Journal of Cerebral Blood Flow and Metabolism最新文献

{"title":"FTO promotes post-stroke neuroprotection by m⁶A demethylation of c-Jun.","authors":"Anil K Chokkalla, Suresh L Mehta, Soomin Jeong, Hui-Lung Sun, Qing Dai, Raghu Vemuganti","doi":"10.1177/0271678X251340808","DOIUrl":"10.1177/0271678X251340808","url":null,"abstract":"<p><p><i>N</i>⁶-methyladenosine (m⁶A) is a critical epitranscriptomic regulator of neuronal function. Cerebral ischemia induces m⁶A hypermethylation due to decreased expression of m⁶A demethylase fat mass and obesity-associated (FTO) protein. Previously, we showed that cerebral overexpression of FTO with an adeno-associated virus (AAV) 9 protects the post-stroke brain. We presently evaluated the mechanistic basis for FTO-dependent m⁶A demethylation in post-ischemic neuroprotection using the mice transient middle cerebral artery occlusion model of experimental stroke. Based on the bioinformatic predictions and m⁶A abundance, pro-apoptotic transcription factor Jun proto-oncogene (c-Jun) with 19 m⁶A sites was chosen as an exemplary target. FTO overexpression normalized the post-stroke m⁶A hypermethylation of c-Jun without altering its transcript levels. FTO-dependent m⁶A demethylation suppressed translation of c-Jun. Consequently, several c-Jun target genes are transcriptionally repressed, and the post-ischemic neuronal apoptosis is decelerated, as seen by decreased cleaved caspase-3 levels and TUNEL⁺ neurons in the FTO AAV9 treated group compared to the control AAV9 treated group. Moreover, replenishing c-Jun precluded the FTO-mediated post-stroke neuroprotection and functional recovery. Collectively, this study demonstrated that the FTO/m⁶A/c-Jun axis ameliorates post-stroke neuronal apoptosis and brain damage, leading to better functional outcomes.</p>","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"1877-1890"},"PeriodicalIF":4.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12081378/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144078364","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":"Amplitude fluctuations of cerebrovascular oscillations and CSF movement desynchronize during NREM3 sleep.","authors":"Vidhya V Nair, Brianna R Kish, Hideyuki Oshima, Adam M Wright, Qiuting Wen, A J Schwichtenberg, Yunjie Tong","doi":"10.1177/0271678X251337637","DOIUrl":"10.1177/0271678X251337637","url":null,"abstract":"<p><p>Fluctuations in cerebral blood volume (CBV) are a dominant mechanism aiding cerebrospinal fluid (CSF) movement in the brain during wakefulness and non-rapid eye movement (NREM) sleep. However, it is unclear if the amplitudes of CBV oscillations also change in proportion to the changes in amplitude of CSF movement across specific NREM sleep states. It is also not known if the coupling strength between them varies between NREM sleep states. To investigate these relationships, we measured cerebral hemodynamics and craniad CSF movement at the fourth ventricle simultaneously during wakefulness and NREM sleep states using concurrent Electroencephalography and functional Magnetic Resonance Imaging. We found that the amplitude fluctuations of cerebral hemodynamics and CSF oscillations desynchronize from one another only during deep NREM3 state, despite the strong mechanical coupling between CBV changes and CSF movement, which was consistent across all states. This suggests the existence of a different mechanism, linked to the cortical interstitial volume/resistance change, that regulates the NREM3 CSF inflow into the brain.</p>","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"1980-1992"},"PeriodicalIF":4.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12081394/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144078328","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":"Repeatability and reliability of cerebrovascular reactivity in young adults using multi-echo, multi-contrast MRI.","authors":"Elizabeth G Keeling, Maurizio Bergamino, Lauren R Ott, Molly M McElvogue, Ashley M Stokes","doi":"10.1177/0271678X251345292","DOIUrl":"10.1177/0271678X251345292","url":null,"abstract":"<p><p>Cerebrovascular reactivity (CVR) shows promise as a biomarker of vascular integrity and may benefit from a repeatable, reliable, and microvasculature-sensitive acquisition. A combined spin- and gradient-echo (SAGE) functional MRI (fMRI) acquisition may improve repeatability and reliability compared to single spin- (SE) and gradient-echo (GRE) fMRI and provide a microvascular-weighted analysis. The most repeatable and reliable MRI acquisition CVR maps were compared across three CVR paradigms: a breath-hold task, a breath modulation task, and a resting state acquisition. SAGE-fMRI data was acquired in fifteen young adults at two timepoints. Mean gray matter (GM) within-subject coefficient of variation (wCV) and intraclass correlation coefficient (ICC) were compared within the quantitative and weighted SAGE-fMRI CVR maps and single GRE- and SE-fMRI CVR. Total and microvascular MRI inputs with lowest wCV and highest ICC were used to compare three CVR paradigms. Total and microvascular weighted SAGE-fMRI CVR had the lowest wCV and highest ICC across paradigms. The breath-hold paradigm produced significantly higher GM CVR estimates. SAGE repeatably and reliably measures CVR and offers a simultaneous, complementary analysis on total and microvascular scales. The breath-hold paradigm showed significantly higher CVR estimates, but less compliance-dependent protocols may be ideal for applications in patient populations.