G. Taccola , A.G. Steele , R. Apicella , J. Oh , V. Dietz , S. Rajendran , S.M. Barber , A.H. Faraji , P.J. Horner , D.G. Sayenko
{"title":"Interactions between descending and spinal circuits on motor output","authors":"G. Taccola , A.G. Steele , R. Apicella , J. Oh , V. Dietz , S. Rajendran , S.M. Barber , A.H. Faraji , P.J. Horner , D.G. Sayenko","doi":"10.1016/j.expneurol.2025.115347","DOIUrl":"10.1016/j.expneurol.2025.115347","url":null,"abstract":"<div><h3>Introduction</h3><div>Supraspinal influence on spinal networks remains incompletely understood yet is crucial for restoring motor function after neurological insults, including spinal cord injury or stroke. Neuromodulation interventions have been employed with varying success to aid recovery and can be utilized to investigate the relationship between supraspinal and spinal networks.</div></div><div><h3>Material and methods</h3><div>We elicited hindlimb muscle responses by motor cortex stimulation paired with either epidural or transcutaneous spinal stimulation in neurologically intact Long-Evans rats and Yucatan miniature pigs.</div></div><div><h3>Results</h3><div>Our findings indicate that modulation of sensorimotor networks using the two stimulation modalities varies with the intensity of spinal stimulation. Specifically, spinal stimulation at near-motor-threshold levels modulates the magnitude of the weak descending volleys, with pronounced increases in compound motor evoked potential magnitude of up to 400–500 %. As spinal stimulation intensity increased, we observed a transition from modulated cortically evoked motor responses toward modulated spinally evoked motor responses. However, when the intensity of spinal stimulation exceeded the supra-motor-threshold, the conditioned responses were abolished. We also examined the effects of timing between paired cortical and spinal stimulation and found that the highest modulation occurred when delivering spinal stimulation using a latency approximately equal to the central conduction time of cortical stimulation.</div></div><div><h3>Conclusion</h3><div>The capacity of cortical stimulation to modulate the effects of spinal modulation can be described as a convergence of supraspinal and spinal networks on the motor pathway. Overall, our results suggest potential stimulation strategies that capitalize on supraspinal-spinal interactions without the need for targeting individual motor pools with focal spinal stimulation.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115347"},"PeriodicalIF":4.6,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144270264","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":"“Senotherapy as a multitarget intervention in chronic obesity: Modulation of senescence, neuroinflammation, dysbiosis, and synaptic integrity in middle-aged female Wistar rats”","authors":"Rosa Pamela Flores-Torres , Verónica Salas-Venegas , Roberto Santín-Márquez , Marisol De la Vega-Tinajar , Ricardo Jair Ramírez-Carreto , Raúl Librado-Osorio , Armando Luna-López , Adriana Alarcón-Aguilar , Norma Edith López-Díazguerrero , Sofía Morán-Ramos , Anahí Chavarría , Beatriz Gómez-González , Mina Königsberg","doi":"10.1016/j.expneurol.2025.115331","DOIUrl":"10.1016/j.expneurol.2025.115331","url":null,"abstract":"<div><div>The Obesity pandemic is a global health problem that has been reported to be more prevalent in women than in men. Obesity is a risk factor for numerous diseases and has recently been related to deficits in memory and learning processes. Chronic obesity is associated with senescent cell accumulation, peripheral and central inflammation, and cognitive decline. Hence, we aimed to evaluate the use of senotherapy to avoid these processes in a model of middle-aged female Wistar rats with chronic obesity. Rats received a hypercaloric diet (HD) from day 21 to middle age (14 months). The senomorphic sulforaphane (SFN) (0.5 mg/kg, 5 days/week) or the senolytic combination of Dasatinib + Quercetin (D + Q) (5 mg/kg and 50 mg/kg respectively, monthly) were administered from 12 to 14 months. The composition of the gut microbiota, the serum, cortical and hippocampal expression of pro- (IL-6 and IL-1β) and anti-inflammatory (IL-10) cytokines, as well as markers of cellular senescence (SA-β-gal, p21 and γH2AX) in the brain were determined. Also, the declarative memory (NOR test) and learning (Barnes maze) processes, and the expression of molecules involved in synaptic plasticity (BDNF, PSD95, and synaptophysin) were evaluated. HD-fed rats presented gut dysbiosis, local and systemic inflammation, and severe cognitive impairments. Senotherapy reversed inflammation, with SFN demonstrating greater effectiveness. D + Q treatment failed to prevent cognitive deficits or modulate gut microbial composition. In contrast, SFN significantly improved performance in both behavioral tests, increased SYP and PSD-95, and prevented some of the gut microbial changes induced by the HD.