{"title":"Characteristics of SAA, the SII and NT-proBNP levels in patients with ACI and their value in evaluating the prognosis of thrombolytic therapy.","authors":"Xianshi Yang, Ailan Pang, Wei Liu, Hong Xu","doi":"10.1080/01616412.2025.2549030","DOIUrl":"10.1080/01616412.2025.2549030","url":null,"abstract":"<p><strong>Objective: </strong>To explore the features of serum amyloid A (SAA), the systemic immune inflammation index (SII), and N-terminal B-type natriuretic peptide (NT-proBNP) among individuals suffering from acute cerebral infarction (ACI), as well as their potential significance in assessing the adverse outcomes of thrombolytic treatment.</p><p><strong>Methods: </strong>A total of 122 patients with ACI who underwent thrombolytic therapy were included in this single-center retrospective study. Patients were categorized into short-term good prognosis (<i>n</i> = 81) and short-term adverse outcomes (<i>n</i> = 41) groups on the basis of their prognosis within 6 months after the procedure. Risk factors for poor short-term prognosis after thrombolytic therapy in ACI patients were screened via regression analysis, and the predictive value of each risk factor was assessed via receiver operating characteristic (ROC) curves.</p><p><strong>Results: </strong>Preoperative SAA, NT-proBNP, Hcy, CRP, and the SII were significantly higher in the short-term adverse outcomes group than in the good prognosis group (<i>p</i> < 0.05). Specifically, the adverse outcomes group had higher mean levels of SAA, NT-proBNP, and SII (<i>p</i> < 0.001). The combined model (SAA, NT-proBNP, and the SII) had high predictive accuracy, with an AUC of 0.957 (<i>p</i> < 0.05).</p><p><strong>Conclusion: </strong>Pretreatment SAA, SII, and NT-proBNP levels are strongly correlated with adverse short-term outcomes of ACI patients following thrombolytic therapy.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1-10"},"PeriodicalIF":1.5,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144874217","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":"Elevated expression of galectin-3 in microglia exacerbated neuron apoptosis via promoting TNF-α release through the TLR4/NF-κB signaling pathway.","authors":"Cui-Jie Yuan, Meng-Yao Wang, Jiang-Bao Xu, Cheng-Peng Zhan, Yang-Bo Li, Guo-Feng Yu, Wei-Min Dai, Xin-Jiang Yan","doi":"10.1080/01616412.2025.2549442","DOIUrl":"10.1080/01616412.2025.2549442","url":null,"abstract":"<p><strong>Objectives: </strong>High blood levels of galectin-3 (Gal-3) predict poor outcomes after intracerebral hemorrhage (ICH). Our previous study also showed that Gal-3 could aggravate ICH-induced brain injury through increasing neuroinflammatory activation and nerve cell death. In this study, we focus on the role of Gal-3 in nerve cell death after ICH.</p><p><strong>Methods: </strong>An ICH mice model and an <i>in vitro</i> co-stimulation model were established to study Gal-3's effect on neuron cell death via toll-like receptor 4 (TLR4)/nuclear factor kappa-B (NF-κB) pathway. Western blot and immunofluorescence (IF) staining were applied for neuron apoptosis evaluation. Enzyme-linked immunosorbent assay (ELISA) was used to measure the production of neuroinflammation factors.</p><p><strong>Results: </strong>Gal-3 expression in microglia was increased and positively correlated with the severity of neurological impairment after ICH. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and NeuN (or MAP2) double staining assay results revealed that the increasing of neuron cell apoptosis after Gal-3 treatment both in <i>in vivo</i> and <i>in vitro</i> co-stimulation experiments could be reversed by treatment with Gal-3 inhibitor MCP, TLR4 inhibitor TAK-242, NF-κB inhibitor PDTC, or TNF-α inhibitor C87 effectively. ELISA results revealed the same trends of TNF-α release changes from microglia after Gal-3 or inhibitor treatment both <i>in vivo</i> and <i>in vitro</i>. WB results confirmed the Gal-3's role on apoptosis by the expression level of proteins such as FADD, Apaf-1, Bax, Cytochrome C, Caspase-8, and cleaved-Caspase-3 in neuron cells.</p><p><strong>Conclusion: </strong>The upregulation of Gal-3 in microglia after ICH could aggravate neuron cell apoptosis through increasing TNF-α release via TLR4/NF-κB pathway.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1-13"},"PeriodicalIF":1.5,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144883311","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}
Halil Onder, Nidanur Kocabacak, Numan Bulut, Selcuk Comoglu