</p>","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"2030-2046"},"PeriodicalIF":4.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12106380/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142453","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":"Environmental enrichment promotes functional recovery from stroke via enhancing neuroplasticity through the action of β-HB.","authors":"Zhuang-Yin Qu, Chang-Jing Zhang, Ya-Lan Hou, Hui-Lin Li, Long Lin, Ai Teng, Chang-Run Shi, Wen-Shuo Lu, Xiao-Wei Zhang, Fei Li, Lei Chang, Yu-Hui Lin","doi":"10.1177/0271678X251328179","DOIUrl":"10.1177/0271678X251328179","url":null,"abstract":"<p><p>Stroke is a leading cause of adult disability worldwide, unfortunately, no drugs are clinically available to promote functional recovery after stroke. Although animal environmental enrichment is a recognized paradigm for promoting stroke repair, elusive mechanisms hinder its clinical translation. Here, we show that β-hydroxybutyrate (β-HB) level in the peri-infarct cortex is upregulated after environmental enrichment (EE) exposure. Importantly, exogenous supplementation of β-HB promotes functional recovery to a similar extent as EE exposure. Moreover, the beneficial effects of EE on stroke recovery, including functional recovery, neuroplasticity-related proteins upregulation, and structural and functional plasticity enhancement, are abolished by β-HB transporter inhibitor, AR-C155858. Intriguingly, supplementation with (R)-3-hydroxybutyl (R)-β-HB, a ketone ester (KE), substantially increases β-HB level and lessens motor functional impairments. Together, our findings indicate that β-HB is a critical substrate for EE-mediated stroke recovery and supplementation with β-HB monoester drinks may serve as a novel strategy to translate EE from bench to bedside.</p>","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"1918-1931"},"PeriodicalIF":4.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12081400/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144078360","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":"Exploring differences in circulating metabolites of females and males with Alzheimer's disease.","authors":"Sara Serafini, Antonella Angiolillo, Gabriella Ferretti, Giulia Viviani, Carmela Matrone, Alfonso Di Costanzo","doi":"10.1177/0271678X251340513","DOIUrl":"10.1177/0271678X251340513","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a progressive neurodegenerative disorder that leads to cognitive and functional decline and primarily affects the elderly population. Metabolic alterations, particularly in the amino acid and fatty acid pathways, are increasingly being recognized in AD. However, the role of sex in these metabolic changes remains insufficiently understood, despite evidence suggesting that AD may manifest more strongly in females. This study investigated sex-specific metabolic patterns in AD by analyzing routine and non-routine hematological tests, including amino acids and fatty acid profiles. The results showed that certain metabolites such as citrulline and alanine were frequently altered in patients with AD. Notably, docosahexaenoic acid, dihomo-gamma-linolenic acid, and gamma-linolenic acid levels were exclusively elevated in female patients. Additionally, females exhibited significantly lower Aβ42 and higher gamma-linolenic acid levels than males, with the trend becoming more pronounced during the early stages of the disease. Despite these differences, most metabolic markers did not show significant sex-based variation. These findings suggest that while some sex-specific metabolic differences exist in AD, a larger cohort is needed to confirm these patterns and fully understand the influence of sex on AD-related metabolic changes.</p>","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"2004-2015"},"PeriodicalIF":4.