrey Drapeau, Mathilde Paré, Marc-Antoine Roy, Lawrence Labrecque, Nassif Chamoun, Mahmoudreza Taghizadeh, Joel Stephen Burma, Saqib Saleem, Catherine Fortier, Mohsen Agharazii, Patrice Brassard","doi":"10.1177/0271678X261501258","DOIUrl":"https://doi.org/10.1177/0271678X261501258","url":null,"abstract":"<p><p>Chronic kidney disease (CKD) is associated with blood pressure (BP) instability and increased cerebrovascular risk, but how CKD alters cerebral pressure-flow relationship remains unclear. Seventeen adults with moderate to severe CKD and 17 controls completed a multimetric protocol including resting supine recordings to assess spontaneous BP-middle cerebral artery mean blood velocity (MCAv) interactions using wavelet phase synchrony index and Granger based conditional joint transfer entropy, acute BP increases via 3 min isometric handgrip at 30% maximal voluntary contraction, acute BP decreases using sit to stand, and forced ABP oscillations using repeated squat-stands at 0.05 Hz and 0.10 Hz. Mean arterial pressure, MCAv, and end-tidal carbon dioxide partial pressure (PETCO<sub>2</sub>) were continuously recorded. Transfer function metrics and MCAv responses to transient mean arterial pressure increases and decreases were comparable between groups. Directional sensitivity was present in both groups at 0.05 Hz only. Wavelet phase synchrony index was elevated in ultra low frequency bands (0.030-0.035 Hz and 0.035-0.040 Hz), and Granger based conditional joint transfer entropy increased by 55% in forward MAP→MCAv information transfer in CKD persisting after PETCO<sub>2</sub> correction. No between-group differences were detected using the linear assessments employed in this study, whereas nonlinear analyses identified differences during spontaneous resting conditions.</p>","PeriodicalId":520660,"journal":{"name":"Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism","volume":" ","pages":"271678X261501258"},"PeriodicalIF":4.5,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149229769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"EXPRESS: Cardio‑Glymphatic Association: Left‑Heart Dysfunction in CSVD and Its Association With Glymphatic‑Related Cognitive Impairment.","authors":"Changqing Zhan, Wenyu Wang, Xueping Lu, Xinling Xie, Yitong Li, Chu-Chung Huang","doi":"10.1177/0271678X261501635","DOIUrl":"https://doi.org/10.1177/0271678X261501635","url":null,"abstract":"<p><p>Cerebral small vessel disease (CSVD) is a leading cause of vascular cognitive impairment. The glymphatic system, a brain-wide waste clearance pathway, may be impaired in CSVD, but its upstream drivers and role linking systemic factors to cognitive impairment remain unclear. This study explored whether glymphatic dysfunction statistically mediates the association between left-heart dysfunction and cognitive impairment in CSVD. We enrolled 80 CSVD-VCI, 80 CSVD-NCI, and 80 normal controls aged 50-80 years. All participants underwent neuropsychological assessment, cardiac ultrasound (measuring left ventricular ejection fraction [LVEF], left ventricular end-diastolic diameter [LVEDD], and left atrial diameter [LAD]), and brain MRI to measure the DTI-ALPS index of glymphatic activity. The DTI-ALPS index was progressively reduced: NC > CSVD-NCI > CSVD-VCI. It correlated positively with LVEF and negatively with LAD, and was associated with multiple cognitive domains. Mediation analysis suggests that DTI-ALPS statistically significantly mediated the effects of LVEF and LAD on cognitive performance. These cross-sectional findings suggest that glymphatic dysfunction is a key feature of CSVD and may represent a potential correlative link connecting left-heart dysfunction to cognitive impairment, consistent with a potential cardio-glymphatic pathway in CSVD pathophysiology.