Experimental Neurology最新文献

{"title":"The interaction effects of hypertension and aging on brain network in spontaneously hypertensive rats: A resting-state functional magnetic resonance imaging study","authors":"Yingying Yang ,&nbsp;Qingfeng Zhu ,&nbsp;Lixin Wang ,&nbsp;Duo Gao ,&nbsp;Yanmin Zhao ,&nbsp;Tiefeng Li ,&nbsp;Juan Du ,&nbsp;Defeng Liu ,&nbsp;Hongtao Niu ,&nbsp;Zuojun Geng","doi":"10.1016/j.expneurol.2026.115687","DOIUrl":"10.1016/j.expneurol.2026.115687","url":null,"abstract":"<div><div>Although both hypertension and aging are considered primary risk factors for cognitive impairment, the combined effects of hypertension and aging on the functional network of the brain remain poorly understood. We aimed to investigate the interactions between hypertension and aging on the brain functional network in spontaneously hypertensive rats (SHRs). Using resting-state functional magnetic resonance imaging, we investigated the interactive effects of hypertension and aging on the brain network in terms of topological metrics and connectivity patterns. We detected changes in the functional connectivity density, topological metrics and functional network connectivity in 20-week-old and 80-week-old SHRs compared with those in age-matched Wistar–Kyoto rats. The functional hub in the brain shifted from the retrosplenial granule to the caudate putamen in SHRs from the young adult stage to the aged stage, while the small-world topology was preserved. We investigated the effects of interactions between hypertension and aging on functional connectivity involving a large-scale increased network in aged SHRs. We identified alterations in the functional hub and network associated with hypertension and aging. Our study supports the viewpoints of compensatory functional reorganization and neural plasticity. Network analysis is a promising technique for exploring brain function in rats and could provide potential neuroimaging biomarkers. It is essential to identify a neuroimaging biomarker that not only allows the prediction of brain abnormalities but also helps in understanding the neurobiological mechanisms underlying hypertension and aging.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"400 ","pages":"Article 115687"},"PeriodicalIF":4.2,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146178600","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":"The TAK1-YAP Axis synergistically suppresses oxidative stress and apoptosis via a non-canonical signaling pathway: A neuroprotective mechanism in ischemic stroke.","authors":"Enzhuang Pan, Juan Chen, Yue Xin, Yaxin Gao, Jingquan Dong, Yingda Xu, Jingyuan Zhou, Xinyu Zhou, Huizhen Chen, Panpan Zhao","doi":"10.1016/j.expneurol.2026.115817","DOIUrl":"https://doi.org/10.1016/j.expneurol.2026.115817","url":null,"abstract":"<p><p>Ischemic stroke (IS) is one of the leading causes of global disability and mortality, yet effective treatments targeting oxidative stress (OS) and neuronal apoptosis remain lacking. This study investigates the neuroprotective role of Yes-associated protein (YAP) in IS and its regulatory mechanisms. Using clinical IS patient serum samples, a mouse middle cerebral artery occlusion (MCAO) model, and an in vitro oxygen-glucose deprivation/reoxygenation (OGD/R) model, we found that YAP protein levels were significantly downregulated post-ischemia, correlating with aggravated OS and neuronal apoptosis. Overexpression of Yap1 via adeno-associated virus (AAV) vectors reduced infarct volume, restored cerebral blood flow, and improved neurological and cognitive functions in MCAO mice. Mechanistically, YAP alleviated oxidative damage by enhancing the activity of antioxidant enzymes (e.g., GSH-Px, SOD) and inhibited apoptosis, as validated by TUNEL and Annexin V/PI assays. Intriguingly, under ischemic conditions, YAP phosphorylation was regulated by TAK1 rather than the canonical Hippo signaling pathway. Knockdown of TAK1 synergized with YAP activation to mitigate oxidative damage and neuronal apoptosis. These findings reveal the critical neuroprotective role of YAP in IS and identify the TAK1-YAP interaction as a therapeutic target. This study provides a mechanistic foundation for developing YAP-based interventions for IS.