Experimental Neurology最新文献

{"title":"Expression of concern: \"Mitoquinone attenuates blood-brain barrier disruption through Nrf2/PHB2/OPA1 pathway after subarachnoid hemorrhage in rats\" [EXP NEUROL, Volume 317 (2019) Pages 1-9].","authors":"","doi":"10.1016/j.expneurol.2025.115295","DOIUrl":"https://doi.org/10.1016/j.expneurol.2025.115295","url":null,"abstract":"","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"391 ","pages":"115295"},"PeriodicalIF":4.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274558","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":"Retraction Notice to “High cholesterol content in neurons increases BACE, β-amyloid and phosphorylated tau levels in rabbit hippocampus” [Experimental Neurology 200 (2006) 460–467]","authors":"Othman Ghribi , Brian Larsen , Matthew Schrag , Mary M. Herman","doi":"10.1016/j.expneurol.2025.115449","DOIUrl":"10.1016/j.expneurol.2025.115449","url":null,"abstract":"","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"394 ","pages":"Article 115449"},"PeriodicalIF":4.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144948221","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":"Expression of concern: \"Therapeutic application of gene silencing MMP-9 in a middle cerebral artery occlusion-induced focal ischemia rat model\" [EXP NEUROL, Volume 216 (2009) Pages 35-46].","authors":"","doi":"10.1016/j.expneurol.2025.115299","DOIUrl":"https://doi.org/10.1016/j.expneurol.2025.115299","url":null,"abstract":"","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"391 ","pages":"115299"},"PeriodicalIF":4.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274561","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":"CCR5 as a key modulator in neurocognitive disorders","authors":"Chew Tin Zar Aung ,&nbsp;Khawla Abuaqel ,&nbsp;Miou Zhou","doi":"10.1016/j.expneurol.2025.115450","DOIUrl":"10.1016/j.expneurol.2025.115450","url":null,"abstract":"<div><div>This integrative review explores the emerging role of C<img>C chemokine receptor type 5 (CCR5) as a critical regulator of neuroinflammation, synaptic plasticity, and cognitive function in the central nervous system. Initially identified as an immune receptor and a co-receptor for HIV entry, CCR5 is now increasingly recognized for its multifaceted role across diverse neurocognitive disorders. CCR5 is upregulated in neurons and glial cells in multiple neurological disorders, including Alzheimer's disease (AD), HIV-associated neurocognitive disorder (HAND), traumatic brain injury (TBI), multiple sclerosis (MS), Lewy body dementia (LBD), Parkinson's disease (PD), Huntington's disease (HD), stroke, and vascular dementia (VaD), where it regulates neuroinflammatory cascades, neuronal injury, and cognitive function. CCR5 also interacts with disease-specific pathological mechanisms, including amyloidosis, tau phosphorylation, cofilin-actin rod formation, and dendritic spine degeneration. Both genetic and pharmacologic inhibition of CCR5 have been shown to reduce microglial and astrocyte activation, preserve blood-brain barrier integrity, restore synaptic plasticity, and enhance cognitive performance in various clinical and preclinical models. While the preponderance of studies supports CCR5 inhibition as a therapeutic strategy to mitigate neuroinflammation and cognitive decline, some research has reported a protective role of CCR5 in AD, PD, stroke, and VaD, highlighting the complexity of its function. The divergent findings emphasize the need for the consideration of genetic background, cell-type-specific mutation or inhibition, the low prevalence of the homozygous CCR5Δ32 mutation in association studies, and context-specific approaches in the design of future studies. Such considerations will be essential for advancing CCR5 targeted interventions in neurocognitive disorders.