Neuroreport最新文献

{"title":"Effects of ononin on cognitive and learning-memory functions in mild cognitive impairment.","authors":"Lei Yang, Wenya Zhao, Jiaojiao Zhao, Siruan Chen, Xia Qin, Zuxiao Yang, Dezhi Kong, Wei Zhang","doi":"10.1097/WNR.0000000000002264","DOIUrl":"10.1097/WNR.0000000000002264","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to investigate the potential of ononin in alleviating mild cognitive impairment (MCI) and to determine whether its effects depend on the functional recovery of neurons in the nucleus tractus solitarius (NTS).</p><p><strong>Methods: </strong>Four-month-old APP/PS1 mice were treated with 30-mg/kg ononin via oral gavage for 8 consecutive days. Cognitive behavior was assessed using the novel object recognition test, Y-maze test, and open field test. Cortical perfusion was measured by laser speckle contrast imaging. The activation of NTS neurons was detected using c-Fos immunofluorescence staining, while dendritic complexity and neuronal firing frequency were evaluated via Golgi staining and patch-clamp electrophysiology, respectively.</p><p><strong>Results: </strong>Ononin treatment significantly improved the novel object recognition index and spontaneous alternation rate in the Y-maze test in APP/PS1 mice. It also enhanced cerebral blood flow perfusion and increased the number of c-Fos-positive cells in the NTS, hippocampal CA1 region, and cortex. Furthermore, ononin increased dendritic intersections and restored dendritic spine density in NTS neurons to normal levels, along with significantly elevating their firing frequency.</p><p><strong>Conclusion: </strong>Ononin may ameliorate MCI-like cognitive deficits in APP/PS1 mice by activating NTS neurons, restoring synaptic plasticity, and improving cerebral perfusion. These findings suggest that the NTS could serve as a potential target for early intervention in Alzheimer's disease.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"308-318"},"PeriodicalIF":1.7,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147654649","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glutaredoxin-1 attenuates transactive response DNA-binding protein 43-induced neurotoxicity by suppressing oxidative stress and transactive response DNA-binding protein 43 aggregation.","authors":"Ji Min Lee, Eugene Bok, Sang Ryong Kim, Jaekwang Kim","doi":"10.1097/WNR.0000000000002266","DOIUrl":"10.1097/WNR.0000000000002266","url":null,"abstract":"<p><strong>Objective: </strong>Cytoplasmic aggregation of transactive response DNA-binding protein 43 (TDP-43) represents pathological hallmarks of TDP-43 proteinopathies. Accumulating evidence indicates that oxidative stress plays a pivotal role in these disorders by promoting TDP-43 aggregation and subsequent neurotoxicity. Glutaredoxin-1 (Grx1) is a key antioxidant enzyme that maintains cellular redox homeostasis. In this study, we investigated the role of Grx1 in TDP-43 proteinopathy.</p><p><strong>Methods: </strong>We examined the effects of Grx1 in neuro-2a cells expressing human wild-type TDP-43 (N2a-hTDP-43), a cellular model of TDP-43 proteinopathy characterized by increased oxidative stress, TDP-43 aggregation, and neurotoxicity.</p><p><strong>Results: </strong>In N2a-hTDP-43 cells, Grx1 expression was increased in parallel with elevated oxidative stress. Increasing Grx1 significantly suppresses intracellular oxidative stress and cytoplasmic TDP-43 aggregation in N2a-hTDP-43 cells. Notably, increasing Grx1 significantly reduces cleaved caspase-3 levels in N2a-hTDP-43 cells, indicating reduced neurotoxicity.</p><p><strong>Conclusion: </strong>Collectively, our findings demonstrate that Grx1 attenuates neurotoxicity by suppressing oxidative stress and TDP-43 aggregation, highlighting its potential as a therapeutic target for TDP-43 proteinopathies.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"319-323"},"PeriodicalIF":1.7,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13124251/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147777347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms of dexmedetomidine-induced cerebral protection following ischemic brain injury via the brain-derived neurotrophic factor-tyrosine kinase receptor B pathway.","authors":"Alimujiang Simayi, Li Qu, Xiao-Li Wang, Wan-Ying Cao, Xuan Zhao, Gui-Ping Xu","doi":"10.1097/WNR.0000000000002256","DOIUrl":"10.1097/WNR.0000000000002256","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the protective effects of dexmedetomidine on cerebral ischemia-reperfusion injury through the activation of the brain-derived neurotrophic factor (BDNF)/tyrosine kinase receptor B (TrkB) signaling pathway.</p><p><strong>Methods: </strong>This study utilized hippocampal neuronal oxygen-glucose deprivation/reoxygenation (OGD/R) models and rat middle cerebral artery occlusion models, with dexmedetomidine intervention.