Chi Zhang, Xingwang Yong, Yuezhou Cao, Yi-Cheng Hsu, Haibin Shi, Feiyun Wu, Yi Zhang, Shanshan Lu
{"title":"Amide proton transfer MRI may reflect effective reperfusion and predict functional outcomes in patients with ischemic stroke.","authors":"Chi Zhang, Xingwang Yong, Yuezhou Cao, Yi-Cheng Hsu, Haibin Shi, Feiyun Wu, Yi Zhang, Shanshan Lu","doi":"10.1177/0271678X241297110","DOIUrl":"10.1177/0271678X241297110","url":null,"abstract":"<p><p>Perfusion imaging is useful to assess tissue recovery in patients with acute ischemic stroke (AIS); however, it cannot reflect tissue metabolism. We postulated that amide proton transfer (APT) imaging can characterize the tissue status after reperfusion therapy, thus providing prognostic value for 90-day functional outcomes. We included 63 patients with AIS and large-vessel occlusion (LVO). The APT signals, including APT<sup>#</sup> and NOE<sup>#</sup> (nuclear Overhauser enhancement) were quantified. Ischemic lesions observed on APT<sup>#</sup> and diffusion-weighted imaging (DWI) were classified according to their mismatch patterns (APT<sup>#</sup> < DWI; APT<sup>#</sup> ≥ DWI). Predictors of 90-day good outcomes (modified Rankin scale score 0-2) were evaluated. Patients with successful reperfusion exhibited higher APT<sup>#</sup>, smaller percentage change of APT<sup>#</sup>, and a greater likelihood of presenting APT<sup>#</sup> < DWI compared to those with poor reperfusion (all <i>P</i> < 0.05). The APT<sup>#</sup> (odds ratio [OR] = 11.48, <i>P</i> = 0.046) and a mismatch pattern of APT<sup>#</sup> < DWI (OR = 7.41, <i>P</i> = 0.020) independently predicted good outcomes besides the clinical parameters. A mismatch pattern of APT<sup>#</sup> ≥ DWI was a significant marker of poor outcomes despite successful reperfusion (<i>P</i> = 0.002). Our study provides preliminary evidence that APT may reveal tissue recovery after reperfusion and predict good outcomes at 90 days in patients with AIS and LVO.</p>","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"421-430"},"PeriodicalIF":4.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11846100/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142545710","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":"Intravenous administration of muse cells improves cerebral ischemia outcome via immunomodulation in the spleen.","authors":"Yuya Kato, Daiki Aburakawa, Ryosuke Tashiro, Yuan Zhou, Sherif Rashad, Hidenori Endo, Teiji Tominaga, Kuniyasu Niizuma","doi":"10.1177/0271678X241290363","DOIUrl":"10.1177/0271678X241290363","url":null,"abstract":"<p><p>Ischemic stroke is a leading cause of disability and death globally. Stem cell therapies are emerging as a frontier for enhancing post-stroke recovery, with Muse cells-a subclass of pluripotent stem cells-demonstrating considerable promise. Muse cells are notable not only for their potential in cell replacement but also for their role in modulating immune responses following cerebral infarction. In the present study, we administered Muse cells intravenously to mice after inducing a stroke via distal middle cerebral artery occlusion. We evaluated motor outcomes, splenocyte populations, cytokine profiles, and gene expression 2 weeks after inducing stroke. Additionally, comparisons were drawn between outcomes in splenectomized mice and those receiving adoptive splenocyte transfer to discern the specific influence of the spleen on treatment efficacy. Our findings revealed that Muse cell therapy facilitates motor recovery, an effect that is compromised in the absence of the spleen. Spleens in treated mice exhibited a shift in neutrophil counts, increased cytokine activity, and a notable uptick in the expression of genes related to protein folding. These insights affirm the potential therapeutic effect of Muse cells in post-stroke treatment strategies, with their efficacy attributed, at least in part, to immunomodulatory pathways involving the spleen.</p>","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"542-557"},"PeriodicalIF":4.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11563515/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142466523","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}
Yao Wang, Ziwei Yang, Xiumei Zheng, Xiao Liang, Lin Wu, Chengsi Wu, Jiankun Dai, Yuan Cao, Meng Li, Fuqing Zhou