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115331"},"PeriodicalIF":4.6,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144270444","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}
Simone Beretta , Davide Carone , Tae-Hee Cho , Martina Viganò , Susanna Diamanti , Jacopo Mariani , Francesco Andrea Pedrazzini , Elisa Bianchi , Cristiano Pini , Radu Bolbos , Marlene Wiart , Carlo Ferrarese , Fabien Chauveau
{"title":"Head-down tilt 15° increases cerebral perfusion before recanalization in acute ischemic stroke. A pre-clinical MRI study","authors":"Simone Beretta , Davide Carone , Tae-Hee Cho , Martina Viganò , Susanna Diamanti , Jacopo Mariani , Francesco Andrea Pedrazzini , Elisa Bianchi , Cristiano Pini , Radu Bolbos , Marlene Wiart , Carlo Ferrarese , Fabien Chauveau","doi":"10.1016/j.expneurol.2025.115343","DOIUrl":"10.1016/j.expneurol.2025.115343","url":null,"abstract":"<div><div>We investigated the therapeutic effect of head-down tilt at −15° (HDT15) on cerebral collateral flow and early infarct growth in a rat model of large vessel occlusion stroke, using multi-modal MRI. Endovascular occlusion of the proximal middle cerebral artery was induced for 90 min in Wistar rats (<em>n</em> = 28), followed by reperfusion. Rats were randomly assigned to HDT15 or flat position for 60 min, starting 30 min after occlusion. Multi-modal brain MRI, including perfusion, angiographic and structural sequences were acquired before treatment, after 60 min of treatment and 24 h after reperfusion. The primary outcome was change in cerebral perfusion after the 60-min treatment, assessed by time-to-peak (rTTP), adjusted for baseline collateral score. The secondary outcome was infarct growth in the first 24 h. The perfusion shift analysis, comparing post- versus pre-treatment changes in time-to-peak maps, showed a significant increase in cerebral perfusion in the HDT15 group (common odds ratio 1.50; 95 % CI 1.41–1.60; <em>p</em> < 0.0001), but not in the flat group (common odds ratio 0.97; 95 % CI 0.92–1.03; <em>p</em> = 0.3503). Early infarct growth at 24 h was +15.4 % in the HDT15 group (224 versus 192 mm<sup>3</sup>; 95 % CI -26.9 to 85.9; <em>p</em> = 0.2272) and + 31.4 % in the flat group (343 versus 250 mm<sup>3</sup>; 95 % CI 2.4 to 165.1; <em>p</em> = 0.0447). In conclusion, MRI-based analysis indicated that HDT15 acutely increased cerebral perfusion in large vessel occlusion and exerted a tissue-saving effect before recanalization in experimental ischemic stroke.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115343"},"PeriodicalIF":4.6,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144263620","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}
Jeong W. Seo , Brian M. Balog , Margaret Pinkevitch, Jon P. Niemi, Marius Patru, Sanika Paranjape, Richard E. Zigmond
{"title":"Somatosensory neurons respond heterogeneously to a conditioning lesion","authors":"Jeong W. Seo , Brian M. Balog , Margaret Pinkevitch, Jon P. Niemi, Marius Patru, Sanika Paranjape, Richard E. Zigmond","doi":"10.1016/j.expneurol.2025.115342","DOIUrl":"10.1016/j.expneurol.2025.115342","url":null,"abstract":"<div><div>Regeneration of peripheral neurons after a nerve crush is enhanced if the axons have received a prior injury, a phenomenon known as the conditioning lesion response (CLR). Neurons in the mouse L3-L5 dorsal root ganglia (DRGs) that project into the sciatic nerve are commonly used to examine the CLR. These ganglia contain a diverse population of somatosensory neurons, which exhibit dramatic heterogeneity in their response to a CL. As reported previously, the nociceptors [i.e., isolectin B4 binding (IB4+) and calcitonin gene-related peptide positive (CGRP+) neurons] do not show enhanced axonal growth in culture after an in vivo CL, whereas the remaining neurons on average do. We asked whether the