</p><p><strong>Results: </strong>Compared with the sham-operated group, the model group rats exhibited a significant increase in Zea-Longa scores, a marked prolongation of the escape latency, a notable reduction in the number of platform crossings, a significant increase in the percentage of cerebral infarct size, and a marked decrease in the expression of BDNF, TrkB, and Bcl-2 proteins and mRNA ( P  < 0.05). The dexmedetomidine group showed significantly better outcomes in all above parameters compared to the model group. Compared with the control group, the OGD/R group exhibited a reduction in hippocampal neuronal cell viability, a significant increase in apoptosis rate, elevated expression of Bax and C-caspase-3 proteins, a marked decrease in Bcl-2 protein levels, and a significant reduction in the expression of BDNF and TrkB proteins and mRNA ( P  < 0.05).</p><p><strong>Conclusion: </strong>Dexmedetomidine exerts significant neuroprotective effects by activating the BDNF/TrkB signaling pathway, thereby alleviating ischemic brain injury.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"297-307"},"PeriodicalIF":1.7,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147777294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CircOGDH promotes oxygen-glucose deprivation/reoxygenation-induced neuron injury by targeting the miR-195-5p/brain-specific angiogenesis inhibitor 1-associated protein 2 axis.","authors":"Ruibin Zheng, Zhanhai Huang, Hongchuan Zhou, Liguo Zhang","doi":"10.1097/WNR.0000000000002261","DOIUrl":"10.1097/WNR.0000000000002261","url":null,"abstract":"<p><strong>Objective: </strong>Stroke remains a major cause of disability and death worldwide, with inflammation and oxidative stress that play important roles in its pathogenesis. This study aimed to explore the role of circOGDH in stroke and its mechanism of action.</p><p><strong>Methods: </strong>SH-SY5Y cells were transfected with circOGDH, miR-195-5p, and brain-specific angiogenesis inhibitor 1-associated protein 2 (BAP2) vectors, and oxygen-glucose deprivation/reoxygenation (OGD/R) models were established. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide was used to assess cell proliferation and flow cytometry was used to measure reactive oxygen species (ROS) activity and apoptotic rates. Inflammatory factor ELISAs were performed. Superoxide dismutase activity and malondialdehyde concentration were measured using assay kits. Luciferase reporters were used to analyze molecular binding.</p><p><strong>Results: </strong>CircOGDH or BAP2 knockdown or miR-195-5p overexpression inhibited the effects of OGD/R on SH-SY5Y cells, including decreased proliferation and superoxide dismutase activity, as well as increased apoptosis, ROS production, malondialdehyde concentration, and inflammatory factor levels. In SH-SY5Y cells, circOGDH targeted miR-195-5p to upregulate BAP2 expression. miR-195-5p inhibition or BAP2 overexpression eliminated circOGDH knockdown-elicited protection of SH-SY5Y cells against OGD/R.</p><p><strong>Conclusion: </strong>CircOGDH aggravates OGD/R-caused SH-SY5Y cell injury and promotes inflammatory factor secretion and oxidative stress by targeting miR-195-5p to upregulate BAP2 expression.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"277-285"},"PeriodicalIF":1.7,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147531274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Control of mirror activity by transcranial direct current stimulation of the supplementary motor area.","authors":"Akihiro Matsuura, Manami Hada, Yuji Nishioka, Futoshi Mori","doi":"10.1097/WNR.0000000000002262","DOIUrl":"10.1097/WNR.0000000000002262","url":null,"abstract":"<p><strong>Objective: </strong>We investigated whether transcranial direct current stimulation (tDCS) applied to the supplementary motor area (SMA) modulates mirror activity induced by transcranial magnetic stimulation (TMS) during a unilateral precision pinch task.</p><p><strong>Methods: </strong>Healthy subjects performed a left-hand precision pinch task during the delivery of single-pulse TMS to the left primary motor cortex (M1) to evoke mirror activity in the right hand. Anodal, cathodal, and sham tDCS were applied over the SMA via a randomized crossover design. Motor-evoked potentials recorded from the right first dorsal interosseous muscle were used to quantify mirror activity. Pinch performance variability was evaluated.</p><p><strong>Results: </strong>Although anodal tDCS tended to increase mirror activity, the effect did not differ significantly from that of sham tDCS. In contrast, cathodal tDCS significantly reduced mirror activity compared with the effects of sham and anodal tDCS. Pinch performance variability did not differ among the tDCS conditions, indicating that mirror activity changed independently of motor performance. Resting motor-evoked potential amplitudes elicited by single-pulse TMS were not significantly altered by tDCS targeting the SMA.</p><p><strong>Conclusion: </strong>Mirror activity is modulated by SMA excitability. The findings indicate that cathodal tDCS applied to the SMA reduces mirror activity, potentially through alterations in cortical network interactions between the SMA and M1.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"286-289"},"PeriodicalIF":1.7,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147504012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Altered gray matter volume in major depressive disorder patients with psychomotor retardation.","authors":"Yiyun Wang, Lijin Yuan, Xiaoyun Luo, Jigang Lian, Yun Zhu, Zonglin Shen","doi":"10.1097/WNR.0000000000002263","DOIUrl":"10.1097/WNR.0000000000002263","url":null,"abstract":"<p><strong>Background: </strong>Psychomotor retardation (PMR) is a clinically significant but under-investigated neuropsychiatric manifestation of major depressive disorder (MDD). Its neuroanatomical features remain poorly understood. This study aims to examine differences in gray matter volume (GMV) alterations between MDD patients with and without PMR.