Neurological Research最新文献

{"title":"ELK3 expression as a prognostic marker in patients with glioma.","authors":"Shanquan Jing, Li Wang, Wei Liu, Conghui Li","doi":"10.1080/01616412.2025.2490088","DOIUrl":"10.1080/01616412.2025.2490088","url":null,"abstract":"<p><strong>Objective: </strong>This study aims to elucidate the expression and clinical relevance of ELK3 in gliomas and to predict its biological functions using comprehensive database analyses.</p><p><strong>Methods: </strong>We utilized data from glioma patients in the Chinese Glioma Genome Atlas (CGGA) and The Cancer Genome Atlas (TCGA) to investigate ELK3 expression across different tumor grades. The impact of ELK3 expression on patient survival was evaluated using Kaplan-Meier survival analysis, and both univariate and multivariate Cox regression analyses. Additionally, Pearson correlation analysis identified genes associated with ELK3 expression, and these genes underwent functional enrichment analysis via Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG).</p><p><strong>Results: </strong>Our findings demonstrate a positive correlation between ELK3 expression and glioma grade, with significant differences in expression observed across grades II, III, and IV (<i>p</i> < 0.05). Elevated ELK3 expression was associated with poorer patient outcomes (<i>p</i> < 0.05). Analyses from both CGGA and TCGA confirmed ELK3 as an independent prognostic factor for gliomas. Functional enrichment analysis revealed significant associations of ELK3 with critical immune-related pathways, including neutrophil activation, T cell activation, and antigen presentation.</p><p><strong>Conclusion: </strong>ELK3 is established as an independent prognostic marker in gliomas, intimately linked with pivotal immune-related pathways. These insights highlight the potential of ELK3 as both a biomarker and a therapeutic target in the management of glioma, offering avenues for improved prognostic assessments and therapeutic strategies.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"550-556"},"PeriodicalIF":1.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143803902","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 effect of proprioceptive neuromuscular facilitation techniques on pain, motor functions, fatigue and health related quality of life in individuals with multiple sclerosis: a randomized, single-blind study.","authors":"Bircan Yucekaya, Seda Nur Kemer, Elif Asan, Huseyin Gerdan, Nilay Comuk Balci, Deniz Cakır, Mine Pekesen Kurtça, Murat Keskin, Murat Terzi","doi":"10.1080/01616412.2025.2490086","DOIUrl":"10.1080/01616412.2025.2490086","url":null,"abstract":"<p><strong>Purpose: </strong>This study aimed to evaluate the effects of PNF on pain, motor function, fatigue, and quality of life in MS patients.</p><p><strong>Method: </strong>A randomized, controlled, single-blind study was conducted. Forty-four patients were randomly assigned to either the PNF Group (PNFG, <i>n</i> = 22, 16 female) or the Control Group (CG, <i>n</i> = 22, 16 female). PNFG underwent supervised combined aerobic and PNF training thrice weekly for 8 weeks, while CG followed a home exercise regimen. Various measures were employed, including the Visual Analogue Scale (VAS) for pain, Timed Up and Go (TUG) test, Functional Reach Test (FRT), Six-Minute Walk Test (6-MWT), Fatigue Severity Scale (FSS), Fatigue Impact Scale (FIS), Dexterity Questionnaire-24 (DextQ-24) and Multiple Sclerosis Quality of Life-54 (MSQoL-54).</p><p><strong>Results: </strong>PNFG exhibited significant improvements in VAS (<i>p</i> = 0.000), FRT (<i>p</i> = 0.001), TUG (<i>p</i> = 0.000), 6-MWT (<i>p</i> = 0.000), FIS (<i>p</i> = 0.007), DextQ-24 (<i>p</i> = 0.033), MSQoL-54 scores (Physical Health Composite, Mental Health Composite, <i>p</i> = 0.005, <i>p</i> = 0.002, respectively) (<i>p</i> < 0.05). CG also showed improvements in VAS (<i>p</i> = 0.018), TUG (<i>p</i> = 0.000), 6-MWT (<i>p</i> = 0.000), FSS (<i>p</i> = 0.006), psychosocial function (<i>p</i> = 0.007), MSQoL-54 (Physical Health Composite, Mental Health Composite, <i>p</i> = 0.017, <i>p</i> = 0.001, respectively), DextQ-24 ADL scores (<i>p</i> = 0.045) (<i>p</i> < 0.05). PNFG outperformed CG in DextQ-24 (Dressing, <i>p</i> = 0.038) and MSQoL-54 subscales (emotional well-being, energy, health perception, <i>p</i> = 0.007, <i>p</i> = 0.037, <i>p</i> = 0.044, respectively) (<i>p</i> < 0.05).</p><p><strong>Conclusions: </strong>This is the first randomized controlled trial to show that PNF improves upper limb motor function (skill) and quality of life in MS patients. PNF and home physiotherapy effectively improved pain, motor function, fatigue and quality of life, with the PNF group achieving better outcomes. Both modalities offered accessible rehabilitation options.