failure to produce a CLR was an inherent property of certain neurons. Two difficulties in interpreting previous findings are that only about half of the neurons in these ganglia project into the sciatic nerve and that both IB4 binding and CGRP immunoreactivity decrease after axotomy. Therefore, a possibility not considered previously is that neurons that are still CGRP+ or IB4+ after sciatic nerve transection have not been axotomized. Genetic mutants that express a reporter in CGRP neurons such that its expression is unchanged after axotomy demonstrate that the absence of a CLR is an inherent property of these neurons; however, expression of a reporter in the MrgD (Mas-related gene D)/IB4 neurons demonstrate that these neurons in fact do exhibit a CLR. Among the CGRP-/IB4- neurons, two populations found to exhibit a CLR are tropomyosin receptor kinase C+ (TrkC+) and MrgD+ neurons.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115342"},"PeriodicalIF":4.6,"publicationDate":"2025-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265802","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}
Valentina La Cognata, Maria Guarnaccia, Giovanna Morello, Giulia Gentile, Sebastiano Cavallaro
{"title":"Predicting amyotrophic lateral sclerosis in the pre-symptomatic phase: Insights from SOD1G93A mouse gene expression profiles","authors":"Valentina La Cognata, Maria Guarnaccia, Giovanna Morello, Giulia Gentile, Sebastiano Cavallaro","doi":"10.1016/j.expneurol.2025.115329","DOIUrl":"10.1016/j.expneurol.2025.115329","url":null,"abstract":"<div><div>Amyotrophic lateral sclerosis (ALS) is a fast-paced fatal disease that requires immediate intervention to slow down the course of pathology and improve patients’ quality of life. However, in most cases, ALS is diagnosed too late. For this reason, an accurate diagnostic test is urgently needed to identify ALS patients early, enabling a timely introduction of novel therapeutics and effective monitoring of disease progression. To address this significant unmet medical need, we explored a transcriptome-based signature to predict ALS during the preclinical phase. Using publicly available gene expression profiles from central nervous system (lumbar isolated motor neurons and spinal cord homogenates) of transgenic SOD1G93A mice with different genetic background and their respective control littermates, covering pre-symptomatic to late stages of the disease, we identified 463 differentially expressed genes (DEGs), primarily involved in immune response and metabolic processes. Based on this ALS gene-associated signature, we tested three machine learning binary classifiers (Support Vector Machine, Neural Network and Linear Discriminant Analysis), which demonstrated highly significant predictive power in discriminating mutant SOD1G93A from controls mice, even at pre-symptomatic stages. This was evident in both the discovery cohort and in two additional peripheral cross-tissue validation datasets from preclinical SOD1G93A sciatic nerve and muscles. Our study provides the first proof of concept for early ALS detection using a machine learning-based transcriptomic classifier. This could lead to earlier diagnosis, potentially enabling effective monitoring of disease progression and earlier interventions.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115329"},"PeriodicalIF":4.6,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144231588","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}
Oscar E. Ruiz , Joost B. Wagenaar , Bella Mehta , Ilias Ziogas , Lyndie Swanson , Kim C. Worley , Yenisel Cruz-Almeida , Alisa J. Johnson , Jyl Boline , Jacqueline Boccanfuso , RE-JOIN Consortium, Maryann E. Martone , Nele A. Haelterman
{"title":"A guide to developing harmonized research workflows in a team science context","authors":"Oscar E. Ruiz , Joost B. Wagenaar , Bella Mehta , Ilias Ziogas , Lyndie Swanson , Kim C. Worley , Yenisel Cruz-Almeida , Alisa J. Johnson , Jyl Boline , Jacqueline Boccanfuso , RE-JOIN Consortium, Maryann E. Martone , Nele A. Haelterman","doi":"10.1016/j.expneurol.2025.115333","DOIUrl":"10.1016/j.expneurol.2025.115333","url":null,"abstract":"<div><div>Large, interdisciplinary team science initiatives are increasingly leveraged to uncover novel insights into complex scientific problems. Such projects typically aim to produce large, harmonized datasets that can be analyzed to yield breakthrough