Experimental Neurology最新文献

{"title":"Protein tau phosphorylation in the proline rich region and its implication in the progression of Alzheimer's disease","authors":"Paula Merino-Serrais ,&nbsp;José Miguel Soria ,&nbsp;Cristina Aguirre Arrabal ,&nbsp;Alfonso Ortigado-López ,&nbsp;María Ángeles García Esparza ,&nbsp;Alberto Muñoz ,&nbsp;Félix Hernández ,&nbsp;Jesús Ávila ,&nbsp;Javier DeFelipe ,&nbsp;Gonzalo León-Espinosa","doi":"10.1016/j.expneurol.2024.115049","DOIUrl":"10.1016/j.expneurol.2024.115049","url":null,"abstract":"<div><div>Tau has a wide variety of essential functions in the brain, but this protein also plays a determining role in the development of Alzheimer's disease (AD) and other neurodegenerative diseases called tauopathies. This is due to its abnormal aggregation and the subsequent formation of neurofibrillary tangles. Tau hyperphosphorylation appears to be a critical step in its transformation into an aggregated protein. However, the exact process, including the cellular events that trigger it, remains unclear. In this study, we employed immunocytochemistry assays on hippocampal sections from AD cases and from tauopathy cases (Braak stage III) with no evidence of cognitive decline, and the P301S mouse model to investigate the colocalization patterns of Tau phosphorylated (p) at specific residues (S202-T205, S214, and T231) within the proline-rich region. Our results show pyramidal neurons in the hippocampus of P301S mice in which Tau is intensely phosphorylated at residues S202 and T205 (recognized by the AT8 antibody), but with no detectable phosphorylation at S214 or T231. These non-colocalizing neurons displayed intensely labeled aggregated pTau deposits distributed through the soma and dendritic processes. However, most of the hippocampal pyramidal neurons are labeled with pTauS214 or pTauT231 antibodies and typically showed a homogeneous and diffuse pTau distribution (not aggregated). This different labeling likely reflects a Tau conformational step, potentially related to the transition from a diffuse tau phosphorylation phenotype (Type 2) into an NFT-like or Type 1 phenotype. We further observed that dendrites of CA3 pyramidal cells are intensely labeled with pTau214 in the <em>stratum lucidum</em>, but not with AT8 or pTauT231. By contrast, analysis of tissue from AD patients or other human tauopathy cases (Braak stage III) with no evidence of cognitive decline revealed extensive colocalization with both antibody combinations in CA1. The complete or mature tangle development may follow a different mechanism in the P301S mouse model or may require more time to achieve the maturity state found in AD cases. Further studies would be necessary to address this question.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"383 ","pages":"Article 115049"},"PeriodicalIF":4.6,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142617564","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":"MAPK signaling pathway in spinal cord injury: Mechanisms and therapeutic potential","authors":"Fei-xiang Lin ,&nbsp;Hou-yun Gu ,&nbsp;Wei He","doi":"10.1016/j.expneurol.2024.115043","DOIUrl":"10.1016/j.expneurol.2024.115043","url":null,"abstract":"<div><div>Spinal cord injury (SCI) is a severe disabling injury of the central nervous system that can lead to motor, sensory, and autonomic dysfunction below the level of the injury. According to its pathophysiological process, SCI can be divided into primary injury and secondary injury. Currently, multiple therapeutic strategies have been proposed to alleviate secondary injury and overcome the occurrence of neurodegenerative events. Although current treatment modalities have achieved varying degrees of success, they cannot effectively intervene or treat its pathological processes, which may be due to the complex treatment and protection mechanisms involved. Research has confirmed that signaling pathways play a crucial role in the pathological processes of SCI and the mechanisms of neuronal recovery. Mitogen-activated protein kinase (MAPK) signaling pathway plays a crucial role in neuronal differentiation, growth, survival and axon regeneration after central nervous system injury. Meanwhile, the MAPK signaling pathway is an important pathway closely related to the pathological processes of SCI. The MAPK signaling pathway is abnormally