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"537-549"},"PeriodicalIF":1.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143803906","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":"Dexmedetomidine protects against cerebral ischemia-reperfusion injury in mice by interfering with the crosstalk between autophagy and ferroptosis.","authors":"Cong Luo, Yi Ou, Yujie Xu, Fengxian Yu","doi":"10.1080/01616412.2025.2524741","DOIUrl":"https://doi.org/10.1080/01616412.2025.2524741","url":null,"abstract":"<p><strong>Objective: </strong>Previous studies show DEX protects against focal cerebral ischemia by hindering autophagy. However, the exact mechanisms are unclear. This study hypothesizes DEX may protect neurons by regulating the crosstalk between autophagy and ferroptosis.</p><p><strong>Methods: </strong>In this study, male C57/BL6 mice were used in an MCAO model divided into five groups. After MCAO and reperfusion, treatments with DEX, DEX+Erastin, or DEX+rapamycin were administered. Neurological deficits and cerebral infarction volumes were measured 24 hours later. Electron microscopy and molecular techniques were used to analyze autophagy and ferroptosis markers to explore DEX's neuroprotective mechanism.</p><p><strong>Results: </strong>Compared to sham controls, the model group showed significantly increased cerebral infarction volume and neurobehavioral scores (<i>p</i> < 0.05). DEX treatment reversed these effects, demonstrating neuroprotection against ischemic injury. Simultaneously, DEX treatment safeguards mitochondrial integrity by suppressing autophagy lysosomes. It also upregulates the expression of glutathione (GSH) protein, solute carrier family 7 member 11 (SLC7A11) protein, and glutathione peroxidase 4 (GPX4). Moreover, DEX inhibits the levels of malondialdehyde (MDA), ferrous ion (Fe2+), microtubule-associated protein 1A/1B-light chain 3 (LC3), and Beclin1 proteins (all <i>p</i> values < 0.05), thereby intervening in the crosstalk between the autophagy and ferroptosis pathways and ultimately exerting its neuroprotective function. Notably, DEX's effects were negated by ferroptosis inducer Erastin or autophagy inducer RAPA.</p><p><strong>Conclusion: </strong>Dexmedetomidine modulates the crosstalk between autophagy and ferroptosis pathways, thereby protecting the mouse brain against ischemia-reperfusion injury and providing novel insights for the future treatment of ischemic stroke.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1-12"},"PeriodicalIF":1.7,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144507095","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":"Electroacupuncture improved depressive behaviors and synaptic plasticity of post-stroke depressed mice via inhibiting the JNK signaling pathway.","authors":"Chunhua Lai, Weimin He, Hua Yang, Junyu Lai, Siyun Huang","doi":"10.1080/01616412.2025.2520017","DOIUrl":"https://doi.org/10.1080/01616412.2025.2520017","url":null,"abstract":"<p><strong>Objectives: </strong>The safety and effectiveness of electroacupuncture (EA) in treating depression have been scientifically validated. Recent evidence indicates that the c-Jun N-terminal kinase (JNK) pathway is a therapeutic target for anti-depression. This study examines the effects and mechanisms of EA on middle cerebral artery occlusion (MCAO) surgery and chronic-stress-induced post-stroke depression (PSD) mice.</p><p><strong>Methods: </strong>C57BL/6 mice were randomly divided into the sham, MCAO, MCAO+stress, and MCAO+EA+stress groups. After the behavior test, H&E staining was conducted to detect hippocampal changes. TUNEL assay was performed to detect apoptosis. Western blot and RT-PCR were performed to assess the protein levels. Immunohistochemistry was used to detect NF200 and 5-HT expressions.</p><p><strong>Results: </strong>EA treatment was found to ameliorate depressive behavior in mice by inhibiting neuro-apoptosis and microglia-mediated neuroinflammation. Furthermore, EA protected the hippocampal synaptic plasticity through up-regulating the protein expression of 5-hydroxytryptamine (5-HT), neurofilament-200 (NF-200), postsynaptic density protein 95 (PSD95), synaptophysin (Syn), and brain-derived neurotrophic factor (BDNF), along with increasing the counts of hippocampal synapses. The JNK signaling pathway was continuously activated after MCAO and stress treatments, and EA inhibited the JNK signaling pathway by decreasing the JNK and c-Jun phosphorylation levels and the downstream AP-1 expression.</p><p><strong>Conclusion: </strong>To summarize, EA effectively suppresses the activation of the JNK signaling pathway, thereby improving PSD-related depressive behavior by enhancing synaptic plasticity and reducing neuro-apoptosis and neuro-inflammation. This study lays a foundation for the clinical application of EA in alleviating PSD-related depressive behaviors, positioning it as a potential alternative therapy for addressing depressive symptoms in PSD.