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"394 ","pages":"Article 115450"},"PeriodicalIF":4.2,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144932741","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":"By inhibiting pyroptosis to reduce neuroinflammation, PEG-bHb may prevent the development of secondary injury after traumatic brain injury","authors":"Qiang Zeng ,&nbsp;Guoxing You ,&nbsp;Weidan Li ,&nbsp;Jianlei An ,&nbsp;Zhiyong Huang ,&nbsp;Xiaoyong Zhang ,&nbsp;Hong Zhou ,&nbsp;Yao Xiao ,&nbsp;Ying Wang ,&nbsp;Lian Zhao","doi":"10.1016/j.expneurol.2025.115447","DOIUrl":"10.1016/j.expneurol.2025.115447","url":null,"abstract":"<div><div>Changes in severe pathological microenvironment of traumatic brain injury (TBI) have important implications for neurological repair, including oxidative stress and intense neuroinflammatory responses. Pyroptosis, a regulated cellular demise process characterized by membrane permeabilization, constitutes a primary contributor to post-traumatic brain injury induced neural inflammatory responses. Regulating the pyroptosis pathway may alleviate secondary brain injury. Polyethylene glycol-conjugated bovine hemoglobin (PEG-bHb) is a type of hemoglobin-based oxygen carriers (HBOCs) and is designed for oxygen delivery in transfusion therapy. PEG-bHb exhibits the capacity to bind and release oxygen, promoting oxygen supply in hypoxic tissues. In vivo studies have found that PEG-bHb can elevate regional oxygen saturation after TBI in prehospital stage, effectively inhibit pyroptosis, attenuate neuroinflammation and oxidative stress, and effectively attenuate the development of secondary brain injury. Furthermore, PEG-bHb has been demonstrated to protect the blood-brain barrier (BBB) by reducing the permeability of BBB and attenuating brain edema. PEG-bHb has been shown to enhance motor, learning, and memory abilities following TBI. Thus, PEG-bHb can act as a promising candidate for TBI treatment.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"394 ","pages":"Article 115447"},"PeriodicalIF":4.2,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144913352","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":"Erratum to’Neuroprotective and gut health benefits of Ugni molinae in preclinical Huntington's disease models' [Experimental Neurology, Volume 393 (2025) 115406]","authors":"Marisol Cisternas-Olmedo ,&nbsp;Valentina Urra-Alvarez ,&nbsp;Tomás J. Huerta ,&nbsp;Valentina Urbina-Muñoz ,&nbsp;Barbara Saavedra ,&nbsp;Ivania Valdés ,&nbsp;Erick Riquelme ,&nbsp;Mauricio Saez ,&nbsp;Rodrigo Pérez-Arancibia ,&nbsp;Carla Delporte ,&nbsp;René L. Vidal","doi":"10.1016/j.expneurol.2025.115444","DOIUrl":"10.1016/j.expneurol.2025.115444","url":null,"abstract":"","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"394 ","pages":"Article 115444"},"PeriodicalIF":4.2,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144926195","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":"KIF23 inhibition protects against perioperative neurocognitive disorders by hindering ROS/caspase-3/GSDME-mediated pyroptosis – Authors' reply","authors":"Shaoqun Tang,&nbsp;Xi Yu,&nbsp;Wei Wang,&nbsp;Zhongyuan Xia","doi":"10.1016/j.expneurol.2025.115445","DOIUrl":"10.1016/j.expneurol.2025.115445","url":null,"abstract":"","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"394 ","pages":"Article 115445"},"PeriodicalIF":4.2,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144948233","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":"Letter to the editor: “KIF23 inhibition protects against perioperative neurocognitive disorders by hindering ROS/caspase-3/GSDME-mediated pyroptosis” by Tang et al.","authors":"Parth Aphale,&nbsp;Himanshu Shekhar,&nbsp;Shashank Dokania","doi":"10.1016/j.expneurol.2025.115446","DOIUrl":"10.1016/j.expneurol.2025.115446","url":null,"abstract":"","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"394 ","pages":"Article 115446"},"PeriodicalIF":4.2,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144908210","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":"Farrerol confers neuroprotection in spinal cord injury by regulating macrophages/microglia polarization through the JAK2/STAT3 pathway","authors":"Yue Chen ,&nbsp;Lü Ren ,&nbsp;Jinzhi Xia ,&nbsp;Bohan Li ,&nbsp;Yi Yang ,&nbsp;Jing Li ,&nbsp;Lu Tao ,&nbsp;Xue Song ,&nbsp;Hezuo Lü ,&nbsp;Jianguo Hu","doi":"10.1016/j.expneurol.2025.115448","DOIUrl":"10.1016/j.expneurol.2025.115448","url":null,"abstract":"<div><h3>Background and aims</h3><div>Spinal cord injury (SCI) causes secondary damage characterized by neuroinflammation and imbalanced macrophages/microglia polarization, worsening neuronal loss and functional decline. Farrerol (FAR), a natural flavonoid with anti-inflammatory properties, has not been studied for SCI treatment. This work assesses FAR's neuroprotection through macrophages/microglia polarization regulation and explores its mechanisms.