{"title":"Investigation of changes in the choice reaction time with levodopa in patients with Parkinson's disease.","authors":"Halil Onder, Nidanur Kocabacak, Numan Bulut, Selcuk Comoglu","doi":"10.1080/01616412.2025.2549042","DOIUrl":"https://doi.org/10.1080/01616412.2025.2549042","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the alterations in the choice reaction time (RT) with levodopa in Parkinson's disease (PD) patients. Via concurrent clinical assessments, we aimed to provide perspectives regarding the clinical significance of these alterations and responsible pathophysiology.</p><p><strong>Methods: </strong>Participants were recruited from consecutive PD patients who applied to our Movement Disorders Polyclinics between September/2024 October/2024. Demographic, clinical features, and the MDS-UPDRS-3 scale (-on and -off) were evaluated. The Blazepod technology was used to measure choice RT.</p><p><strong>Results: </strong>We included 25 PD patients with a mean age of 65.7 ± 9.0 y (F/M = 9/16). The comparative analyses between medication-off and -on states revealed that the MDS-UPDRS-3 scores decreased significantly during the medication-on states (<i>p</i> < 0.001, d = 1.09). Besides, all the parameters related to reaction time including RT, number of hits, and errors improved during medication-on state (d = 0.71, d = 0.88, d = 0.72, respectively). The RT-off showed moderate positive correlations with the UPDRS-3 scores (CC:0.416, <i>p</i> = 0.039). The left side RT-off and also the right-side RT-off showed moderate positive correlations with the left-side UPDRS-3-'off' scores (CC:0.499, <i>p</i> = 0.011, CC:0.440, <i>p</i> = 0.028, respectively).</p><p><strong>Conclusion: </strong>In conclusion, we found significant improvements in all the measures of choice RT after levodopa intake which reached moderate-large effects sizes. Our findings suggest that RT impairment in PD may involve shared neural mechanisms, with possible lateralized contributions that require further investigation. The RT measures may also constitute an alternative method for measuring LR and needs to be tested in the distinct clinical scenarios in future-related studies.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1-12"},"PeriodicalIF":1.5,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144874218","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":"The predictive, preventive, and personalized medicine of multiple sclerosis: ferroptosis and circulating proteins.","authors":"Yao Xiong, Daifeng Yang, Shanshan Cai","doi":"10.1080/01616412.2025.2541908","DOIUrl":"https://doi.org/10.1080/01616412.2025.2541908","url":null,"abstract":"<p><strong>Objective: </strong>Based on the principles of Predictive, Preventive, and Personalized Medicine (PPPM), this study aimed to identify ferroptosis-related genes associated with multiple sclerosis (MS) and to explore the underlying mechanisms through genetic approaches.</p><p><strong>Materials and methods: </strong>Summary statistics of circulating proteins were obtained from the UK Biobank Pharma Proteomics Project (UKB-PPP), ferroptosis-related genes were curated from the FerrDb database, and MS genome-wide association study (GWAS) data were sourced from the International Multiple Sclerosis Genetics Consortium (IMSGC). Two-sample Mendelian randomization (MR) analyses were performed to assess the causal relationships between proteins, ferroptosis-related genes, and MS risk. Mediation MR analysis was conducted to explore the potential mediating role of ferroptosis-related genes. The primary analytical method was inverse variance weighting (IVW), supplemented by MR-Egger and weighted median approaches.</p><p><strong>Results: </strong>After Bonferroni correction, one ferroptosis-related gene (Ferritin Mitochondrial, FTMT) and 21 circulating proteins were significantly associated with MS. Eleven protein-gene pairs were identified. Mediation analysis further revealed that FTMT mediated the effects of several proteins on MS risk, including CD8A (17.6%), CFB (9.0%), ENPP6 (9.5%), GZMA (22.9%), KIR2DL2 (17.4%), KIR2DL3 (16.9%), and TNXB (13.2%).</p><p><strong>Conclusions: </strong>This study highlights the critical role of FTMT in linking circulating proteins to MS pathogenesis through ferroptosis regulation, providing novel insights into predictive, preventive, and personalized medicine strategies for MS management.