</p>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":" ","pages":"115817"},"PeriodicalIF":4.2,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147856154","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":"Chronic activation of corticospinal tract neurons after pyramidotomy injury enhances neither behavioral recovery nor axonal sprouting.","authors":"Zimei Wang, Matthew Brannigan, Logan Friedrich, Murray G Blackmore","doi":"10.1016/j.expneurol.2026.115810","DOIUrl":"https://doi.org/10.1016/j.expneurol.2026.115810","url":null,"abstract":"<p><p>Modulation of neural activity is a promising strategy to influence the growth of axons and improve behavioral recovery after damage to the central nervous system. The benefits of neuromodulation likely depend on optimization across multiple input parameters. Here we used a chemogenetic approach to achieve continuous, long-term elevation of neural activity in murine corticospinal tract (CST) neurons. To specifically target CST neurons, AAV2-retro-DIO-hM3Dq-mCherry or matched mCherry control was injected to the cervical spinal cord of adult Emx1-Cre transgenic mice. Pilot studies verified efficient transgene expression in CST neurons and effective elevation of neural activity as assessed by cFos immunohistochemistry. In subsequent experiments mice were administered either DIO-hM3Dq-mCherry or control DIO-mCherry, were pre-trained on a pellet retrieval task, and then received unilateral pyramidotomy injury to selectively ablate the right CST. Mice then received continual clozapine via drinking water and weekly testing on the pellet retrieval task, followed by cortical injection of a viral tracer to assess cross-midline sprouting by the spared CST. After sacrifice at eight weeks post-injury immunohistochemistry for cFos verified elevated CST activity in hM3Dq-treated animals and immunohistochemistry for PKC-gamma verified unilateral ablation of the CST in all animals. Despite the chronic elevation of CST activity, however, both groups showed similar levels of cross-midline CST sprouting and similar success in the pellet retrieval task. These data indicate that continuous, long-term elevation of activity that is targeted specifically to CST neurons does not affect compensatory sprouting or directed forelimb movements.</p>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":" ","pages":"115810"},"PeriodicalIF":4.2,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147856192","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":"Variability-dominated auditory cortical dysfunction and targeted VNS modulation in a Mecp2^+/- model of Rett syndrome.","authors":"Ghazaal Tahmasebi, Katherine S Adcock, Crystal T Engineer","doi":"10.1016/j.expneurol.2026.115811","DOIUrl":"https://doi.org/10.1016/j.expneurol.2026.115811","url":null,"abstract":"<p><strong>Objective: </strong>Rett syndrome is a neurodevelopmental disorder caused by mutations in the X-linked transcriptional regulator MECP2, which causes widespread abnormalities in cortical network activity and sensory processing. In rodent models, Mecp2^+/- rats recapitulate key clinical features of Rett syndrome, including disrupted auditory cortical responses and impaired spike timing fidelity. Given its potential to normalize abnormal cortical activity, vagus nerve stimulation (VNS) may offer a promising therapeutic approach. This study examined auditory local field potential (LFP) responses in Mecp2^+/- rats and assesses the modulatory effects of VNS.</p><p><strong>Methods: </strong>Auditory cortical LFPs were recorded in response to speech, noise, and tone stimuli in Mecp2^+/- rats, VNS-treated Mecp2^+/- rats, and wild-type littermates. LFP component latency, amplitude, trial-to-trial variability, and oscillatory band power were quantitatively analyzed across groups.</p><p><strong>Results: </strong>Mecp2^+/- rats were characterized by delayed and weakened LFP responses, widespread increases in trial-to-trial variability of latency, amplitude, and power, and stimulus-dependent changes in spectral power, with the most pronounced abnormalities for speech, followed by tones and then noise. VNS partially normalized these abnormalities by improving speech-evoked latency and variability and reducing noise-evoked power variability. However, tone-evoked responses were largely unchanged with VNS, indicating a selective rescue of specific components and stimulus classes rather than a global restoration of auditory function. These findings demonstrate robust auditory cortical processing deficits in a preclinical model of Rett syndrome and highlight the potential of VNS to partially restore cortical function. The results support further development of targeted neuromodulatory interventions to ameliorate sensory processing abnormalities in Rett syndrome.