</div></div><div><h3>Methods</h3><div>C57BL/6 mice with spinal cord injury were randomly assigned to three groups: Sham, SCI, and SCI + FAR. Motor function was evaluated using locomotor scoring, while lesion size, myelin integrity, and neuronal apoptosis were assessed via histology, immunofluorescence, and Western blot. Spinal inflammatory cytokine, macrophages/microglia activation, and polarization were analyzed by qRT-PCR, ELISA, immunofluorescence, and flow cytometry. LPS-stimulated BV2 microglia and BV2-HT22 co-cultures evaluated FAR's effects on cytokine secretion, macrophages/microglia phenotypes, and neuronal survival. Signaling mechanisms were further examined via Western blot and immunofluorescence.</div></div><div><h3>Results</h3><div>FAR treatment significantly enhanced motor recovery in SCI mice, evidenced by elevated Basso Mouse Scale (BMS) scores, increased inclined plane angles, improved swimming performance, and refined gait patterns. It reduced lesion area, preserved myelin integrity, and attenuated neuronal apoptosis. FAR downregulated pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), suppressed macrophages/microglia hyperactivation while upregulating IL-10, and shifted M1/M2 polarization toward neuroprotective M2 phenotypes. In LPS-stimulated BV2 microglia, FAR attenuated inflammatory responses, inhibited M1 markers, enhanced M2 markers, and rescued HT22 neuronal apoptosis in co-cultures. These therapeutic effects may be mediated through suppression of JAK2/STAT3 phosphorylation.</div></div><div><h3>Conclusions</h3><div>FAR promotes functional recovery after spinal cord injury by modulating macrophages/microglia M1/M2 polarization through JAK2/STAT3 pathway inhibition, thereby attenuating neuroinflammation and neuronal death. These findings provide novel evidence supporting targeted immunomodulation for SCI treatment.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"394 ","pages":"Article 115448"},"PeriodicalIF":4.2,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144913206","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":"Long-term intermittent theta burst stimulation alleviates Parkinson's disease-related cognitive impairment by modulating GluN2B in the dorsal hippocampus","authors":"Xiang Wu ,&nbsp;Yanping Hui ,&nbsp;Ling Wang ,&nbsp;Hongfei Qiao ,&nbsp;Yixuan Wang ,&nbsp;Yihua Bai ,&nbsp;Qingfeng Sun ,&nbsp;Shasha Gao ,&nbsp;Qiaojun Zhang ,&nbsp;Libo Li","doi":"10.1016/j.expneurol.2025.115439","DOIUrl":"10.1016/j.expneurol.2025.115439","url":null,"abstract":"<div><div>Cognitive impairment is one of the typical non-motor symptoms of Parkinson's disease (PD) that severely affects the quality of life of patients. However, limited treatments are currently available, suggesting the urgent need for new therapeutic approaches. Intermittent theta burst stimulation (iTBS), an updated pattern of high-frequency repetitive transcranial magnetic stimulation, can potentially improve cognitive function. However, its efficacy on PD-related cognitive impairment and the mechanism underlying it remain unclear. In this study, we found that unilateral 6-hydroxydopamine (6-OHDA) lesions of the substantia nigra pars compacta (SNc) impaired hippocampus-dependent memory, decreased the expression of GluN2B at both the total and membrane protein levels, reduced the concentration of intracellular Ca²⁺, and resulted in hyperactive theta power in the dorsal hippocampus (dHip) in rats. Fourteen days of iTBS treatment improved the impaired hippocampus-dependent memory in the lesioned rats, which could last for at least 10 days. In addition, iTBS treatment up-regulated the expression of GluN2B at total and membrane protein levels, elevated intracellular Ca²⁺ concentration, and normalized the aberrantly high theta power in the dHip. Furthermore, iTBS treatment failed to improve hippocampus-dependent memory and normalize the aberrant theta power after knocking down the hippocampal GluN2B. Collectively, these findings suggest that 14-day iTBS treatment alleviates hippocampus-dependent memory impairment in PD, which is achieved by up-regulating the expression of the GluN2B, followed by increasing the level of intracellular Ca²⁺ concentration and normalizing hyperactive theta rhythm in the dHip.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"394 ","pages":"Article 115439"},"PeriodicalIF":4.2,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144890749","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}