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1-9"},"PeriodicalIF":1.5,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144855885","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":"Predictors of botulinum toxin type A response in patients with migraine: a meta-analysis.","authors":"Shaoqi Wu, Chang Zhou","doi":"10.1080/01616412.2025.2541293","DOIUrl":"https://doi.org/10.1080/01616412.2025.2541293","url":null,"abstract":"<p><strong>Background: </strong>Migraine is one of the most common neurological diseases, imposing a heavy burden on society. Botulinum toxin type A (BT-A) has been approved as a safe and effective preventive treatment; however, not all patients report effectiveness after BT-A treatment. Thus, identifying BT-A responders in advance is valuable for treatment. Several studies have shown that some characteristics of headache, like a shorter disease duration and the absence of medication overuse, are potential predictors of clinical response. This meta-analysis aims to identify predictors linked to BT-A in people with migraine.</p><p><strong>Methods: </strong>PubMed, Web of Science, Embase and the Cochrane Library were searched for studies. All cohort studies reporting the factors of responders and non-responders to BT-A injection were selected.</p><p><strong>Results: </strong>Eleven studies met the criteria for selection. Of the 18 factors identified, only six were reported in at least three studies. BT-A response was associated with disease duration (MD: -2.37, CI: [-4.03, -0.83], <i>p</i> = 0.0002). In sensitivity analysis, the outcome of headache days was also statistically significant (MD: 1.02, CI: [0.45, 1.59], <i>p</i> = 0.0004).</p><p><strong>Conclusion: </strong>The findings of this meta-analysis support disease duration and headache days as predictive factors of BT-A response in people with migraine. Injecting BT-A at an early stage might be beneficial for migraine patients. However, the predictors were based on a small number of studies; thus, more studies are needed to prove the outcome. Several other factors may be associated with the response to BT-A but reported in a few studies. Therefore, more studies are needed to evaluate additional predictors.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1-15"},"PeriodicalIF":1.5,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144847961","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}
Shupeng Guo, Ti Li, Lili Luan, Jialin Deng, Yuntao Luo
{"title":"Sophocarpine prevents LPS and IFN-γ-stimulated oxidative stress and neuroinflammation of BV-2 microglia by regulating the AMPK/NF-κB signaling pathway.","authors":"Shupeng Guo, Ti Li, Lili Luan, Jialin Deng, Yuntao Luo","doi":"10.1080/01616412.2025.2545351","DOIUrl":"https://doi.org/10.1080/01616412.2025.2545351","url":null,"abstract":"<p><strong>Background: </strong>Microglia can be continuously activated to produce proinflammatory cytokines and reactive oxygen species, leading to progressive neurodegeneration. Sophocarpine (ScP) has been reported to exhibit neuroprotective and anti-inflammatory activities, but it remains unclear whether microglia are involved in these effects.</p><p><strong>Methods: </strong>BV-2 cells were exposed to ScP, AMP-activated protein kinase (AMPK) agonist AICAR, and the AMPK inhibitor Compound C for 30 min before being treated with lipopolysaccharide (LPS) and IFN-γ for 24 h. The levels of oxidative response and inflammation were detected by kits, immunofluorescence, ELISA, and western blotting. The AMPK/NF-κB expression was measured using western blotting. In vivo effects were next verified using LPS-induced neuroinflammatory mouse models.</p><p><strong>Results: </strong>Overall, 1, 2, and 4 μM ScP had no effects on BV-2 cells. After BV-2 cells were stimulated with LPS and IFN-γ, the levels of antioxidant enzymes were decreased, whereas the levels of allograft inflammatory factor 1 (Iba-1) and inflammatory mediators were increased. After LPS and IFN-γ stimulation, the levels of phosphorylated (p)-AMPK protein were decreased, whilst the levels of p-IκBα and p-p65 protein were increased. ScP then reduced the levels of Iba-1, inflammatory mediators, p-IκBα, and p-p65 proteins, whilst increasing the levels of antioxidant enzymes and p-AMPK. ScP treatment reduced the extent of neuronal damage in mice, significantly improving inflammation and oxidative stress damage. The antioxidant and anti-inflammatory effects of ScP were found to be enhanced after AICAR intervention.</p><p><strong>Conclusion: </strong>ScP can inhibit LPS and IFN-γ-stimulated oxidative response and neuroinflammation in BV-2 cells through the AMPK/NF-κB axis.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1-19"},"PeriodicalIF":1.5,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144835857","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":"Association of hemoglobin glycation index with poor prognosis in critically ill patients with ischemic stroke: a cohort study.","authors":"Kaiwu Meng, Sushuang Yang, Yiran Liu, Xinyan He, Wenqin Luo, Ling He, Dian He","doi":"10.1080/01616412.2025.2542948","DOIUrl":"https://doi.org/10.1080/01616412.2025.2542948","url":null,"abstract":"<p><strong>Background: </strong>The hemoglobin glycation index (HGI), quantifying interindividual hemoglobin glycation variability, predicts cardiovascular outcomes but lacks exploration in cerebrovascular prognosis. We evaluated its nonlinear association with mortality in critically ill ischemic stroke (IS) patients.</p><p><strong>Methods: </strong>This retrospective cohort analyzed 2,035 ICU-admitted IS patients (MIMIC-IV database). HGI was computed as measured HbA1c minus regression-predicted HbA1c (fasting glucose-derived). Restricted cubic splines and multivariable Cox models assessed nonlinear mortality risks (30-/365-day).</p><p><strong>Results: </strong>A U - shaped HGI - mortality relationship emerged. Compared to moderate HGI (Q3), low HGI (Q1) doubled the 30 - day mortality risk (adjusted HR = 2.00, 95% CI: 1.49-2.70) and increased the 365 - day risk by 59% (HR = 1.59, 95% CI: 1.27-1.99). High HGI (Q4) demonstrated a 38% increase in the 30 - day risk (HR = 1.38, 95% CI: 0.99-1.93) and a 24% increase in the 365 - day risk (HR = 1.24, 95% CI: 0.98-1.59). Continuous HGI was inversely correlated with mortality (30 - day HR = 0.86, 95% CI: 0.78-0.95, <i>p</i> = 0.003; 365 - day HR = 0.92, 95% CI: 0.86-0.99, <i>p</i> = 0.038). Threshold analysis identified inflection points (HGI = 0.58 for the 365 - day period; 1.299 for the 30 - day period), with mortality increasing beyond these thresholds.</p><p><strong>Conclusions: </strong>HGI demonstrates a robust U-shaped association with mortality in critical IS, independent of glycemic status. Both extremes independently predict adverse outcomes, with low HGI conferring higher risk. HGI emerges as a novel prognostic biomarker, underscoring glycemic variability's clinical relevance beyond conventional metrics for IS risk stratification.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1-12"},"PeriodicalIF":1.5,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144822127","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}
Cengiz Guven, Ahmet Türk, Seda Koçak, Busra Zencirci, Alper Yalcin, Hasan Aydın, Mevlut Doğukan
{"title":"Cortexin modulates OPG/RANK/RANKL and TRPC1 expression in cerebral ischemia-reperfusion injury.","authors":"Cengiz Guven, Ahmet Türk, Seda Koçak, Busra Zencirci, Alper Yalcin, Hasan Aydın, Mevlut Doğukan","doi":"10.1080/01616412.2025.2536075","DOIUrl":"https://doi.org/10.1080/01616412.2025.2536075","url":null,"abstract":"<p><strong>Objective: </strong>Biomarkers such as Osteoprotegerin (OPG), Receptor Activator of Nuclear Factor κ-B (RANK), its ligand RANKL, and Transient Receptor Potential Canonical 1 (TRPC1) have been implicated in the neuroprotective response to neuronal injury, with their expression potentially influenced by antioxidant treatments. The objective of this study was to investigate the effects of Cortexin on the expression of these biomarkers in brain tissue following cerebral ischemia-reperfusion (I/R) injury.</p><p><strong>Methods: </strong>Thirty-five male Wistar albino rats were divided into five groups: control, ischemia (45 minutes), I/R (7 days), I/R + 1 mg/kg Cortexin, and I/R + 2 mg/kg Cortexin. On day 8, rats were euthanized, and brain and serum samples were collected. Immunohistochemical staining was used to assess biomarker expression in brain tissue, while serum total oxidant status (TOS) and total antioxidant status (TAS) were measured using ELISA.</p><p><strong>Results: </strong>Oxidative stress analysis showed significantly increased TOS levels (<i>p</i> = 0.012; <i>p</i> = 0.005) and decreased TAS levels (<i>p</i> = 0.000; <i>p</i> = 0.000) in the ischemia and I/R groups compared to control. Cortexin significantly reduced TOS (<i>p</i> < 0.01) and increased TAS, with 2 mg/kg Cortexin producing TAS levels higher than control (<i>p</i> < 0.05). Immunohistochemical analysis revealed significantly elevated OPG, RANK, RANKL, and TRPC1 expression in ischemia and I/R groups (<i>p</i> < 0.001). Cortexin treatment significantly decreased expression of all markers (<i>p</i> < 0.01). No significant difference was found between ischemia and I/R groups (<i>p</i> > 0.05), suggesting a sustained inflammatory response.</p><p><strong>Conclusion: </strong>These findings suggest that Cortexin may exert neuroprotective effects by modulating oxidative stress and biomarker expression involved in inflammation and calcium signaling.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1-12"},"PeriodicalIF":1.5,"publicationDate":"2025-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812140","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}
Chenying Hu, Lin Wang, Qinghong Li, Yangbin Ji, Xuefei Yang, Jian Ding