</p>","PeriodicalId":520660,"journal":{"name":"Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism","volume":" ","pages":"271678X261501635"},"PeriodicalIF":4.5,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149229780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"EXPRESS: Reperfusion-sensitive induction of endothelial NDRG1 identifies a dynamic vascular stress response to thrombolysis in ischemic stroke.","authors":"Jonathane Furon, Tamara Etuze, Louis Fosset, Ruben Goulet, Eloïse Lemarchand, Yohann Repesse, Denis Vivien, Fatemeh Dubois","doi":"10.1177/0271678X261501639","DOIUrl":"https://doi.org/10.1177/0271678X261501639","url":null,"abstract":"<p><p>Ischemic stroke (IS) outcome critically depends on the neurovascular unit's capacity to respond to ischemia-reperfusion stress within the salvageable penumbra. Here, we characterize the spatiotemporal regulation of N-myc downstream-regulated gene 1 (NDRG1) and identify it as an early, reperfusion-sensitive marker of endothelial stress. Under physiological conditions, NDRG1 is primarily expressed in neurons and oligodendrocytes, with minimal endothelial expression. Following middle cerebral artery occlusion, NDRG1 undergoes marked spatial and cellular redistribution, becoming strongly induced in endothelial cells across the cerebrovascular tree.Endothelial NDRG1 induction was detectable as early as 6 hours after ischemia and evolved from a vesicular pattern to diffuse vascular labeling by 24 hours. Importantly, recombinant tissue-type plasminogen activator (rtPA) selectively enhanced endothelial NDRG1 expression in peri-lesional vessels in the rtPA-sensitive thrombin model, but not in the rtPA-resistant FeCl<sub>3</sub> model, indicating that NDRG1 induction is linked to effective reperfusion. In vitro, oxygen-glucose deprivation (OGD) recapitulated endothelial NDRG1 induction, further enhanced by rtPA through a pathway involving the LDL receptor family.Collectively, these findings identify endothelial NDRG1 as a dynamic molecular readout of reperfusion-sensitive vascular stress. NDRG1 may serve as a biomarker of endothelial responsiveness to thrombolytic therapy, providing new insight into cerebrovascular adaptations associated with successful reperfusion.</p>","PeriodicalId":520660,"journal":{"name":"Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism","volume":" ","pages":"271678X261501639"},"PeriodicalIF":4.5,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149229835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"EXPRESS: Cerebral Microbleed Burden After Aortic and Cardiac Surgery Is Associated With Extracorporeal Circulation Exposure: Evidence From Young Patients With Heritable Connective Tissue Disorders.","authors":"Gianfranco Vornetti, Riccardo Regazzo, Valentina Barone, Valentina Belacchi, Giuliana La Rosa, Elisabetta Mariucci, Andrea Donti, Caterina Tonon, Raffaele Lodi, Luca Spinardi","doi":"10.1177/0271678X261499072","DOIUrl":"https://doi.org/10.1177/0271678X261499072","url":null,"abstract":"<p><strong>Background and purpose: </strong>Cerebral microbleeds (CMBs) occur after surgery involving extracorporeal circulation (ECC), though confounding risk factors may obscure this association. Patients with heritable connective tissue diseases (HCTDs) requiring early surgery provide an ideal model to investigate ECC-related CMBs. We aimed to assess CMB prevalence, distribution, and surgical correlates in a genetically confirmed HCTD population.</p><p><strong>Methods: </strong>We retrospectively analyzed 111 HCTD patients with brain magnetic resonance. CMBs number and location were correlated with clinical and surgical data, including procedure frequency, type, and, when available, ECC duration.</p><p><strong>Results: </strong>All 58 patients exposed to surgery under ECC exhibited CMBs, compared to only four surgery-naïve individuals. CMBs showed a predominantly lobar pattern. CMB burden was significantly higher in patients with multiple surgeries and longer ECC duration (P<0.001), whereas valve type and surgical technique showed no associationDiscussion:In our cohort, CMBs were identified in all individuals with ECC exposure. The absence of significant differences in CMB burden across surgical techniques weakens the hypothesis that CMBs originate solely from metallic microemboli. In young, normotensive patients with HCTDs, ECC exposure was uniformly associated with CMBs, with burden increasing with repeated procedures and ECC duration.</p>","PeriodicalId":520660,"journal":{"name":"Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism","volume":" ","pages":"271678X261499072"},"PeriodicalIF":4.5,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149229772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Carolyn A Lomahan, Georgios Kalarakis, Marie Luby, Staffan Holmin, Johan Lundberg, Michael V Mazya, Lawrence L Latour, Fabian Arnberg-Sandor