{"title":"Cerebral blood flow alterations and host genetic association in individuals with long COVID: A transcriptomic-neuroimaging study.","authors":"Yao Wang, Ziwei Yang, Xiumei Zheng, Xiao Liang, Lin Wu, Chengsi Wu, Jiankun Dai, Yuan Cao, Meng Li, Fuqing Zhou","doi":"10.1177/0271678X241277621","DOIUrl":"10.1177/0271678X241277621","url":null,"abstract":"<p><p>Neuroimaging studies have indicated that altered cerebral blood flow (CBF) was associated with the long-term symptoms of postacute sequelae of SARS-CoV-2 infection (PASC), also known as \"long COVID\". COVID-19 and long COVID were found to be strongly associated with host gene expression. Nevertheless, the relationships between altered CBF, clinical symptoms, and gene expression in the central nervous system (CNS) remain unclear in individuals with long COVID. This study aimed to explore the genetic mechanisms of CBF abnormalities in individuals with long COVID by transcriptomic-neuroimaging spatial association. Lower CBF in the left frontal-temporal gyrus was associated with higher fatigue and worse cognition in individuals with long COVID. This CBF pattern was spatially associated with the expression of 2,178 genes, which were enriched in the molecular functions and biological pathways of COVID-19. Our study suggested that lower CBF is associated with persistent clinical symptoms in long COVID individuals, possibly as a consequence of the complex interactions among multiple COVID-19-related genes, which contributes to our understanding of the impact of adverse CNS outcomes and the trajectory of development to long COVID.</p>","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"431-442"},"PeriodicalIF":4.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11572096/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142035981","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}
Ye Yuan, Xiao Yang, Yutong Zhao, Jerry J Flores, Lei Huang, Lingui Gu, Ruihao Li, Xingyu Zhang, Shiyi Zhu, Siyuan Dong, Hideki Kanamaru, Qiuguang He, Yihao Tao, Kun Yi, Mingyang Han, Xionghui Chen, Lei Wu, John H Zhang, Zongyi Xie, Jiping Tang
{"title":"Mitochondrial ferritin upregulation by deferiprone reduced neuronal ferroptosis and improved neurological deficits via NDRG1/Yap pathway in a neonatal rat model of germinal matrix hemorrhage.","authors":"Ye Yuan, Xiao Yang, Yutong Zhao, Jerry J Flores, Lei Huang, Lingui Gu, Ruihao Li, Xingyu Zhang, Shiyi Zhu, Siyuan Dong, Hideki Kanamaru, Qiuguang He, Yihao Tao, Kun Yi, Mingyang Han, Xionghui Chen, Lei Wu, John H Zhang, Zongyi Xie, Jiping Tang","doi":"10.1177/0271678X241252110","DOIUrl":"10.1177/0271678X241252110","url":null,"abstract":"<p><p>Ferroptosis contributes to brain injury after germinal matrix hemorrhage (GMH). Mitochondrial ferritin (FTMT), a novel mitochondrial outer membrane protein, reduces oxidative stress in neurodegenerative diseases. In vitro, Deferiprone has been shown to upregulate FTMT. However, the effects of FTMT upregulation by Deferiprone on neuronal ferroptosis after GMH and its underlying mechanism has not been investigated. In our study, 389 Sprague-Dawley rat pups of postnatal day 7 were used to establish a collagenase-induced GMH model and an iron-overload model of intracerebral FeCl<sub>2</sub> injection. The brain expressions of FTMT, N-myc downstream-regulated gene-1 (NDGR1), Yes-associated protein (YAP), ferroptosis-related molecules including transferrin receptor (TFR) and acyl-CoA synthase long-chain family member 4 (ACSL4) were increased after GMH. FTMT agonist Deferiprone improved neurological deficits and hydrocephalus after GMH. Deferiprone or Adenovirus-FTMT enhanced YAP phosphorylation at the Ser<sup>127</sup> site and attenuated ferroptosis, which was reversed by NDRG1 CRISPR Knockout. Iron overload induced neuronal ferroptosis and neurological deficits, which were improved by YAP CRISPR Knockout. Collectively, FTMT upregulation by Deferiprone reduced neuronal ferroptosis and neurological deficits via the NDRG1/YAP signaling pathway after GMH. Deferiprone may serve as a potential non-invasive treatment for GMH patients.</p>","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"510-527"},"PeriodicalIF":4.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11563512/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142347558","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}
