Experimental Neurology最新文献

{"title":"Prolonged antibiotic treatment accelerates neurological recovery and reduces long-term neuroinflammatory gene expression after experimental TBI in mice","authors":"Katharina Ritter ,&nbsp;Katharina Petri ,&nbsp;Julian Denninger ,&nbsp;Yi Zhang ,&nbsp;Yong Wang ,&nbsp;Michael K.E. Schäfer","doi":"10.1016/j.expneurol.2026.115645","DOIUrl":"10.1016/j.expneurol.2026.115645","url":null,"abstract":"<div><h3>Background</h3><div>Neuroprotective effects of antibiotic medications are reported in the context of experimental traumatic brain injury (TBI), but the choice of substances and treatment intervals are inconsistent.</div></div><div><h3>Methods</h3><div>In this study, we tested whether continuous posttraumatic administration of a combined broad-spectrum antibiotic regimen of vancomycin, amoxicillin, and clavulanic acid affects neurological recovery, structural brain damage and neuroinflammation following experimental TBI by controlled cortical impact in 80 adult male C57BL/6 mice.</div></div><div><h3>Results</h3><div>Antibiotic treatment led to accelerated recovery from posttraumatic neuromotor impairment and exploratory behavioural disorders. Reduced astrocytic activation and neuronal loss in the ipsilesional thalamic region in the early (5 days post injury, dpi) and attenuated neuroinflammatory gene expression in the late (30 dpi) period were observed alongside a severe disruption of the intestinal microbial spectrum after five days of antibiotic treatment, while the structural brain damage remained unaffected.</div></div><div><h3>Conclusion</h3><div>We demonstrated accelerated neurological recovery and long-lasting effects of antibiotic treatment on the neuroinflammatory response after experimental TBI. Increased plasma levels of lipopolysaccharide-binding protein and short-chain fatty acids were evaluated, yet not identified as potential modulators. As the observed effects can not entirely be linked to the intestinal dysbiosis, direct modulation of secondary brain damage by the antibiotic substances should be considered as an alternate mechanism.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"398 ","pages":"Article 115645"},"PeriodicalIF":4.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145988873","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":"Investigating the therapeutic potential of nasal administration of mitochondria on blood-brain barrier integrity and vasogenic brain Edema in a rat ischemic stroke model","authors":"Nooshin Sadeghian ,&nbsp;Hamdollah Panahpour ,&nbsp;Mohammad Reza Alipour ,&nbsp;Fereshteh Farajdokht ,&nbsp;Javad Shadman","doi":"10.1016/j.expneurol.2025.115609","DOIUrl":"10.1016/j.expneurol.2025.115609","url":null,"abstract":"<div><div>Mitochondrial dysfunction is an early and critical factor in the development of ischemic stroke. This study investigated the therapeutic potential of intranasally delivered mitochondria to reduce vasogenic cerebral edema and protect blood-brain barrier (BBB) integrity in a rat model of ischemic stroke. Male rats underwent 60 min of middle cerebral artery occlusion to induce stroke and then received daily intranasal mitochondrial treatment (750 μg/50 μl) for two days. Cerebral edema was measured by the wet/dry method, and BBB permeability was assessed using Evans blue dye extravasation. Mitochondrial function was evaluated by assessing mitochondrial swelling, mitochondrial membrane potential (MMP), succinate dehydrogenase (SDH) activity, and reactive oxygen species (ROS) production. Protein levels of matrix metalloproteinase-9 (MMP-9), intercellular adhesion molecule-1 (ICAM-1), and markers of apoptosis were examined by immunofluorescence. The treatment significantly reduced infarct size, improved sensorimotor function, decreased cerebral edema, and preserved BBB integrity. These benefits correlated with improved mitochondrial function—demonstrated by reduced swelling and ROS, and restoration of MMP and SDH activity. Additionally, mitochondrial therapy lowered apoptosis and decreased expression of MMP-9 and ICAM-1. These findings suggest that intranasal mitochondrial administration mitigates cerebral edema and BBB disruption after ischemic stroke. This protective effect is likely achieved by enhancing mitochondrial function and lowering levels of inflammation-related proteins, suggesting a promising neuroprotective strategy targeting mitochondrial dysfunction in stroke.