{"title":"EXPRESS: Cerebral blood flow-oxygen metabolism uncoupling at 24 hours after stroke thrombectomy.","authors":"Carolyn A Lomahan, Georgios Kalarakis, Marie Luby, Staffan Holmin, Johan Lundberg, Michael V Mazya, Lawrence L Latour, Fabian Arnberg-Sandor","doi":"10.1177/0271678X261501263","DOIUrl":"https://doi.org/10.1177/0271678X261501263","url":null,"abstract":"<p><p>BackgroundFollowing successful endovascular therapy (EVT) for acute ischemic stroke, tissue with abnormal perfusion may have impaired oxygen extraction and metabolism. MRI model-based oxygen extraction fraction (OEFmax) and cerebral metabolic rate of oxygen (CMRO2) were characterized in hypoperfusion and hyperemia regions 24 hours post-EVT.MethodsEighty-four patients were included with anterior circulation vessel occlusion, successful recanalization, and an MRI at 24 hours post-EVT. Time-to-maximum (Tmax) and cerebral blood flow (CBF) were evaluated for hypoperfusion and hyperemia. CBF, OEFmax, and CMRO2 were quantified using i) segmentation-based and ii) single slice region of interest (ROI) analyses. Normalized CBF, OEFmax, and CMRO2 were calculated by dividing the segmentation or ROI value by the contralateral value.ResultsSixty-seven (80%) patients had abnormal perfusion; hypoperfusion in 22 (26%), hyperemia in 36 (43%), and both in 9 (11%). Compared to control, hypoperfused regions demonstrated a 62% CBF decrease, 52% CMRO2 decrease, and 68% OEFmax increase (p<0.01). Hyperemic regions demonstrated a 58% CBF increase, 26% CMRO2 increase, and 25% OEFmax decrease (p<0.01). Hyperemia had no significant correlation between normalized CBF and CMRO2 (p=0.14).ConclusionHyperemia regions demonstrated cerebral blood flow-oxygen metabolism uncoupling, suggesting the underlying mechanism as loss of cerebrovascular autoregulation rather than hypermetabolic demand.</p>","PeriodicalId":520660,"journal":{"name":"Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism","volume":" ","pages":"271678X261501263"},"PeriodicalIF":4.5,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149229766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Quinten Deckers, Simone M Uniken-Venema, Kees P Braun, Albert van der Zwan, Tristan P C van Doormaal, Pieter Thomas Deckers, Jeroen Cw Siero, Alex Bhogal
{"title":"EXPRESS: Quantification of arterial hemodynamics in steno-occlusive disease using time-resolved MRI-based angiography.","authors":"Quinten Deckers, Simone M Uniken-Venema, Kees P Braun, Albert van der Zwan, Tristan P C van Doormaal, Pieter Thomas Deckers, Jeroen Cw Siero, Alex Bhogal","doi":"10.1177/0271678X261500385","DOIUrl":"https://doi.org/10.1177/0271678X261500385","url":null,"abstract":"<p><p>BackgroundIntracranial steno-occlusive disease (SOD) assessment benefits from hemodynamic imaging, but comprehensive evaluation often relies on contrast- or radiation-based techniques. Arterial spin labeling (ASL) provides a non-invasive alternative for quantifying tissue-level perfusion and cerebrovascular reactivity, yet does not capture upstream arterial flow dynamics. As a result, non-invasive assessment of macrovascular hemodynamics for SOD remains limited. This study evaluates whether quantitative 4D-MRA provides complementary arterial information beyond established ASL-derived metrics.MethodsTwelve SOD patients (7 women; age 42.3±25.8 years) underwent multi-delay ASL and 4D-MRA before and after acetazolamide. Cerebrovascular reactivity (CVR), arterial transit time (ATT), macrovascular