</p>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":" ","pages":"115811"},"PeriodicalIF":4.2,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147856200","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":"Newborn and juveniles exhibit distinct transcriptional and pathological profiles after brain injury.","authors":"Oluwagbemisola Aderibigbe, Akshara D Thakore, Martin N Griffin, Levi B Wood, Susan S Margulies","doi":"10.1016/j.expneurol.2026.115808","DOIUrl":"https://doi.org/10.1016/j.expneurol.2026.115808","url":null,"abstract":"<p><p>Age and injury severity influence patient outcomes and recovery trajectories after traumatic brain injury (TBI). However, there is a paucity in understanding the effects of age and biomechanical load on molecular changes to the brain after pediatric TBI. We examined frontal lobe transcriptional changes and axonal injury 1 day after sagittal rapid non-impact head rotation (RNR) in newborn 3-5 day old piglets (N = 26) exposed to either Low (43.9 ± 6.3 rad/s) or High (150 ± 2.6 rad/s) loads compared to juvenile 4 week old piglets (N = 40) exposed to scaled High loads (124.3 ± 1.7 rad/s) and to age-matched Shams. In newborns, we identified 780 differentially expressed genes (DEGs) and 333 DEGs in the Low and High groups, respectively, with 91 of these overlapping. While overlapping DEGs and gene sets were consistent with stress, inflammation, BBB disruption, mitochondrial maintenance, extracellular matrix (ECM) and collagen degradation and formation, DEGs specific to the High group signaled damage and exacerbated immune response. Axonal injury volume was significantly larger in the High group than the Low and Sham newborn groups, and increased axon growth and neuronal dysfunction DEGs were also correlated with increased rotational loads. Importantly, age had a profound influence, despite mechanically equivalent rotational loads. Upregulated DEGs from newborn piglets were associated with endothelial cells, while juvenile piglet DEGs were associated with neurons. Additionally, even sham newborns and juveniles displayed distinct microglia morphologies, and TBI changes were observed only in the juveniles. In summary, we conclude that biological differences associated with developmental stage, rather than biomechanical load, dominate the tissues level response. In total, our data reveal the influence of rotational magnitude and emphasizes distinct gene expression, cell response, and tissue pathology changes in newborn versus juvenile brains after TBI.</p>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":" ","pages":"115808"},"PeriodicalIF":4.2,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835497","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":"Microglial P2RY12 mediates migration to and protection of cerebral microvasculature after ischemia–reperfusion via Caveolin-1","authors":"Yuan Wang ,&nbsp;Xiaoyan Li ,&nbsp;Weijie Li ,&nbsp;Chenglong Wang ,&nbsp;Ge Xu ,&nbsp;Shanshan Yu","doi":"10.1016/j.expneurol.2026.115662","DOIUrl":"10.1016/j.expneurol.2026.115662","url":null,"abstract":"<div><div>Disruption of blood-brain barrier (BBB) integrity after cerebral ischemia-reperfusion (I/R) injury contributes to neuroinflammation and neuronal damage. Microglia plays a significant role in the repair processes of the BBB, and the G protein-coupled receptor P2RY12 is involved in microglial chemotactic migration. However, its precise function and associated downstream mechanisms are unclear. Caveolin-1 (Cav-1), a membrane scaffold protein, plays a key role in signal transduction and cellular motility. This study employed in vivo and in vitro experimental models to explore the functional role of the P2RY12-Cav-1 interaction after ischemic stroke. Blocking P2RY12 with PSB0739 worsened neurological deficits and BBB disruption. In contrast, the P2RY12 agonist 2MeSADP attenuated I/R injury, promoted Bv2 cell migration. Disrupting lipid rafts with methyl-β-cyclodextrin (MβCD) abolished these benefits. Co-immunoprecipitation verified P2RY12 interacts with the scaffolding domain of Cav-1. These findings reveal a possible mechanism by which the P2RY12-Cav-1 signaling axis regulates microglial chemotaxis for microvascular protection, offering a potential therapeutic target for the treatment of ischemic stroke.