{"title":"Electroacupuncture activation of the CaMKII/CREB pathway improves dLGN synaptic plasticity in monocular deprivation amblyopic rats.","authors":"Chenying Hu, Lin Wang, Qinghong Li, Yangbin Ji, Xuefei Yang, Jian Ding","doi":"10.1080/01616412.2025.2545542","DOIUrl":"https://doi.org/10.1080/01616412.2025.2545542","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to investigate the therapeutic potential of electroacupuncture(EA) for amblyopia, a common childhood visual disorder caused by early abnormalities such as monocular deprivation(MD). We examined the role of the calcium/calmodulin-dependent protein kinase II/cAMP response element-binding protein(CaMKII/CREB) pathway and enhanced synaptic plasticity in visual function improvement following EA.</p><p><strong>Methods: </strong>An amblyopia model was established using 14-day-old rats by inducing MD during a critical developmental period. MD rats received EA stimulation at the Cuanzhu(BL2) and Fengchi(GB20) acupoints for 14 consecutive days. Visual function was assessed. Structural damage to the retina and dorsal lateral geniculate nucleus(dLGN) was analyzed. CaMKII/CREB pathway and synaptic plasticity proteins(SYN1 and PSD95) activity levels were measured. To confirm CaMKII involvement, the inhibitor KN93 was administered.</p><p><strong>Results: </strong>EA was associated with significant visual function improvement in rats MD with and reduced structural damage to retinal and dLGN cells. EA activated the CaMKII/CREB signaling pathway and upregulated synaptic plasticity protein(SYN1 and PSD95) expression. The therapeutic effects of EA were markedly attenuated when the CaMKII inhibitor KN93 was co-administered, demonstrating that CaMKII signaling is essential for mediating the benefits of EA.</p><p><strong>Conclusion: </strong>EA effectively treated amblyopia in this model by restoring visual function and protecting neural structures by activating the CaMKII/CREB signaling pathway, subsequently enhancing synaptic plasticity. These findings provide a strong theoretical foundation for the clinical application of EA in the treatment of amblyopia.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1-12"},"PeriodicalIF":1.5,"publicationDate":"2025-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812141","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":"<i>FAM111B</i> as a biomarker influences the prognosis and immune microenvironment of low-grade gliomas.","authors":"Shuang Chen, Zhendong Liu, Yanzheng Gao","doi":"10.1080/01616412.2025.2538129","DOIUrl":"https://doi.org/10.1080/01616412.2025.2538129","url":null,"abstract":"<p><strong>Background: </strong>In recent years, FAM111B has been found to be closely related to the occurrence and development of various cancers. However, the role of FAM111B in low-grade glioma (LGG) remains unclear.</p><p><strong>Objective: </strong>This study aims to investigate the regulatory role of FAM111B in the progression of LGG.</p><p><strong>Method: </strong>First, this study explored the expression levels of FAM111B in LGG using various databases. Second, Wilcoxon and Kruskal-Wallis tests were employed to assess the association between FAM111B expression and clinical characteristics. Survival analysis and multivariate Cox regression evaluated the prognostic value of FAM111B expression levels in LGG. Additionally, GSEA was performed to explore pathways associated with FAM111B expression, while Pearson correlation analysis revealed relationships between FAM111B expression and tumor-associated macrophages as well as immune checkpoints.</p><p><strong>Results: </strong>The findings of this study demonstrate that high expression of FAM111B is significantly associated with molecular characteristics of LGG. FAM111B serves as an independent prognostic factor, and the high expression of FAM111B significantly shortens survival of LGG patients. The methylation site cg14859464 was found to negatively regulate FAM111B expression. FAM111B primarily activates pathways related to Cell cycle regulation, DNA replication, and Mismatch repair. Additionally, FAM111B expression showed positive correlations with macrophage marker CD163 and immune checkpoint molecule CD276.</p><p><strong>Conclusion: </strong>This study conducted an in-depth investigation into the biological functions of FAM111B in LGG. We identified FAM111B as an independent prognostic factor associated with unfavorable clinical outcomes in LGG. The findings provide novel insights and actionable targets for the precise diagnosis and effective management of LGG.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1-18"},"PeriodicalIF":1.5,"publicationDate":"2025-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144817208","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}