Shintaro Kimura, Maho Iwata, Hajime Takase, Eng H Lo, Ken Arai
{"title":"Oxidative stress and chronic cerebral hypoperfusion: An overview from preclinical rodent models.","authors":"Shintaro Kimura, Maho Iwata, Hajime Takase, Eng H Lo, Ken Arai","doi":"10.1177/0271678X241305899","DOIUrl":"10.1177/0271678X241305899","url":null,"abstract":"<p><p>Chronic cerebral hypoperfusion (CCH) is an important clinical condition characterized by a prolonged reduction in cerebral blood flow that contributes to several neurodegenerative diseases, including vascular dementia and Alzheimer's disease. A number of rodent models of CCH have been developed that mimic the human pathological conditions of reduced cerebral perfusion. These models have been instrumental in elucidating the molecular and cellular mechanisms involved in CCH-induced brain damage. Oxidative stress is induced by perturbations in cellular pathways caused by CCH, including mitochondrial dysfunction, ion pump dysfunction, and adenosine triphosphate (ATP) depletion. The deleterious stress leads to the accumulation of reactive oxygen species (ROS) and exacerbates damage to neuronal structures, significantly impairing cognitive function. Among the various therapeutic strategies being evaluated, edaravone, a potent antioxidant, is emerging as a promising drug due to its neuroprotective properties against oxidative stress. Initially approved for use in ischemic stroke, research using rodent CCH models has shown that edaravone has significant efficacy in scavenging free radicals and ameliorating oxidative stress-induced neuronal damage under CCH conditions. This mini-review summarizes the current literature on the rodent models of CCH and then discusses the therapeutic potential of edaravone to reduce neuronal and vascular damage caused by CCH-induced oxidative stress.</p>","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"381-395"},"PeriodicalIF":4.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11635795/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813361","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}
Ingrid Magnet, Alexandra-Maria Stommel, Christoph Schriefl, Matthias Mueller, Michael Poppe, Juergen Grafeneder, Christoph Testori, Andreas Janata, Andreas Schober, Daniel Grassmann, Wilhelm Behringer, Wolfgang Weihs, Michael Holzer, Sandra Hoegler, Florian Ettl
{"title":"Neuroprotection with hypothermic reperfusion and extracorporeal cardiopulmonary resuscitation - A randomized controlled animal trial of prolonged ventricular fibrillation cardiac arrest in rats.","authors":"Ingrid Magnet, Alexandra-Maria Stommel, Christoph Schriefl, Matthias Mueller, Michael Poppe, Juergen Grafeneder, Christoph Testori, Andreas Janata, Andreas Schober, Daniel Grassmann, Wilhelm Behringer, Wolfgang Weihs, Michael Holzer, Sandra Hoegler, Florian Ettl","doi":"10.1177/0271678X241281485","DOIUrl":"10.1177/0271678X241281485","url":null,"abstract":"<p><p>Extracorporeal cardiopulmonary resuscitation (ECPR) facilitates resuscitation with immediate and precise temperature control. This study aimed to determine the optimal reperfusion temperature to minimize neurological damage after ventricular fibrillation cardiac arrest (VFCA). Twenty-four rats were randomized (n = 8 per group) to normothermia (NT = 37°C), mild hypothermia (MH = 33°C) or moderate hypothermia (MOD = 27°C). The rats were subjected to 10 minutes of VFCA, before 15 minutes of ECPR at their respective target temperature. After ECPR weaning, rats in the MOD group were rapidly rewarmed to 33°C, and temperature maintained at 33°C (MH/MOD) or 37°C (NT) for 12 hours before slow rewarming to normothermia (MH/MOD). The primary outcome was 30-day survival with overall performance category (OPC) 1 or 2 (1 = normal, 2 = slight disability, 3 = severe disability, 4 = comatose, 5 = dead). Secondary outcomes included awakening rate (OPC ≤ 3) and neurological deficit score (NDS, from 0 = normal to 100 = brain dead). The survival rate did not differ between reperfusion temperatures (NT = 25%, MH = 63%, MOD = 38%, p = 0.301). MH had the lowest NDS (NT = 4[IQR 3-4], MH = 2[1-2], MOD = 5[3-5], p = 0.044) and highest awakening rate (NT = 25%, MH = 88%, MOD = 75%, p = 0.024). In conclusion, ECPR with 33°C reperfusion did not statistically significantly improve survival after VFCA when compared with 37°C or 27°C reperfusion but was neuroprotective as measured by awakening rate and neurological function.</p>","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"476-485"},"PeriodicalIF":4.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11574926/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142154213","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}