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"399 ","pages":"Article 115662"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146025603","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":"Corrigendum to \"Secukinumab attenuates neuroinflammation and neurobehavior defect via PKCβ/ERK/NF-κB pathway in a rat model of GMH\" [Exp Neurol. 2023 Feb; 360:114276].","authors":"Shengpeng Liu, Shuixiang Deng, Yan Ding, Jerry J Flores, Xiaoli Zhang, Xiaojing Jia, Xiao Hu, Jun Peng, Gang Zuo, John H Zhang, Ye Gong, Jiping Tang","doi":"10.1016/j.expneurol.2026.115797","DOIUrl":"https://doi.org/10.1016/j.expneurol.2026.115797","url":null,"abstract":"","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":" ","pages":"115797"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147812911","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":"Initiation site of experimentally-evoked spreading depolarizations influence tissue outcomes in a murine stroke model","authors":"Michael C. Bennett ,&nbsp;Russell A. Morton ,&nbsp;Andrew P. Carlson ,&nbsp;C. William Shuttleworth","doi":"10.1016/j.expneurol.2026.115671","DOIUrl":"10.1016/j.expneurol.2026.115671","url":null,"abstract":"<div><div>Spreading depolarization waves (SDs) are implicated in secondary expansion of brain injuries and are the target for initial clinical intervention trials. However, the assumption that SD directly causes neuronal injury has been challenged by recent findings with experimentally-induced SD in stroke models. The current study addressed this controversy by examining whether stroke consequences are confounded by the precise location of experimental SD initiation. Focal ischemic lesions were generated by transient distal middle cerebral artery occlusion in male mice. Clusters of SDs (6 at 10-min intervals) were induced by either focal KCl application or optogenetic stimulation during occlusion. SDs were initiated either in regions close to the infarct core (penumbral-SD; &lt;50% perfusion) or in less compromised tissue in the same hemisphere (remote-SD; &gt;70% perfusion). Despite the fact that all SDs fully invaded stroke expansion areas, the location of experimental SD induction had significant effects on stroke outcomes measured 48 h after reperfusion. Penumbral-SDs resulted in larger infarct expansion than seen in control stroke mice lacking experimentally-imposed SD. Conversely, remote-SDs led to significantly smaller infarcts than stroke alone. Laser speckle contrast imaging of blood flow in injury expansion areas showed enhanced hypoperfusion responses after penumbral-SDs and larger hyperemic responses after remote-SDs, suggesting that differential vascular responses could contribute to stroke outcomes. Overall, this study helps to reconcile different prior reports by showing that experimentally-induced SDs can either exacerbate or reduce stroke-induced injury depending on the SD initiation site and further strengthens evidence for injurious roles of SDs initiating in vulnerable brain tissue.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"399 ","pages":"Article 115671"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146076269","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":"Imipramine improves motor impairments in a rat model of Parkinson's disease induced by 6-hydroxydopamine; the role of oxidative stress and neurotrophic factors","authors":"Mahdi Hajibabaei ,&nbsp;Bagher Jafarvand ,&nbsp;Elmira Beirami ,&nbsp;Neda Valian","doi":"10.1016/j.expneurol.2026.115646","DOIUrl":"10.1016/j.expneurol.2026.115646","url":null,"abstract":"<div><h3>Introduction</h3><div>Parkinson's disease (PD) is a progressive neurological disorder characterized by the loss of dopaminergic neurons in the substantia nigra and is associated with neuroinflammation, apoptosis, oxidative stress, and motor impairment. Imipramine, a tricyclic antidepressant, has a wide range of biological effects such as anti-inflammatory, anti-apoptotic, and free radical scavenging activities. The present study was designed to investigate the neuroprotective effect of imipramine in a rat model of PD induced by 6-hydroxydopamine (6-OHDA).