</p><p><strong>Methods: </strong>The study enrolled 107 first-episode, treatment-naïve MDD patients (diagnosed per DSM-IV criteria) and 112 age- and sex-matched healthy controls. Participants were divided into two clinical subgroups based on the retardation factor score of the 17-item Hamilton Depression Rating Scale: an MDD with retardation (MDD-WR) group (score ≥ 8, n  = 51) and an MDD without retardation (MDD-WoR) group (score < 8, n  = 56). Structural MRI scans were obtained for all participants.</p><p><strong>Results: </strong>Compared with healthy controls, the MDD-WR group showed significantly smaller GMV in the bilateral posterior cerebellum and left calcarine gyrus. In contrast, the MDD-WoR group demonstrated larger GMV in the left postcentral gyrus (PoCG) and right angular gyrus. Among all of the MDD patients, patients of the MDD-WR group had smaller GMV in the right PoCG, right superior frontal gyrus, and left olfactory bulb compared with the MDD-WoR group.</p><p><strong>Conclusion: </strong>Our findings identify distinct neuroanatomical patterns of GMV changes in MDD patients with PMR compared with those without PMR. This provides novel insights into the neural basis of PMR in MDD.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"290-296"},"PeriodicalIF":1.7,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13061376/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147531285","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nuclear heme oxygenase-1 enhances blood-spinal cord barrier repair via corticotropin-releasing hormone-mediated tight junction phosphorylation.","authors":"Jin Huang, Sheng Chang","doi":"10.1097/WNR.0000000000002268","DOIUrl":"https://doi.org/10.1097/WNR.0000000000002268","url":null,"abstract":"<p><strong>Objective: </strong>The hallmark of secondary spinal cord injury (SCI) is destruction of the blood-spinal cord barrier (BSCB). Nuclear heme oxygenase-1 (NHO-1) is involved in neuroprotection in the central nervous system. Previously, we demonstrated that adenoviral delivery of nuclear-targeted HO-1 (NHO-1) alleviates BSCB disruption, but the molecular mechanisms remain to be clarified. This study was conducted to investigate the specific regulatory mechanisms regulating tight junctions in the BSCB.</p><p><strong>Methods: </strong>A moderate T10 contusion SCI was induced in adult male Sprague-Dawley rats. Nuclear-targeted HO-1 was delivered by adenoviral pretreatment 7 days before injury. Spinal cords were collected at 24 h post-SCI for RNA-seq and quantitative real-time-PCR validation. BSCB permeability (Evans Blue), tight junction phosphorylation (western blot), and locomotor function (Basso, Beattie, and Bresnahan score and footprint analysis) were assessed, with intrathecal corticotropin-releasing hormone (CRH)-R1 agonist (Cortagine) or antagonist (Antalarmin) administered after SCI.</p><p><strong>Results: </strong>RNA-seq identified 10 overlapping differentially expressed genes across pairwise comparisons; subsequent Venn-based prioritization and quantitative real-time-PCR validation identified Crh as the most consistently regulated candidate. Functional assays demonstrated that nuclear HO-1, particularly when combined with CRH receptor activation, decreased leakage of BSCB via enhancing phosphorylation of tight junction protein which disappears after application of CRH inhibitor.</p><p><strong>Conclusion: </strong>These results indicate that nuclear-targeted HO-1 promotes BSCB repair after SCI by transcriptionally upregulating Crh and enhancing CRH-dependent phosphorylation of tight junction proteins (Claudin-5 and Occludin).</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147818241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynamic brain states and molecular signatures in primary angle-closure glaucoma.","authors":"Shui-Feng Wang, Yuan-Zhi He, Zhan-Xiang Hu, Zi-Liang Zheng, Xin Huang","doi":"10.1097/WNR.0000000000002267","DOIUrl":"https://doi.org/10.1097/WNR.0000000000002267","url":null,"abstract":"<p><strong>Background: </strong>Primary angle-closure glaucoma (PACG) has traditionally been regarded as an ocular disorder, but accumulating evidence suggests broader central nervous system involvement. Although previous neuroimaging studies have identified static functional abnormalities, the dynamic properties of large-scale brain networks and their associated molecular signatures in PACG remain insufficiently understood.</p><p><strong>Methods: </strong>We applied Leading Eigenvector Dynamics Analysis to resting-state functional MRI data from 44 patients with PACG and 57 healthy controls to characterize recurrent whole-brain dynamic states. State-specific temporal metrics and spatial patterns were further evaluated using multiple machine learning models. To explore potential biological correlates, imaging-derived spatial patterns were linked to cortical gene expression profiles from the Allen Human Brain Atlas using partial least squares regression, followed by pathway enrichment, cell-type enrichment, and neurotransmitter receptor/transporter mapping analyses.