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12084220/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144078362","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":"Chronic treatment with adenosine A1 receptor antagonist promotes neurogenesis and improves outcome after cerebral ischemia.","authors":"Maria Ardaya, Monica Benito-Muñoz, Esther Rubio-López, Maider Garbizu, Laura Aguado, Naroa Mocha-Muñoz, Leyre Iglesias, Unai Alduntzin, Carlos Matute, Federico N Soria, Vanessa Gómez-Vallejo, Aitzol García-Etxarri, Jordi Llop, Fabio Cavaliere, Abraham Martín","doi":"10.1177/0271678X251345294","DOIUrl":"10.1177/0271678X251345294","url":null,"abstract":"<p><p>Adenosine A1 receptors (A1ARs) are promising targets for stroke treatment, potentially due to their relatively unexplored effects on proliferation and differentiation of newborn neurons. In this study, we investigated the impact of chronic treatment with the A1ARs antagonist DPCPX on neurogenesis following MCAO in rodents, using PET with [¹⁸F]FLT in rats and immunohistochemistry in mice. In addition, we assessed the therapeutic properties of DPCPX on stroke recovery with a comprehensive battery of neurological and behavioral tests. The outcome shows that blocking A1ARs signaling with DPCPX improved immunohistochemical results in 8 to 28 days after MCAO in mice. PET imaging with [¹⁸F]FLT revealed an increase in cellular proliferation following DPCPX treatment in the subventricular zone at day 8 post-ischemia in rats, a result further supported by IHC in SVZ of ischemic animals. Furthermore, DPCPX enhanced the production and integration of newborn neurons while reducing astrocytic differentiation in the ischemic areas. Finally, behavioral tests showed that chronic treatment with DPCPX ameliorated motor and memory deficits after brain ischemia. All taken in consideration, our results provide novel and compelling evidence of the therapeutic potential of the A1AR antagonist DPCPX for ischemic stroke recovery.</p>","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"2016-2029"},"PeriodicalIF":4.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103464/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144135917","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":"A novel approach for modeling <i>in vivo</i> enzyme turnover in the presence of a suicide inhibitor drug: A proof-of-concept brain PET study on MAG lipase.","authors":"Tommaso Volpi, Daniel Holden, Jean-Dominique Gallezot, Nabeel Nabulsi, Keunpoong Lim, David Labaree, Hong Gao, Michael Kapinos, Edmund J Keliher, Kari R Fonseca, Patrick Trapa, Andrea Varrone, Christer Halldin, Kevin P Maresca, Yiyun Huang, Richard E Carson","doi":"10.1177/0271678X251329254","DOIUrl":"10.1177/0271678X251329254","url":null,"abstract":"<p><p>PET imaging allows the study of enzyme concentration and activity <i>in vivo</i>. The enzyme natural turnover <math><mi>α</mi></math>, relevant for drug development, can be estimated if a suicide inhibitor drug is used. The main aim of this study was to develop a model for estimating <math><mi>α</mi></math> by accounting for the presence of residual inhibitor. We analyzed nonhuman primate PET data with monoacyglycerol lipase (MAGL) tracer [¹¹C]PF-06809247, and suicide inhibitor PF-06818883 (0.03-1.27 mg/kg, active compound PF-06807893). As [¹¹C]PF-06809247 is an irreversible tracer, we used simulations to evaluate the impact of flow limitation on identifiability of kinetic parameters. Based on this, MAGL activity estimates were obtained from three outcome parameters: <i>K</i>_i, <i>k</i>₃, <math><msub><mrow><mover><mrow><mi>K</mi></mrow><mo>˜</mo></mover></mrow><mrow><mn>3</mn></mrow></msub></math> (=<math><mfrac><mrow><msub><mrow><mi>K</mi></mrow><mrow><mn>1</mn></mrow></msub><msub><mrow><mi>K</mi></mrow><mrow><mi>i</mi></mrow></msub></mrow><mrow><msub><mrow><mi>K</mi></mrow><mrow><mn>1</mn></mrow></msub><msub><mrow><mo>-</mo><mi>K</mi></mrow><mrow><mi>i</mi></mrow></msub></mrow></mfrac></math>). A new model, which links enzyme activity to the inhibitor drug's plasma concentration, was used to estimate <math><mi>α</mi></math>. Using a conservative statistical cut-off, MAGL turnover half-lives were estimated (<i>K</i>_i: 3.9 h; <i>k</i>₃: 4.6 h; <math><msub><mrow><mover><mrow><mi>K</mi></mrow><mo>˜</mo></mover></mrow><mrow><mn>3</mn></mrow></msub></math>: 6.1 h) - with faster turnover for <i>K</i>_i (flow-limited). Serial PET experiments and measuring the drug's plasma concentration allowed to estimate <math><mi>α</mi></math> correcting for residual suicide inhibition. This approach can be extended to other PET enzyme targets, improving our understanding of enzyme pathological alterations and suicide inhibitor-based therapies.</p>","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"1947-1960"},"PeriodicalIF":4.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12081407/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144078322","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":"Retrograde and anterograde trans-synaptic viral tracing of neuronal connections reveals local and distant effects of ischemic stroke on dendritic spines.","authors":"Myrthe Van Sprengel, Jenna Butterworth, Patrick L Reeson, Craig E Brown","doi":"10.1177/0271678X251345360","DOIUrl":"10.1177/0271678X251345360","url":null,"abstract":"<p><p>Focal stroke leads to complex neurological disturbances with variable recovery. One explanation for this variability is that stroke disrupts local and remote neural circuits via the connectome, termed 'diaschisis'. Past studies have yielded mixed effects of stroke on dendritic structure in distant regions. However, a previous limitation was the