activated after SCI, and inhibiting the activity of MAPK pathway can effectively inhibit inflammation, oxidative stress, pain and apoptosis to promote the recovery of nerve function after SCI. Based on the role of the MAPK pathway in SCI, it may be a potential therapeutic target. This article summarizes the role and mechanism of MAPK pathway in SCI, and discusses the shortcomings and shortcomings of MAPK pathway in SCI field, as well as the potential challenges of targeting MAPK pathway in SCI treatment strategies. This article aims to elucidate the mechanism of the MAPK pathway in SCI to emphasize the role of targeting the MAPK pathway in the treatment of SCI, providing a theoretical basis for the MAPK pathway as a potential therapeutic target for SCI treatment.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"383 ","pages":"Article 115043"},"PeriodicalIF":4.6,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142617575","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":"Mechanisms of time-restricted feeding-induced neuroprotection and neuronal plasticity in ischemic stroke as a function of circadian rhythm","authors":"Soomin Jeong ,&nbsp;Charles K. Davis ,&nbsp;Raghu Vemuganti","doi":"10.1016/j.expneurol.2024.115045","DOIUrl":"10.1016/j.expneurol.2024.115045","url":null,"abstract":"<div><div>Time-restricted feeding (TRF) is known to promote longevity and brain function, and potentially prevent neurological diseases. Animal studies show that TRF enhances brain-derived neurotrophic factor (BDNF) signaling and regulates autophagy and neuroinflammation, supporting synaptic plasticity, neurogenesis and neuroprotection. Feeding/fasting paradigms influence the circadian cycle, with TRF aligning circadian cycle-related gene expression, and thus altering physiological processes. Emerging evidence highlights the role of gut microbiota in neuronal plasticity, based on the observation that TRF significantly alters gut microbiota composition. Hence, the gut-brain axis may be crucial for maintaining cognitive functions and presents a potential therapeutic target for TRF-mediated neuroprotection. In the context of ischemic stroke where neuronal damage is extensive, TRF can be a preconditioning strategy to enhance synaptic plasticity and neuronal resilience, thus improving outcomes after stroke. This review discussed the link between TRF and circadian regulation in neuronal plasticity and its implications for recovery after stroke.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"383 ","pages":"Article 115045"},"PeriodicalIF":4.6,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603665","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 \"Validation of optimised intracranial spectroscopic probe for instantaneous in-situ monitoring and classification of traumatic brain injury\" [Experimental Neurology, 382 (2024) 1-12, 114960].","authors":"Clarissa A Stickland, Zoltan Sztranyovszky, Jonathan J S Rickard, Pola Goldberg Oppenheimer","doi":"10.1016/j.expneurol.2024.115046","DOIUrl":"https://doi.org/10.1016/j.expneurol.2024.115046","url":null,"abstract":"","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":" ","pages":"115046"},"PeriodicalIF":4.6,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603655","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":"Anesthesia/surgery leads to blood-brain barrier disruption via the transcellular and paracellular pathways, and postoperative delirium-like behavior: A comparative study in mice of different ages","authors":"Xudong Hu ,&nbsp;Lixia Liu ,&nbsp;Xin Da ,&nbsp;Sihui Zhu ,&nbsp;Jiawei Wang ,&nbsp;Menglei Shan ,&nbsp;Yinuo Liu ,&nbsp;Ziqing He ,&nbsp;Guanghong Xu","doi":"10.1016/j.expneurol.2024.115044","DOIUrl":"10.1016/j.expneurol.2024.115044","url":null,"abstract":"<div><h3>Aims</h3><div>Postoperative delirium (POD) is a common complication of anesthesia and surgery, with a higher incidence in elderly patients. Disruption of the blood-brain barrier (BBB) is considered one of the key mechanisms underlying POD. Therefore, the present study aimed to investigate the effects of different BBB permeability alteration pathways on POD in mice of various ages.</div></div><div><h3>Methods</h3><div>C57BL/6 J mice aged 4 and 16 months underwent exploratory laparotomy under sevoflurane anesthesia. Behavioral tests were conducted 24 h prior to surgery, as well as 6, 9, and 24 h postoperatively. Frontal cortex tissue was collected to detect the levels of BBB-related proteins and mRNA.