ATT (mATT), and labeled blood volume (LBV) were quantified. Associations and vasodilatory responses were assessed using linear mixed-effects models.ResultsAt baseline, mATT correlated with ATT (β=0.66±0.08, p<0.001). Both decreased following acetazolamide (mATT: 1.07±0.03s to 1.01±0.03s, p=0.029; ATT: 1.63±0.07s to 1.40±0.07s, p<0.001). However, changes in mATT and ATT were not associated with CVR. In contrast, CVR was positively associated with ΔLBV (β=8.84, SE=2.43, p=0.01). Case analyses further demonstrated artery-level delayed inflow and vascular steal.ConclusionQuantitative 4D-MRA provides complementary macrovascular information to ASL in SOD. ΔLBV more consistently reflects cerebrovascular reactivity than transit-based metrics and is sensitive to artery-level delayed inflow and vascular steal.</p>","PeriodicalId":520660,"journal":{"name":"Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism","volume":" ","pages":"271678X261500385"},"PeriodicalIF":4.5,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149229782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"EXPRESS: Increases in Intraluminal Viscosity Disrupt Microvascular Flow Dynamics.","authors":"Cristian Franco, Albert Gonzales","doi":"10.1177/0271678X261501252","DOIUrl":"https://doi.org/10.1177/0271678X261501252","url":null,"abstract":"<p><strong>Background: </strong>Autoregulation of blood flow relies on a balance between pressure-induced constriction and shear stress-mediated dilation. While these mechanisms are well characterized in arterioles, far less is known about how blood enters and is distributed within capillary networks, the site of oxygen and nutrient exchange. Because neuronal function requires rapid, on-demand perfusion, local mechanisms must regulate both capillary inflow and flow distribution. Capillary endothelial cells and pericytes, contractile cells that envelop capillaries, are emerging contributors to these processes, yet capillary-level autoregulation remains poorly defined.</p><p><strong>Methods: </strong>Using an <i>ex vivo</i> pressurized retinal preparation that preserves the arteriole-to-capillary continuum, we examined how intraluminal viscosity, and thus shear stress, regulates endothelial and mural cell signaling during pressure-driven flow.</p><p><strong>Results: </strong>Increased viscosity delayed capillary filling and enhanced endothelial calcium activity in transitional and capillary segments. In contrast, viscosity suppressed pressure-induced calcium signaling in smooth muscle cells and ensheathing pericytes via nitric oxide-dependent inhibition. Chronic elevation of intraluminal viscosity induced arteriolar remodeling and increased tone but impaired endothelial shear sensing and reduced capillary perfusion.</p><p><strong>Conclusion: </strong>These findings reveal fundamental differences in autoregulatory mechanisms between arterioles and capillaries and identify viscosity-driven endothelial signaling as a key determinant of capillary perfusion and flow distribution.</p>","PeriodicalId":520660,"journal":{"name":"Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism","volume":" ","pages":"271678X261501252"},"PeriodicalIF":4.5,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149229796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Max J McLachlan, Brecca Bettcher, Rebecca Langhough, Alexandra DiFilippo, Tobey Betthauser, Andrew McVea, Lisette LeMerise, Matthew Zammit, Ethan Grover, Erin M Jonaitis, Gilda Ennis, Nathaniel Chin, Sanjay Asthana, Sterling C Johnson, Barbara B Bendlin, Bradley T Christian