discoveries using cutting-edge scientific methods. Successfully harmonizing and integrating datasets generated by different technologies and research groups is a considerable task, which requires an extensive supportive framework that is built by all members involved. Such a data harmonization framework includes a shared language to communicate across teams and disciplines, harmonized methods and protocols, (meta)data standards and common data elements, and the appropriate infrastructure to support the framework's development and implementation. In addition, a supportive data harmonization framework also entails adopting processes to decide on which elements to harmonize and to help individual team members implement agreed-upon data workflows in their own laboratories/centers. Building an effective data harmonization framework requires buy-in, team building, and significant effort from all members involved. While the nature and individual elements of these frameworks are project-specific, some common challenges typically arise that are independent of the research questions, scientific techniques, or model systems involved. In this perspective, we build on our collective experiences as part of the REstoring JOINt health and function to reduce pain (RE-JOIN) Consortium to provide guidance for developing research-centered data collection and analysis pipelines that enable downstream integrated analyses within and across diverse teams.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115333"},"PeriodicalIF":4.6,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144247215","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}
G. Smith , C. Santana-Gomez , R.J. Staba , N.G. Harris
{"title":"Unbiased population-based statistics to obtain pathologic burden of injury after experimental TBI","authors":"G. Smith , C. Santana-Gomez , R.J. Staba , N.G. Harris","doi":"10.1016/j.expneurol.2025.115332","DOIUrl":"10.1016/j.expneurol.2025.115332","url":null,"abstract":"<div><div>Reproducibility of scientific data is a current concern throughout the neuroscience field. There are multiple on-going efforts to help resolve this problem. Within the preclinical neuroimaging field, the continued use of a region-of interest (ROI) type approaches combined with the well-known spatial heterogeneity of traumatic brain injury pathology is a barrier to the replicability and repeatability of data. Here we propose the conjoint use of an unbiased analysis of the whole brain after injury together with a population-based statistical analysis of sham-control brains as one approach that has been used in clinical research to help resolve this issue. The approach produces two volumes of pathology that are outside the normal range of sham brains, and can be interpreted as whole brain burden of injury. Using diffusion weighted imaging-derived scalars from a tensor analysis of data acquired from adult, male rats at 2, 9 days, 1 and 5 months after lateral fluid percussion injury (LFPI) and in shams (<em>n</em> = 73 and 12, respectively), we compared a data-driven, z-score mapping method to a whole brain and white matter-specific analysis, as well as an ROI-based analysis with brain regions preselected by virtue of their large group effect sizes. We show that the data-driven approach is statistically robust, providing the advantage of a large group effect size typical of a ROI analysis of mean scalar values derived from the tensor in regions of gross injury, but without the large multi-region statistical correction required for interrogating multiple brain areas, and without the potential bias inherent with using preselected ROIs. We show that the technique correctly captures the expected longitudinal time-course of the diffusion scalar volumes based on the spatial extent of the pathology and the known temporal changes in scalar values in the LFPI model.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115332"},"PeriodicalIF":4.6,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144240051","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}
Tan Zhang , Yitong Jia , Nan Wang , Xiaoke Chai , Qiheng He , Tianqing Cao , Qingchun Mu , Qing Lan , Jizong Zhao , Yi Yang