</div></div><div><h3>Results</h3><div>At 6 and 9 h after anesthesia/surgery, 4-month-old mice showed poorer performance on behavioral tests than their untreated counterparts. However, 16-month-old mice exhibited worse behavioral test results at 6, 9, and 24 h after surgery. Anesthesia/surgery 6 h postoperatively increased the expression of vesicle-associated proteins, and BBB leakage in 4-month-old mice. In 16-month-old mice, anesthesia/surgery altered the expression of tight junction proteins, vesicle-associated proteins, and BBB leakage at 6 and 24 h postoperatively.</div></div><div><h3>Conclusion</h3><div>Overall, our results suggest that anesthesia/surgery leads to age-dependent cognitive decline, and is associated with differences in the BBB injury pathways among mice of different ages. The transcellular pathway (transcytosis), compared to the paracellular pathway (tight junction), is more vulnerable to damage following anesthesia/surgery. This study provides new evidence for the improvement of POD through protection of the BBB.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"383 ","pages":"Article 115044"},"PeriodicalIF":4.6,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142589652","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":"Connecting the dots in neuroscience research: The future of evidence synthesis.","authors":"Kaitlyn Hair, María Arroyo Araujo, Sofija Vojvodic, Maria Economou, Charis Wong, Francesca Tinsdeall, Sean Smith, Torsten Rackoll, Emily S Sena, Sarah K McCann","doi":"10.1016/j.expneurol.2024.115047","DOIUrl":"https://doi.org/10.1016/j.expneurol.2024.115047","url":null,"abstract":"<p><p>Making progress in neuroscience research involves learning from existing data. In this perspective piece, we explore the potential of a data-driven evidence ecosystem to connect all primary data streams, and synthesis efforts to inform evidence-based research and translational success from bench to bedside. To enable this transformation, we set out how we can produce evidence designed with evidence curation in mind. All data should be findable, understandable, and easily synthesisable, using a combination of human and machine effort. This will require shifts in research culture and tailored infrastructure to support rapid dissemination, data sharing, and transparency. We also discuss improvements in the way we can synthesise evidence to better inform primary research, including the potential of emerging technologies, big-data approaches, and breaking down research silos. Through a case study in stroke research, one of the most well-established areas for synthesis efforts, we demonstrate the progress in implementing elements of this ecosystem, with an emphasis on the need for coordinated efforts between laboratory researchers and synthesists.</p>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":" ","pages":"115047"},"PeriodicalIF":4.6,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603652","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":"Temporal development of seizure threshold and spontaneous seizures after neonatal asphyxia and the effect of prophylactic treatment with midazolam in rats","authors":"Ricardo Schmidt ,&nbsp;Björn Welzel ,&nbsp;Annika Merten ,&nbsp;Hannah Naundorf ,&nbsp;Wolfgang Löscher","doi":"10.1016/j.expneurol.2024.115042","DOIUrl":"10.1016/j.expneurol.2024.115042","url":null,"abstract":"<div><div>Birth asphyxia (BA) and subsequent hypoxic-ischemic encephalopathy (HIE) is one of the most serious birth complications affecting full-term infants and can result in severe disabilities including mental retardation, cerebral palsy, and epilepsy. Animal models of BA and HIE are important to characterize the functional and behavioral correlates of injury, explore cellular and molecular mechanisms, and assess the potential of novel therapeutic strategies. Here we used a non-invasive, physiologically validated rat model of BA and acute neonatal seizures that mimics many features of BA and HIE in human infants to study (i) the temporal development of epilepsy with spontaneous recurrent seizures (SRS) in the weeks and months after the initial brain injury, (ii) alterations in seizure threshold