</p><p><strong>Results: </strong>Compared with healthy controls, PACG patients showed prolonged dwell time in one recurrent dynamic state, suggesting reduced flexibility of large-scale brain dynamics. Machine learning models showed promising classification performance within the current dataset, with the most informative features primarily located in default mode network regions. Transcriptomic decoding revealed enrichment of genes related to synaptic signaling, ion channel activity, neurotransmitter transport, and neuronal communication. Cell-type enrichment analyses further implicated excitatory neurons, inhibitory neurons, and astrocytes. In addition, a significant spatial association with VMAT2 suggested that monoaminergic systems may be relevant to the observed imaging phenotype.</p><p><strong>Conclusion: </strong>PACG is associated with altered large-scale brain dynamics, particularly involving default mode network-related state instability. These imaging abnormalities show spatial associations with molecular, cellular, and neurotransmitter-related signatures.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147818269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Opposite modulation of sensorimotor rhythms in 3-8 years children by passive hand movement and hand movement observation.","authors":"Vladimir Lipatov, Anna Rebreikina, Olga Sysoeva","doi":"10.1097/WNR.0000000000002254","DOIUrl":"10.1097/WNR.0000000000002254","url":null,"abstract":"<p><strong>Objective: </strong>Sensorimotor rhythms can be potential markers of atypical child development; however, many paradigms used in research of sensorimotor rhythms are difficult to use in children with developmental disabilities. In this paper, we explored two experimental paradigms for sensorimotor rhythms investigation that can potentially be used in children with developmental disorders.</p><p><strong>Methods: </strong>Electroencephalography was recorded in typically developing children aged 3-8 years ( N  = 58), during the inclusive passive hand movement paradigm (PHM), the hand movement observation on video paradigm (VWH), and control condition (video with fractals). The difference in the mu-rhythm power was analyzed between experimental and control conditions at the central electrodes (C3 and C4).</p><p><strong>Results: </strong>The PHM causes significant desynchronization of the mu rhythm in the 6-13 and 13-30 Hz ranges, predominantly in the right motor region, suggesting activation of motor programs. In contrast, the VWH paradigm caused an increase in the mu rhythm in the 6-13 Hz range relative to the control condition, predominantly over left motor cortex, suggesting deactivation or underdevelopment of motor representation in children of such age during hand movement observation.</p><p><strong>Conclusion: </strong>While PHM consistently elicits mu rhythm desynchronization, observation of hand movement could induce the opposite effect, which needs further investigation.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"215-221"},"PeriodicalIF":1.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147504311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Involvement of 75NTR extracellular domain in rotenone-induced Parkinson's disease cell models.","authors":"Yifei You, Anyan Ren, Nan Wang, Fang Chen, Xianzhi Wang, Chen Li, Hongcai Wang","doi":"10.1097/WNR.0000000000002258","DOIUrl":"10.1097/WNR.0000000000002258","url":null,"abstract":"<p><strong>Objective: </strong>While the p75 neurotrophin receptor (p75NTR) is critically implicated in the aggregation of α-synuclein (α-syn), a defining pathological hallmark of Parkinson's disease, the distinct functional contributions of its structural domains remain largely unresolved.</p><p><strong>Methods: </strong>To investigate this, we employed a rotenone-induced cellular Parkinson's disease model utilizing SH-SY5Y neuroblastoma cells transfected with plasmids encoding specific p75NTR truncation mutants.</p><p><strong>Results: </strong>Overexpression of a mutant representing the p75NTR extracellular domain (HA-p75Δ151, lacking residues 277-427) significantly exacerbated both α-syn expression levels and its aggregation phenotype. This effect is potentially attributable to the aberrant activation of caspase-1. Conversely, unlike full-length p75NTR which enhanced α-syn ubiquitination, the HA-p75Δ151 truncation failed to modulate ubiquitination dynamics. Furthermore, expression of this extracellular domain fragment induced cell cycle dysregulation and promoted cell death.</p><p><strong>Conclusion: </strong>These findings delineate the p75NTR extracellular domain-induced α-syn proteotoxic stress. This domain-specific mechanism advances our understanding of Parkinson's disease pathogenesis and highlights the therapeutic potential of targeting specific p75NTR domains.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"247-257"},"PeriodicalIF":1.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147503965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}