</div></div><div><h3>Methods</h3><div>Male Wistar rats were treated with daily intraperitoneal administration of imipramine (20 mg/kg, for 14 days) starting 72 h after 6-OHDA injection (20 μg/rat; 4 μl in the right medial forebrain bundle (MFB)). The motor performance was assessed using the rotarod, beam, pole, and apomorphine-induced rotation tests. The protein levels of neurotrophic factors (BDNF, GDNF, and NT3) and factors involved in oxidative stress (MDA, CAT, SOD, GST, and GSH) were measured in the striatum by ELISA technique. The neuronal survival was also evaluated by Nissl staining.</div></div><div><h3>Results</h3><div>Our results showed that 6-OHDA caused motor impairments and neuronal cell death. It also significantly reduced the protein levels of neurotrophic factors and induced an oxidative stress response in the striatum of rats. Whereas, imipramine treatment effectively reduced 6-OHDA-induced motor deficits and neuronal cell death. This improvement was accompanied by an increase in neurotrophic factors, especially GDNF, as well as a reduction in oxidative stress through increased SOD levels.</div></div><div><h3>Conclusion</h3><div>These findings provide direct evidence that imipramine treatment contributes to improve of neuronal cell death and motor deficits, perhaps by increasing the striatal levels of SOD and GDNF, which play a key role in the survival of dopaminergic neurons. Further studies are also needed to elucidate the precise underlying molecular mechanisms of neuroprotective effects of imipramine.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"399 ","pages":"Article 115646"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145988894","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":"Mismatch between oxygen delivery and consumption in the cerebral watershed during subacute global hypoperfusion","authors":"Baoqiang Li ,&nbsp;Hewei Cao ,&nbsp;Hajime Takase ,&nbsp;Srinivasa Rao Allu ,&nbsp;Yimeng Wu ,&nbsp;Buyin Fu ,&nbsp;Sergei A. Vinogradov ,&nbsp;Eng H. Lo ,&nbsp;Ken Arai ,&nbsp;Cenk Ayata ,&nbsp;Sava Sakadžić","doi":"10.1016/j.expneurol.2026.115666","DOIUrl":"10.1016/j.expneurol.2026.115666","url":null,"abstract":"<div><div>Hemodynamically significant carotid artery stenosis is a common clinical condition that can lead to chronic cerebral hypoperfusion. Despite the well-recognized pivotal role of pial collaterals in maintaining cerebral perfusion during focal arterial occlusions, regulation of microvascular blood flow and oxygenation in the cerebral watershed “pial-collateral territory” during chronic hypoperfusion remains unexplored. To answer this question, we applied 2-photon microscopy and Doppler optical coherence tomography to assess the changes in cerebral blood flow, capillary red-blood-cell (RBC) flux, and intravascular oxygen partial pressure (PO₂), seven days after bilateral common-carotid artery stenosis (BCAS). The measurements were performed in the middle-cerebral-artery (MCA) territory and the watershed between the MCA and anterior-cerebral-artery territories in the awake, head-restrained C57BL/6 mice, through a glass-sealed cranial window. The results showed that BCAS induced a significant decrease in microvascular perfusion in the watershed area compared to the MCA territory, with the largest RBC flux reduction observed in the subcortical white matter. The watershed area exhibited a larger drop between arterial and venous PO₂ and the calculated oxygen saturation, indicating a significant increase in oxygen extraction fraction following BCAS. Structural analysis of the microvasculature showed significant BCAS-induced dilation of pial collaterals, suggesting a potential compensatory mechanism to improve blood flow in the hypoperfused watershed. However, microvascular morphology did not change in either region, implying an absence of structural remodeling at this early stage. Collectively, these findings point to an oxygen supply-consumption mismatch and heightened vulnerability in the watershed areas, particularly affecting the subcortical white matter, during flow-limiting cervical artery stenosis.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"399 ","pages":"Article 115666"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146046322","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}