and hippocampal EEG that may precede the onset of SRS, and (iii) the effect of prophylactic treatment with midazolam. For this purpose, a total of 89 rat pups underwent asphyxia or sham asphyxia at postnatal day 11 and were examined over 8–10.5 months. In vehicle-treated animals, the incidence of electroclinical SRS progressively increased from 0 % at 2.5 months to 50 % at 6.5 months, 75 % at 8.5 months, and &gt; 80 % at 10.5 months after asphyxia. Unexpectedly, post-asphyxial rats did not differ from sham-exposed rats in seizure threshold or interictal epileptiform discharges in the EEG. Treatment with midazolam (1 mg/kg i.p.) after asphyxia, which suppressed acute symptomatic neonatal seizures in about 60 % of the rat pups, significantly reduced the incidence of SRS regardless of its effect on neonatal seizures. This antiepileptogenic effect of midazolam adds to the recently reported prophylactic effects of this drug on BA-induced neuroinflammation, brain damage, behavioral alterations, and cognitive impairment in the rat asphyxia model of HIE.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"383 ","pages":"Article 115042"},"PeriodicalIF":4.6,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142589807","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":"Early α-synuclein/synapsin III co-accumulation, nigrostriatal dopaminergic synaptopathy and denervation in the MPTPp mouse model of Parkinson's Disease","authors":"Marcello Serra ,&nbsp;Gaia Faustini ,&nbsp;Viviana Brembati ,&nbsp;Maria Antonietta Casu ,&nbsp;Marina Pizzi ,&nbsp;Micaela Morelli ,&nbsp;Annalisa Pinna ,&nbsp;Arianna Bellucci","doi":"10.1016/j.expneurol.2024.115040","DOIUrl":"10.1016/j.expneurol.2024.115040","url":null,"abstract":"<div><div>Parkinson's disease (PD) is characterized by the loss of nigrostriatal dopaminergic neurons and the presence of Lewy bodies (LB), intraneuronal inclusions mainly composed of α-synuclein (α-Syn) fibrils. Compelling evidence supports that, in PD brains, synapses are the sites where neurodegeneration initiates several years before the manifestation of motor symptoms. Furthermore, the amount of α-Syn deposited at synaptic terminals is several orders greater than that constituting LB. This hints that pathological synaptic α-Syn aggregates may be the main trigger for the retrograde synapse-to-cell body degeneration pattern characterizing early prodromal phases of PD. Identifying reliable biomarkers of synaptopathy is therefore crucial for early diagnosis. Here, we studied the alterations of key dopaminergic and non-dopaminergic striatal synaptic markers during the initial phases of axonal and cell body degeneration in mice subjected to 3 or 10 administrations of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine + probenecid (MPTPp), a model for early prodromal PD. We found that MPTPp administration resulted in progressive deposition of α-Syn, advancing from synaptic terminals to axons and dopaminergic neuron cell bodies. This was accompanied by marked co-accumulation of Synapsin III (Syn III), a synaptic protein previously identified as a component of α-Syn fibrils in post-mortem PD brains and as a main stabilizer of α-Syn aggregates, as well as very early and severe reduction of vesicular monoamine transporter 2 (VMAT2), dopamine transporter (DAT) and tyrosine hydroxylase (TH) immunoreactivity in nigrostriatal neurons. Results also showed that striatal α-Syn accumulation and VMAT2 decrease, unlike other markers, did not recover following washout from 10 MPTPp administrations, supporting that these changes were precocious and severe. Finally, we found that early changes in striatal α-Syn, Syn III, VMAT2 and DAT observed following 3 MPTPp administrations, correlated with nigrostriatal neuron loss after 10 MPTPp administrations. These findings indicate that α-Syn/Syn III co-deposition characterizes very early stages of striatal dopaminergic dysfunction in the MPTPp model and highlight that VMAT2 and Syn III could be two reliable molecular imaging biomarkers to predict dopamine neuron denervation and estimate α-Syn-related synaptopathy in prodromal and early symptomatic phases of PD.