{"title":"Recent advances in potential mechanisms of epidural spinal cord stimulation for movement disorders","authors":"Tan Zhang , Yitong Jia , Nan Wang , Xiaoke Chai , Qiheng He , Tianqing Cao , Qingchun Mu , Qing Lan , Jizong Zhao , Yi Yang","doi":"10.1016/j.expneurol.2025.115330","DOIUrl":"10.1016/j.expneurol.2025.115330","url":null,"abstract":"<div><h3>Background</h3><div>Epidural spinal cord stimulation (eSCS) has emerged as a promising neuromodulation technique for treating movement disorders. The underlying mechanisms of eSCS are still being explored, making it a compelling area for further research.</div></div><div><h3>Objective</h3><div>This review aims to provide a comprehensive analysis of the mechanisms of eSCS, its stimulation parameters, and its clinical applications in movement disorders. It seeks to synthesize the current understanding of how eSCS interacts with the central nervous system to enhance motor function and promotes neural plasticity for sustained recovery.</div></div><div><h3>Methods</h3><div>A literature search was performed in databases such as Web of Science, Scopus, and PubMed to identify studies on eSCS for movement disorders.</div></div><div><h3>Results</h3><div>The therapeutic effects of eSCS are achieved through both immediate facilitative actions and long-term neural reorganization. By activating sensory neurons in the dorsal root, facilitating proprioceptive input and modulating spinal interneurons, eSCS enhances motor neuron excitability. Additionally, eSCS influences corticospinal interactions, increasing cortical excitability and promoting corticospinal circuit remodeling. Neuroplasticity plays a critical role in the long-term efficacy of eSCS, with evidence suggesting that stimulation can enhance axonal sprouting, synaptic formation, and neurotrophic factor expression while reducing neuroinflammation. Its regulation of the sympathetic nervous system further enhances recovery by improving blood flow, muscle tone, and other physiological parameters.</div></div><div><h3>Conclusions</h3><div>Epidural spinal cord stimulation shows promise in enhancing motor function and promoting neuroplasticity, but further research is needed to optimize treatment protocols and establish long-term efficacy.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115330"},"PeriodicalIF":4.6,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144222863","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":"AXL-mediate GEF-H1 phosphorylation was involved in microglia synapse phagocytosis in 5xFAD mice","authors":"Genyu Chen , Jian Zhang , Aiwen Dong , Lingmin Xiao , Pinyuan Huang , Tianwen Huang , Qinyong Ye , En Huang","doi":"10.1016/j.expneurol.2025.115327","DOIUrl":"10.1016/j.expneurol.2025.115327","url":null,"abstract":"<div><div>Studies indicated that microglial synapse phagocytosis played a critical role in synapse loss and pathogenesis in Alzheimer's disease. AXL was one of key phagocytic receptors and was upgraded in disease associated microglia. This study aimed to investigate the role of AXL-mediated microglial synapse phagocytosis in AD mice model. Our data indicated that AXL was increased in microglia in 5xFAD mouse AD model. The lentivirus PLV-CXC3CR1-shAXl was applied to especially knockdown the AXL expression in microglia and the shAXL treatment ameliorated the cognitive impairment in 5xFAD mice. AXL knockdown decreased the 6E10 positive amyloid plaques, the diffusion index of amyloid plaques and the level of phosphorylated Tau. shAXL treatment increased microglial complexity and reduced the microglial synapse phagocytosis. This study further demonstrated that GEF-H1 was identified as a substrate of AXL and mainly phosphorylated at Y470 by AXL. The AXL-mediated GEF-H1-Y470 phosphorylation enhanced the phagocytic capacity of BV2. It seems paradoxical that amyloid plaque load and microglial phagocytosis were both decreased at the same time when the AXL was knockdown, but these indicated that microglia phagocytosis related synapse loss played a more critical role in cognitive impairment and AD pathogenesis than amyloid plaque load. Our study demonstrated that the activated AXL in microglia in 5xFAD enhanced synapse phagocytosis via phosphorylating GEF-H1 at Y470, which led to synapse loss and cognitive impairment. The application of AXL blockage would be a potential therapeutic strategy for AD treatment.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115327"},"PeriodicalIF":4.6,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144203860","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}