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"398 ","pages":"Article 115609"},"PeriodicalIF":4.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145833403","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":"Role of A-delta low threshold mechanoreceptors and tropomyosin receptor kinase B plasticity in at-level aversive pain after spinal cord injury","authors":"Shangrila Parvin,&nbsp;Kyeongran Jang,&nbsp;Sandra M. Garraway","doi":"10.1016/j.expneurol.2025.115628","DOIUrl":"10.1016/j.expneurol.2025.115628","url":null,"abstract":"<div><div>The mechanisms of neuropathic pain after spinal cord injury (SCI) are not fully understood, although spinal and peripheral processes are involved. Maladaptive tropomyosin receptor kinase-B (TrkB) signaling has been implicated in pain hypersensitivity after SCI. A-delta-low threshold mechanoreceptors (Aδ-LTMRs) innervate the hairy skin and normally signal directional touch and are identified by their preferential TrkB expression. This study investigated whether Aδ-LTMRs play a role in at-level pain after thoracic contusion SCI. Using a modified light-dark chamber conditioned place aversion (CPA) paradigm, we assessed chamber preferences and transitions between chambers in response to mechanical stimulation, and optogenetic stimulation of Aδ-LTMRs in the trunk skin of adult TrkB^Cre mice of both sexes. Respiratory rates (RRs) were monitored at baseline and during truncal stimulation. The expression of brain-derived neurotrophic factor (BDNF), TrkB and pERK1/2 in the lesioned spinal cord and skin, and histological changes in Aδ-LTMRs in trunk skin were assessed. In addition, electrophysiological studies examined changes in Aδ-LTMRs membrane and firing properties, and response to bath-applied 7, 8-dihydroxyflavone (7,8-DHF), a TrkB agonist. The results showed that whereas brush stimulation evoked an aversive response at 4 weeks post-SCI that was accompanied by increased RRs, targeted stimulation of Aδ-LTMRs produced an aversive response 7 weeks post-SCI. SCI increased BDNF, TrkB and pERK1/2 expression in the skin, and augmented 7,8-DHF-induced inward current in Aδ-LTMRs. Together, these results suggest that plasticity of Aδ-LTMR, including an increase in TrkB signaling in the periphery, contribute to at-level affective pain following chronic SCI in adult mice.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"398 ","pages":"Article 115628"},"PeriodicalIF":4.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145882229","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":"Abnormal upregulation of SPP1 promotes fibrotic scar after peripheral nerve repair (FS-PNR) by driving M2 macrophage polarization","authors":"Jingyuan Fan ,&nbsp;Zhe Li ,&nbsp;Nan Zhang ,&nbsp;Shuolin Wang ,&nbsp;Canbin Zheng ,&nbsp;Qingtang Zhu ,&nbsp;Honggang Wang ,&nbsp;Jian Qi ,&nbsp;Liwei Yan","doi":"10.1016/j.expneurol.2025.115612","DOIUrl":"10.1016/j.expneurol.2025.115612","url":null,"abstract":"<div><div>Fibrotic scar after peripheral nerve repair (FS-PNR) hinder axon regeneration and functional recovery. However, the mechanism underlying FS-PNR formation remains elusive. SPP1, a glycoprotein known to promote fibrosis in multiple organ systems, was abnormally upregulated in human peripheral nerve fibrotic scar tissues, though its cellular functions in FS-PNR were undefined. Using single- nucleus RNA sequencing, we confirmed SPP1 upregulation in FS-PNR patients and identified repair Schwann cells (rSCs) as its primary cellular source, with macrophages as key targets. To investigate this axis, we established an animal model replicating clinical FS-PNR pathology, validated by histopathological and functional assessments. Notably, SPP1 elevation correlated with increased M2 macrophage infiltration within fibrotic scars. Genetic ablation of SPP1 in mice significantly reduced scar formation and improved functional outcomes. Transcriptomic analysis revealed that SPP1 depletion promoted macrophage M1 polarization. Further <em>in vitro</em> studies demonstrated that SPP1 drives fibrogenesis by inducing macrophage M2 polarization. Together, our findings implicate SPP1 as a novel mediator of FS-PNR pathology <em>via</em> rSCs-macrophage crosstalk.