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"383 ","pages":"Article 115040"},"PeriodicalIF":4.6,"publicationDate":"2024-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142581877","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":"Comparing white and gray matter responses to lobar intracerebral hemorrhage in piglets and the effects of deferoxamine","authors":"Yingfeng Wan ,&nbsp;Qing Xie ,&nbsp;Ya Hua,&nbsp;Guohua Xi,&nbsp;Richard F. Keep,&nbsp;Aditya Pandey","doi":"10.1016/j.expneurol.2024.115041","DOIUrl":"10.1016/j.expneurol.2024.115041","url":null,"abstract":"<div><h3>Background</h3><div>Intracerebral hemorrhage (ICH) often impacts patient white matter. However, preclinically, the effects of ICH are mostly studied in rodents with sparse white matter. This study used a lobar porcine ICH model to examine differences in the effects of ICH on white and gray matter as well as the role of the iron chelator deferoxamine (DFX), on attenuation of such injury.</div></div><div><h3>Methods</h3><div>This two-part study was performed in piglets. Firstly, piglets had a needle (Sham) or 2.5 ml blood injection (ICH) and were euthanized at day 3. Secondly, animals were treated with vehicle or DFX after ICH and were euthanized at day 3. White and gray matter edema, the number of oligodendrocytes (mature and immature) and neurons, and the number of Perls' (iron), ferritin and heme oxygenase (HO)-1 positive cells were examined.</div></div><div><h3>Results</h3><div>At day 3, ICH induced greater edema formation in white than gray matter. This marked white matter edema was associated with a loss of mature, but not immature, oligodendrocytes. ICH also induced neuronal death in gray matter. There were also marked increases in Perls', ferritin and HO-1 positive cells after ICH in both white and gray matter, but significantly more in the former. DFX attenuated ICH-induced brain edema in white but not gray matter and this was associated with increased survival of mature oligodendrocytes. DFX also increased survival of neurons in the gray matter and it reduced the number of Perls', ferritin and HO-1 positive cells in both tissue types.</div></div><div><h3>Conclusions</h3><div>While there were commonalities in perihematomal changes between white and gray matter after ICH, there was greater edema in white matter which may be linked to the susceptibility of mature oligodendrocytes to ICH injury. Similarly, while DFX reduced perihematomal iron overload in both white and gray matter, it only significantly reduced edema in white matter where it increased the number of mature oligodendrocytes.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"383 ","pages":"Article 115041"},"PeriodicalIF":4.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142566616","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":"Multifaceted role of thrombin in subarachnoid hemorrhage: Focusing on cerebrospinal fluid circulation disorder","authors":"Yajun Qian ,&nbsp;Junjie Wang ,&nbsp;Jiarui Chen ,&nbsp;Weibo Lin ,&nbsp;Huimin Shen ,&nbsp;Yuanjian Fang ,&nbsp;Wenhua Yu","doi":"10.1016/j.expneurol.2024.115036","DOIUrl":"10.1016/j.expneurol.2024.115036","url":null,"abstract":"<div><div>Subarachnoid hemorrhage (SAH) is a severe neurological condition characterized by high morbidity and mortality. The unfavorable prognosis of SAH is closely associated with early brain injury (EBI) and delayed cerebral ischemia (DCI), wherein thrombin plays a role as part of the secondary injury components following hemorrhage in these two pathological processes. Additionally, thrombin contributes to disruptions in the circulation of cerebrospinal fluid (CSF), thereby giving rise to a spectrum of sequelae following SAH, including cerebral edema, hydrocephalus, cognitive impairments, and depressive symptoms. This review aims to provide a comprehensive understanding of the pathological role of thrombin in EBI, DCI, and CSF circulation following SAH, with a specific focus on its impact on the glymphatic-meningeal lymphatic system—a crucial mechanism for waste clearance and neurohomeostatic regulation. Additionally, this review offers an overview of current pharmacological interventions and treatment modalities targeting pathogenic mechanisms, aiming to mitigate brain injury and promote neurological recovery post-SAH.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"383 ","pages":"Article 115036"},"PeriodicalIF":4.6,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142563639","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}