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1-16"},"PeriodicalIF":1.7,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144497539","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":"Kenpaullone attenuates amyloid-beta deposition and neuroinflammation, improving memory in a 5XFAD mouse model of Alzheimer's disease.","authors":"Shukur Wasman Smail, Azad Hasan Kheder, Hero Khalid Mustafa, Shang Ziyad Abdulqadir, Kovan Faidhalla Jalal, Raya Kh Yashooa, Mohammad B Ghayour, Arash Abdolmaleki, Mudhir Sabir Shekha","doi":"10.1080/01616412.2025.2520983","DOIUrl":"https://doi.org/10.1080/01616412.2025.2520983","url":null,"abstract":"<p><p>Kenpaullone is known for its neuroprotective and anti-inflammatory properties. We explored the potential of a specific intervention to influence cognitive abilities and disease-related brain changes in a mice model replicating key aspects of Alzheimer's disease (AD). We employed 5XFAD transgenic mice, which develop Aβ plaques and cognitive impairments that mirror those observed in individuals with Alzheimer's disease (AD). The animals were treated with Kenpaullone (1 mg/kg, 3 mg/kg, and 5 mg/kg) or a vehicle (DMSO). The study evaluated memory using the Morris water maze (MWM) and the novel object recognition (NOR) task. This study employed immunohistochemistry, ELISA, and Western blot to analyze Aβ plaques and proinflammatory factors, investigating neurodegeneration. In contrast, the expression of genes related to neurodegeneration and apoptosis was evaluated using polymerase chain reaction (PCR). Administration of Kenpaullone yielded significant improvements in cognitive performance in the 5XFAD mice. Mice that received the 5 mg/kg treatment demonstrated the highest improvement in spatial learning and recognition memory. Furthermore, Kenpaullone decreased the burden of amyloid-beta plaques in key brain regions associated with memory (hippocampus and cortex), along with decreased levels of proinflammatory cytokines. Furthermore, Kenpaullone treatment resulted in a downregulation of genes related to neurodegeneration and apoptosis, suggesting a potential therapeutic benefit in mitigating neural apoptosis in AD. Our results suggest that Kenpaullone holds promise for improving cognitive function and mitigating neuropathological changes in AD, warranting further exploration as a potential medicinal substance.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1-14"},"PeriodicalIF":1.7,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144497540","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":"Efficacy and safety of hematopoietic and mesenchymal stem cells in multiple sclerosis: a meta-analysis.","authors":"Shampa Maji, Archana Mishra, Anand Srinivasan, Rituparna Maiti","doi":"10.1080/01616412.2025.2521712","DOIUrl":"https://doi.org/10.1080/01616412.2025.2521712","url":null,"abstract":"<p><strong>Objective: </strong>Currently available treatment options for multiple sclerosis (MS) have limited efficacy and/or safety concerns. Various mesenchymal stem cells and hematopoietic stem cells have been evaluated in recent clinical trials. The present meta-analysis was conducted to assess the safety and efficacy of stem cell therapy in multiple sclerosis.</p><p><strong>Methods: </strong>PubMed/MEDLINE, EMBASE, Cochrane Database, Scopus, and clinical trial registries were searched, and 11 RCTs were included. Quality assessment was performed using the risk-of-bias assessment 2 tool, and the random-effects model was used to estimate the effect size. Subgroup analysis, sensitivity analysis, and meta-regression were performed as applicable. PRISMA reporting guidelines were followed for reporting.</p><p><strong>Results: </strong>A total data of 691 patients from 11 RCTs were included, and it showed that there was a greater change in EDSS score from baseline in the stem cell therapy arm as compared to the control arm (MD:-0.35; 95%CI: -0.79 to 0.08; <i>p</i> = 0.104), but was not significant statistically. The change in number of T2 lesions was also not statistically significant between the groups (MD:-0.75; 95%CI: -4.16 to 2.66; <i>p</i> = 0.619). Number of patients with at least one TEAE were comparable between the groups (OR:0.99; 95%CI: 0.61 to 1.62; <i>p</i> = 0.977).</p><p><strong>Conclusion: </strong>Stem cell therapy is safe; however, it is no better than control (mostly placebo, mitoxantrone and conventional disease-modifying therapy) in the treatment of MS. Well-designed, adequately powered randomized controlled trials focusing on standardized stem cell types, routes, and dosing are essential to clarify their therapeutic role in multiple sclerosis.