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"398 ","pages":"Article 115612"},"PeriodicalIF":4.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145814284","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":"Age and sex dependent hippocampal neuronal hyperactivity in Alzheimer model mice","authors":"E. Hegnet,&nbsp;S. Häkli,&nbsp;H. Koivisto,&nbsp;P.O. Miettinen,&nbsp;N. Jin,&nbsp;I. Gureviciene,&nbsp;H. Tanila","doi":"10.1016/j.expneurol.2025.115632","DOIUrl":"10.1016/j.expneurol.2025.115632","url":null,"abstract":"<div><div>Both seizures and epileptiform discharges have been reported in various amyloid plaque- forming mouse models of Alzheimer's disease (AD). These mice also show premature mortality possibly related to epileptic seizures. Yet, the relationship between epileptic manifestations and amyloid pathology remains elusive. We utilized deltaFosB as a marker for sustained neuronal hyperactivity to localize the epileptic focus and compared it with age and sex differences in premature mortality between APP/PS1, 5xFAD and wildtype littermate mice and epileptiform discharges (EDs) during sleep in cortex and hippocampus. APP/PS1 mice showed elevated FosB/deltaFosB (shortly FosB) staining in the dentate granule (DG) cells and CA1-CA3 pyramidal cells. These were also the origins of identified epileptiform discharges (EDs) in LFP recordings. APP/PS1 mice showed much higher premature mortality than 5xFAD mice, females more than males. FosB staining intensity in APP/PS1 mice was robustly elevated compared to wildtype mice and peaked at 3 months of age. In contrast, FosB intensity in 5xFAD was lower than in wildtype mice at 1 and 3 months of age, showing a modest elevation at 10 months. In APP/PS1 mice between 1.5 and 3 months of age, the DG amyloid load correlated positively with FosB intensity. Furthermore, the DG FosB intensity showed a positive correlation with the frequency of EDs during sleep. These findings suggest that FosB staining intensity can be used as a proxy for local epileptiform activity in AD model mice and help unveil cellular and molecular basis of AD related neuronal hyperactivity and epilepsy.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"398 ","pages":"Article 115632"},"PeriodicalIF":4.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145892378","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":"Biochanin A exerts neuroprotective effects in Parkinson's disease both in vivo and in vitro by improving mitochondrial dysfunction through the Sirt1 signaling pathway","authors":"Shuxiang Tian ,&nbsp;Mingguang Niu ,&nbsp;Qian Qian,&nbsp;Kexian Zhang,&nbsp;Han Yang,&nbsp;Yang Xiao,&nbsp;Xinyue Jin,&nbsp;Yanyan Yin","doi":"10.1016/j.expneurol.2025.115636","DOIUrl":"10.1016/j.expneurol.2025.115636","url":null,"abstract":"<div><div>The accumulation of reactive oxygen species (ROS) leading to mitochondrial dysfunction is the pathological characteristics underlying the damage to dopaminergic neurons in the substantia nigra (SN) of Parkinson's disease (PD). Therefore, through improving mitochondrial dysfunction may be a potential strategy for PD treatment. Biochanin A (Bioch A), as a natural isoflavone phytoestrogen, has been implicated in studies for its therapeutic potential in neurodegenerative diseases. However, the precise molecular mechanisms by which it modulates PD-related neuronal damage remain unclear, limiting its clinical translational application. This study focuses on the neuroprotective mechanism of Bioch A, systematically revealing the key pathways and regulatory mechanisms through which it exerts its neuroprotective effects in PD by targeting mitochondrial dysfunction. By establishing lipopolysaccharide (LPS)-induced PD model mice and tumor necrosis factor-α (TNF-α)-induced SH-SY5Y cell models, combined with in vivo and in vitro