Diana G Bohannon, Laurie L Wellman, Marcus Kaul, Elena V Galkina, Ming-Lei Guo, Prasun K Datta, Woong-Ki Kim
{"title":"Type-1-to-type-2 transition of brain microvascular pericytes induced by cytokines and disease-associated proteins: Role in neuroinflammation and blood-brain barrier disruption.","authors":"Diana G Bohannon, Laurie L Wellman, Marcus Kaul, Elena V Galkina, Ming-Lei Guo, Prasun K Datta, Woong-Ki Kim","doi":"10.1177/0271678X241296270","DOIUrl":"10.1177/0271678X241296270","url":null,"abstract":"<p><p>While the concept of pericyte heterogeneity in the brain microvasculature is becoming more widely accepted, little is known about how they arise, or their functional contributions to the blood-brain barrier (BBB). We therefore set out to examine the distribution of subtypes of pericytes at the BBB and sought to elucidate some of their functional characteristics by examining their unique mRNA expression patterns. We demonstrate that type-1 pericytes (PC1) that are associated with young healthy brains and BBB homeostasis, can transition into type-2 pericytes (PC2) that are associated with disease and BBB breakdown, both in vitro and in vivo, in the presence of both endogenous and disease associated ligands. We identified PC1 and PC2 in single-cell RNA-sequencing from vascular enriched mouse brain and identified transcriptional differences between PC1 and PC2. PC2 showed increased expression of genes associated with phagocytosis and peripheral immune cell infiltration. On the contrary, PC1 displayed increased expression of genes involved in hedgehog signaling, which is known to promote tight junction formation at the BBB. Our data support the PC1-to-PC2 transition as an origin of PC diversity and suggest a functional role for PC1 in maintaining BBB homeostasis and PC2 in responding to pathological conditions.</p>","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"405-420"},"PeriodicalIF":4.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11563511/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142545713","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}
Aishat O Ameen, Sebastian W Nielsen, Martin W Kjær, Jens V Andersen, Emil W Westi, Kristine K Freude, Blanca I Aldana
{"title":"Metabolic preferences of astrocytes: Functional metabolic mapping reveals butyrate outcompetes acetate.","authors":"Aishat O Ameen, Sebastian W Nielsen, Martin W Kjær, Jens V Andersen, Emil W Westi, Kristine K Freude, Blanca I Aldana","doi":"10.1177/0271678X241270457","DOIUrl":"10.1177/0271678X241270457","url":null,"abstract":"<p><p>Disruptions to the gut-brain-axis have been linked to neurodegenerative disorders. Of these disruptions, reductions in the levels of short-chain fatty acids (SCFAs), like butyrate, have been observed in mouse models of Alzheimer's disease (AD). Butyrate supplementation in mice has shown promise in reducing neuroinflammation, amyloid-β accumulation, and enhancing memory. However, the underlying mechanisms remain unclear. To address this, we investigated the impact of butyrate on energy metabolism in mouse brain slices, primary cultures of astrocytes and neurons and <i>in-vivo</i> by dynamic isotope labelling with [U-<sup>13</sup>C]butyrate and [1,2-<sup>13</sup>C]acetate to map metabolism via mass spectrometry. Metabolic competition assays in cerebral cortical slices revealed no competition between butyrate and the ketone body, β-hydroxybutyrate, but competition with acetate. Astrocytes favoured butyrate metabolism compared to neurons, suggesting that the astrocytic compartment is the primary site of butyrate metabolism. <i>In-vivo</i> metabolism investigated in the 5xFAD mouse, an AD pathology model, showed no difference in <sup>13</sup>C-labelling of TCA cycle metabolites between wild-type and 5xFAD brains, but butyrate metabolism remained elevated compared to acetate in both groups, indicating sustained uptake and metabolism in 5xFAD mice. Overall, these findings highlight the role of astrocytes in butyrate metabolism and the potential use of butyrate as an alternative brain fuel source.</p>","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"528-541"},"PeriodicalIF":4.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11563520/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142347557","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}