lack of sampling specifically from neurons directly connected to those within the infarct. To overcome this, we used retrograde and anterograde trans-synaptic AAVs to examine dendritic spine density in neurons that provide inputs to, or receive outputs (pre- and post-synaptic) from primary forelimb somatosensory cortex at 1 or 6 weeks after stroke. For both pre- and post-synaptic neurons, spine density was generally lower in superficial and deep neurons in peri-infarct and motor cortex at 1 week, which recovered by 6 weeks. By contrast, no changes in spine density were observed in ipsilateral secondary somatosensory (S2) or contralateral primary somatosensory cortex at 1 week, although there was an increase in spines in select S2 neurons at 6 weeks. Our data show that some cortical connections are more disrupted by stroke than others, particularly those in peri-infarct and motor cortex which could serve as an important substrate for stroke recovery and future therapies.</p>","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"1891-1904"},"PeriodicalIF":4.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12106386/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142522","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":"Combination of alpha-1 antitrypsin (A1AT) and anti-TNFα as a neuroprotective strategy in the early stages after ischemic stroke.","authors":"Paula García-Rodríguez, Laura Ramiro, Alba Simats, Feifei Ma, Anna Rosell, Joan Montaner","doi":"10.1177/0271678X251340234","DOIUrl":"10.1177/0271678X251340234","url":null,"abstract":"<p><p>Neuroprotection after ischemic stroke has been focused on targeting one pathway of the ischemic cascade. In this study, we have hypothesized that combination therapy with alpha-1 antitrypsin (A1AT) and a blocker of tumor necrosis factor (TNFα) could be beneficial in the acute phases after ischemia. Following a detailed safety assessment of the co-administration of both drugs, we tested their neuroprotective effect in a transient mouse model of proximal middle cerebral artery occlusion (MCAo) by evaluating infarct extension and functional outcomes. Anti-TNFα (20 mg/kg) and A1AT were administered at different doses (ranging from 60 mg/kg to 700 mg/kg), as a single therapy during occlusion or at different time-points following reperfusion. Results showed that the administration of A1AT (60 mg/kg) in combination with anti-TNFα (20 mg/kg) was safe and effective when given during occlusion by reducing infarct volume at 24 h by 27% compared with the vehicle group (p = 0.0001). In conclusion, the synergy of the anti-apoptotic and anti-inflammatory properties of both drugs can reduce infarct volume in a stroke mouse model when given in the hyperacute phase. This approach shows promise as an early intervention strategy for stroke patients and underscores the potential of drug repurposing to develop new stroke treatments.</p>","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"1993-2003"},"PeriodicalIF":4.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12081373/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144078288","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":"Neuronal deterioration associated with hyperexcitability under mild chronic cerebral hypoperfusion.","authors":"Takuya Urushihata, Manami Takahashi, Masafumi Shimojo, Yuhei Takado, Nobuhiro Nitta, Yosuke Tajima, Kazuto Masamoto, Iwao Kanno, Yutaka Tomita, Naruhiko Sahara, Masaya Takahashi, Takayuki Obata, Hiroshi Ito, Tetsuro Yamashita, Tetsuya Suhara, Makoto Higuchi, Hiroyuki Takuwa","doi":"10.1177/0271678X251328971","DOIUrl":"10.1177/0271678X251328971","url":null,"abstract":"<p><p>Chronic cerebral hypoperfusion (CCH) has been indicated to impair cognitive and diverse brain functions. However, the neural mechanisms linking these cerebrovascular and phenotypic alterations remain unclear. Here, we investigated the effect of CCH on neuronal activity in male mice with unilateral common carotid artery occlusion using optical imaging and MRI. Our examinations revealed enhanced neuronal activity in concurrence with increased glutamate and tissue acidosis up to seven days after occlusion. At 21-28 days after occlusion, neuronal activity decreased below baseline, while the acidotic but not the hyperglutamatergic state persisted. Notably, pharmacological blockade of the N-methyl-D-aspartate-type glutamate receptor, initiated at an early stage of CCH, suppressed the onset of neuronal hyperexcitation and subsequent deficits in neuronal activity. Altogether, we provide experimental evidence that CCH induces a glutamate surge and results in neuronal hyperexcitation at an early phase, which thereafter gives rise to a non-lethal but progressive deterioration of neuronal functions.</p>","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"1932-1946"},"PeriodicalIF":4.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511680/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144078332","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}