experiments confirmed that Bioch A significantly alleviates dopaminergic neuronal damage by downregulating ROS levels, modulating adenosine triphosphate (ATP) production, promoting mitochondrial biogenesis, and improving abnormal mitochondrial dynamics. More importantly, this study has for the first time revealed that the Sirt1 pathway is a core target for Bioch A in regulating mitochondrial dysfunction. Furthermore, Bioch A promotes mitochondrial biogenesis by activating the Sirt1 pathway and reduces apoptosis levels by promoting mitochondrial fusion. In conclusion, this study provides novel experimental evidence for Bioch A's regulation of mitochondrial dysfunction, establishing the Sirt1 pathway as a key neuroprotective target. This discovery paves the way for Bioch A's clinical translation and targeted therapeutic research in PD.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"398 ","pages":"Article 115636"},"PeriodicalIF":4.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145896397","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: “Comparison of blood-brain barrier permeability changes in gyrencephalic (ferret & non-human primate) and lissencephalic (rat) models following blast overpressure exposures” by Kakulavarapu V. Rama Rao, et al.","authors":"W. Brad Hubbard ,&nbsp;Rania Abutarboush ,&nbsp;Stephen T. Ahlers ,&nbsp;Pamela J. VandeVord","doi":"10.1016/j.expneurol.2025.115602","DOIUrl":"10.1016/j.expneurol.2025.115602","url":null,"abstract":"","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"398 ","pages":"Article 115602"},"PeriodicalIF":4.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145843581","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":"Lipopolysaccharide-binding protein: The missing link in sleep and inflammation","authors":"Ye Qin ,&nbsp;Lei Sun ,&nbsp;Xuyuan Fan ,&nbsp;Jie Chen ,&nbsp;Jun Zhang ,&nbsp;Longfei Du","doi":"10.1016/j.expneurol.2025.115610","DOIUrl":"10.1016/j.expneurol.2025.115610","url":null,"abstract":"<div><div>Sleep disorders represent a major global health issue, and their association with systemic low-grade inflammation has become increasingly clear. Lipopolysaccharide-binding protein (LBP), a key mediator of the immune response to gut microbiota-derived endotoxins, has emerged as a potential regulatory molecule in inflammation-related sleep disorders. Elevated LBP levels are closely linked to a variety of sleep disorders. LBP induces sleep dysregulation through multiple mechanisms, including mediating peripheral and central immune inflammation, disrupting neurotransmitter balance, and perturbing biological rhythms. Both preclinical and clinical studies have observed abnormal LBP changes in different sleep disorder models. LBP serves as a critical interface molecule connecting peripheral immune activation and central sleep regulation. Targeting the LBP signaling pathway provides a new perspective for understanding and treating immune-mediated sleep disorders, yet its translational application still faces challenges. This review systematically summarizes clinical and preclinical studies on the role of LBP in sleep, neuroimmunity, and related diseases, aiming to clarify the potential pathophysiological mechanisms of LBP in sleep disorders and explore its prospects as a therapeutic target.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"398 ","pages":"Article 115610"},"PeriodicalIF":4.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145833498","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":"Astrocytic TPK1 mitigates amyloid pathology via TFEB-mediated endocytosis","authors":"Shu-Zhen Zhang ,&nbsp;Yuan Ma ,&nbsp;Yu Ding ,&nbsp;Yan-Qing Yin ,&nbsp;Bing-Wei Wang ,&nbsp;Gang Hu ,&nbsp;Jia-Wei Zhou","doi":"10.1016/j.expneurol.2026.115640","DOIUrl":"10.1016/j.expneurol.2026.115640","url":null,"abstract":"<div><div>Alzheimer's disease (AD), the leading cause of dementia, is characterized by amyloid-beta (Aβ) plaques, neurofibrillary tangles, and progressive neurodegeneration. Deregulation of glial cell activity plays an important role in the amyloid pathology. However, it is still unclear how changes in astrocytes contribute to Aβ deposition and clearance in AD. Here, we showed that deficiency of astrocytic thiamine pyrophosphokinase 1 (<em>Tpk1</em>), exacerbated Aβ burden leading to exacerbated spatial memory deficits in a mouse model of AD. While selective overexpression of <em>Tpk1</em> in astrocytes ameliorated cognitive decline and significantly reduced hippocampal and cortical Aβ plaque burden. Enhanced <em>Tpk1</em> expression augmented astrocyte endocytic capacity. Mechanistically, <em>Tpk1</em>-promoted endocytic activity depended on the activation of transcription factor EB (TFEB)-mediated pathways. Collectively, our findings demonstrate that astrocytic TPK1 mitigates cognitive impairment in 5xFAD mice by upregulating TFEB expression, thereby enhancing astrocyte-mediated engulfment and degradation of neurotoxic aggregates, including Aβ. This study suggests that astrocytic TPK1/TFEB pathway is a promising target for developing disease-modifying AD therapies.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"398 ","pages":"Article 115640"},"PeriodicalIF":4.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145931587","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 effects of traumatic brain injury and the impact of biperiden treatment in a male rat model","authors":"Viviam Sanabria ,&nbsp;Matheus B. Braga ,&nbsp;Simone Romariz ,&nbsp;Christiane Gimenes ,&nbsp;Michele Longoni Calió ,&nbsp;Maira Licia Foresti ,&nbsp;Luiz Eugênio Mello ,&nbsp;Beatriz M. Longo","doi":"10.1016/j.expneurol.2025.115626","DOIUrl":"10.1016/j.expneurol.2025.115626","url":null,"abstract":"<div><div>Traumatic brain injury (TBI) disrupts brain function and may lead to post-traumatic epilepsy (PTE), a long-term complication. Anticholinergic drugs, such as biperiden, have shown potential in modulating neural plasticity. This study evaluated whether biperiden treatment influences motor and cognitive recovery, seizure susceptibility, and neurovascular and inflammatory responses in rats subjected to the lateral fluid percussion injury (LFPI) model. Adult male Wistar rats underwent LFPI or sham surgery and were treated with saline or biperiden (8 mg/kg) administered intraperitoneally every 8 h for 10 days, starting 6 h after trauma. Neuromotor battery tests were assessed over 28 days, spatial memory at 30 days using the Barnes Maze, and seizure susceptibility was tested with pentylenetetrazol (PTZ) at 90 days after trauma as a second hit. Plasma samples were collected 10 days after trauma for Single Molecular Array (SIMOA) analysis of trauma biomarkers, neurofilament light chain (NfL), and total tau. Histological and immunofluorescence analyses were conducted at 91 days. TBI significantly increased plasma NfL levels compared to the Naive group, indicating neuronal damage. Animals that underwent LFPI and were treated with saline solution were called TBI-SAL group, while animals that underwent LFPI and were treated with biperiden solution were called TBI-BIP group. TBI-SAL group exhibited memory impairments and random search strategies in the Barnes Maze. Both TBI groups (those treated with saline and with biperiden) exhibited higher seizure susceptibility to PTZ at 30 mg/kg, but biperiden slightly reduced seizure intensity. Histological analyses revealed larger lesion volumes, reduced NeuN expression in hippocampal regions (CA1, CA3), and altered astrocytic and microglial morphology in the TBI-SAL group. Notably, biperiden treatment promoted vascular remodeling, characterized by an increase in vessel density, in the motor cortex and hippocampal regions, suggesting potential modulation of post-traumatic neuroinflammation. Biperiden enhanced vascular remodeling and partially mitigated long-term histopathological changes after TBI, though its protective effects on cognitive and seizure-susceptibility responses were limited. These findings highlight biperiden's potential to influence vascular and inflammatory responses in the injured brain.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"398 ","pages":"Article 115626"},"PeriodicalIF":4.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145882227","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}