Isabell Nessel, Luke Whiley, Simon C Dyall, Adina T Michael-Titus
{"title":"A plasma lipid signature in acute human traumatic brain injury: Link with neuronal injury and inflammation markers.","authors":"Isabell Nessel, Luke Whiley, Simon C Dyall, Adina T Michael-Titus","doi":"10.1177/0271678X241276951","DOIUrl":"10.1177/0271678X241276951","url":null,"abstract":"<p><p>Traumatic brain injury (TBI) leads to major membrane lipid breakdown. We investigated plasma lipids over 3 days post-TBI, to identify a signature of acute human TBI and assess its correlation with neuronal injury and inflammation. Plasma from patients with TBI (Abbreviated Injury Scale (AIS)3 - serious injury, n = 5; AIS4 - severe injury, n = 8), and controls (n = 13) was analysed for lipidomic profile, neurofilament light (NFL) and cytokines, and the omega-3 index was measured in red blood cells. A lipid signature separated TBI from controls, at 24 and 72 h. Major species driving the separation were: lysophosphatidylcholine (LPC), phosphatidylcholine (PC) and hexosylceramide (HexCer). Docosahexaenoic acid (DHA, 22:6) and LPC (0:0/22:6) decreased post-injury. NFL levels were increased at 24 and 72 h post-injury in AIS4 TBI vs. controls. Interleukin (IL-)6, IL-2 and IL-13 were elevated at 24 h in AIS4 patients vs. controls. NFL and IL-6 were negatively correlated with several lipids. The omega-3 index at admission was low in all patients (controls: 4.3 ± 1.1% and TBI: 4.0 ± 1.1%) and did not change significantly over 3 days post-injury. We have identified specific lipid changes, correlated with markers of injury and inflammation in acute TBI. These observations could inform future lipid-based therapeutic approaches.</p>","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"443-458"},"PeriodicalIF":4.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11572080/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142072918","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}
Nuwan D Nanayakkara, Liesel-Ann Meusel, Nicole D Anderson, J Jean Chen
{"title":"Estimation of cerebrovascular reactivity amplitude and lag using breath-holding fMRI and the global BOLD signal: Application in diabetes and hypertension.","authors":"Nuwan D Nanayakkara, Liesel-Ann Meusel, Nicole D Anderson, J Jean Chen","doi":"10.1177/0271678X241270420","DOIUrl":"10.1177/0271678X241270420","url":null,"abstract":"<p><p>In this work, we demonstrate a data-driven approach for estimating cerebrovascular reactivity (CVR) amplitude and lag from breathhold (BH) fMRI data alone. Our approach employs a frequency-domain approach that is independent of external recordings. CVR amplitude is estimated from the BOLD frequency spectrum and CVR lag is estimated from the Fourier phase using the global-mean BOLD signal as reference. Unlike referencing to external recordings, these lags are specific to the brain. We demonstrated our method in detecting regional CVR amplitude and lag differences across healthy (CTL), hypertensive (HT) and hypertension-plus-type-2-diabetes (HT + DM) groups of similar ages and sex ratios, with a total <i>N</i> of 49. We found CVR amplitude to be significantly higher in CTL compared to HT + DM, with minimal difference between CTL and HT. Also, voxelwise CVR lag estimated in the Fourier domain is a more sensitive marker of vascular dysfunction than CVR amplitude. CVR lag in HT is significantly shorter than in CTL, with minimal difference between CTL and HT + DM. Our results support the importance of joint CVR amplitude and lag assessments in clinical applications.</p>","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"459-475"},"PeriodicalIF":4.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11572012/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142119918","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}