{"title":"EXPRESS: Synaptic density PET mediates the relationship between Alzheimer's disease pathology and cognitive performance.","authors":"Max J McLachlan, Brecca Bettcher, Rebecca Langhough, Alexandra DiFilippo, Tobey Betthauser, Andrew McVea, Lisette LeMerise, Matthew Zammit, Ethan Grover, Erin M Jonaitis, Gilda Ennis, Nathaniel Chin, Sanjay Asthana, Sterling C Johnson, Barbara B Bendlin, Bradley T Christian","doi":"10.1177/0271678X261501266","DOIUrl":"https://doi.org/10.1177/0271678X261501266","url":null,"abstract":"<p><strong>Introduction: </strong>Synaptic loss is one of the strongest post-mortem predictors of Alzheimer's disease (AD) severity and may impact how pathology affects cognition. This study compared regional [<sup>11</sup>C]UCB-J synaptic density across the AD continuum and evaluated the extent to which synaptic density mediates relationships between AD biomarkers.</p><p><strong>Methods: </strong>Seventy-two participants completed PET scans, MRIs, and cognitive testing. Participants were categorized into subgroups representing typical AD progression. Regional synaptic density was compared across subgroups and pathological variables. Standard mediation and moderated mediation analyses were performed using amyloid and tau as predictors/moderators and MoCA score as outcome.</p><p><strong>Results: </strong>The amyloid+/tau+/impaired subgroup showed lower synaptic density than controls, particularly for transverse temporal, inferior parietal, and hippocampal regions (Cohen's d=1.60, 1.57, 1.50). Hippocampal synaptic density had the strongest associations with tau (β=-0.473); transverse temporal synaptic density had the strongest association with amyloid (β=-0.543) and age (β=-0.614). Eight of twelve assessed brain regions demonstrated significant indirect effects across mediation frameworks. The inferior parietal lobe showed the largest mediation for amyloid (45.3%) and tau (28.9%).</p><p><strong>Discussion: </strong>These findings support the hypothesis that synaptic loss is a primary mechanism contributing to clinical AD and suggest that synaptic density imaging can provide complementary information to the existing AD framework.</p>","PeriodicalId":520660,"journal":{"name":"Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism","volume":" ","pages":"271678X261501266"},"PeriodicalIF":4.5,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149229800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"EXPRESS: A novel mouse model of cerebral venous sinus thrombosis based on photochemical-induction combined with in situ injection.","authors":"Chengbin Zhou, Huimin Jiang, Yifan Zhou, Weiyue Zhang, Hui Li, Wei Ma, Lu Liu, Xiao Xue, Chunxiao Lu, Xiaoming Zhang, Zilin Xu, Ran Duan, Qian Feng, Liuguan Bian, Xunming Ji, Chen Zhou","doi":"10.1177/0271678X261499069","DOIUrl":"https://doi.org/10.1177/0271678X261499069","url":null,"abstract":"<p><p>Cerebral venous sinus thrombosis (CVST) is a distinct cerebrovascular disorder characterized by impaired venous drainage and blood-brain barrier dysfunction, yet its pathophysiology remains poorly understood due to a lack of refined experimental models. We developed a novel, clinically relevant mouse model of CVST by integrating localized intraluminal induction with photochemical occlusion of the superior sagittal sinus (SSS). Model fidelity was validated using laser speckle contrast imaging, MRI, and histological analysis. Our approach produced consistent, spatially restricted SSS thrombosis, resulting in pronounced acute-stage brain edema and venous infarction. Notably, MRI combined with TTC staining identified a peri-infarct region suggestive of a venous penumbra. Functional assessments revealed significant acute motor deficits followed by recovery at day 7, whereas cognitive impairments persisted longer. Compared with conventional FeCl₃ or systemic Rose Bengal photothrombosis models, this integrated method exhibited superior anatomical specificity and minimized off-target tissue injury. This study introduces a reproducible CVST model that successfully recapitulates the key hemodynamic and pathological features of human venous stroke, providing a robust platform for mechanistic investigations and the evaluation of targeted therapeutic interventions.</p>","PeriodicalId":520660,"journal":{"name":"Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism","volume":" ","pages":"271678X261499069"},"PeriodicalIF":4.5,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149198792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}