</p><p><strong>Prospero registration number: </strong>CRD42023457808.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1-11"},"PeriodicalIF":1.7,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144497538","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":"Cognitive impairment and quality of life in patients with carotid artery stenosis pre-revascularization: a scoping review.","authors":"Mohammad Minwer Alnaeem","doi":"10.1080/01616412.2025.2523907","DOIUrl":"10.1080/01616412.2025.2523907","url":null,"abstract":"<p><strong>Background: </strong>Carotid artery stenosis (CAS) reduces cerebral blood flow and is frequently associated with cognitive impairment and reduced quality of life (QoL), particularly in severe CAS. Although carotid revascularization (stenting or endarterectomy) can improve blood flow and potentially enhance cognitive function and QoL, the impact of CAS before revascularization remains unclear.</p><p><strong>Objective: </strong>This review aimed to synthesize the literature exploring the relationship between CAS, cognitive impairment, and QoL, focusing on pre-revascularization outcomes.</p><p><strong>Method: </strong>A comprehensive scoping review was conducted using PubMed, CINAHL, MEDLINE, EMBASE, PsycINFO, EBSCO, and Scopus to identify relevant studies published between 2015 and 2023.</p><p><strong>Results: </strong>This review identified consistent evidence linking severe CAS (≥70%) to significant cognitive decline, particularly in areas such as memory, attention, and executive function. Although carotid revascularization showed promise in improving cognitive performance, the extent of recovery varied. Studies also highlighted the profound impact of CAS on QoL, with patients frequently experiencing anxiety, depression, and physical limitations. While revascularization procedures were associated with improvements in physical functioning and overall well-being, emotional recovery often delayed.</p><p><strong>Conclusion: </strong>CAS substantially affects both cognitive functioning and QoL, even before revascularization. Although some studies suggested that revascularization may lead to improvements in cerebral perfusion and certain domains of cognitive function, the trajectory of psychosocial and emotional recovery; including depressive symptoms, anxiety, and fear of future cerebrovascular events, demonstrates delayed improvement. These emotional outcomes mediate overall QoL and should be a focus of both clinical assessment and future longitudinal studies. Standardization of cognitive and psychosocial outcome measures is essential.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1-12"},"PeriodicalIF":1.7,"publicationDate":"2025-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144369099","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":"Multimerin-1 modulates macrophage M2 polarization and enhances tumor cell stemness in glioblastoma.","authors":"Chao Huang, Xue-Bin Yu, Yong-Zhi Zhou, Xiao-Bing Zhang, Chang-Ming Dong, Wu-Qiao Bao","doi":"10.1080/01616412.2025.2520060","DOIUrl":"https://doi.org/10.1080/01616412.2025.2520060","url":null,"abstract":"<p><strong>Objectives: </strong>Glioblastoma (GBM) is one of the most aggressive brain tumors, with a poor prognosis. Brain tumor stem cells (BTSCs) play a central role in GBM progression and recurrence. This study aimed to identify key BTSC-related genes associated with GBM prognosis and explore their potential biological functions.</p><p><strong>Methods: </strong>BTSC-related differentially expressed genes (DEGs) were identified by integrating gene expression data from public databases. Functional enrichment analyses were conducted to explore their biological relevance in GBM. The key variables associated with GBM risk and prognosis were selected using the machine learning method. Immune cell infiltration in GBM was explored through CIBERSORT. Finally, the effects of MMRN1 on cell stemness and macrophage polarization were investigated using in vitro experiments.</p><p><strong>Results: </strong>A total of 26 upregulated BTSC-related DEGs in GBM were identified, which were enriched in immune response and pathways in cancer. MMRN1 and age were the key variables associated with GBM risk and prognosis. Higher MMRN1 expression and older age indicated a poor prognosis. MMRN1 expression was significantly elevated in GBM tissues, especially in BTSCs. Mechanistically, MMRN1 activated the TLR7/8/9-IRF5 signaling pathway and promoted M2 macrophage polarization. In vitro validation confirmed that MMRN1 overexpression enhanced GBM cell stemness and induced macrophage M2 polarization.</p><p><strong>Discussion: </strong>MMRN1 is a critical BTSC-related biomarker that contributes to GBM progression by enhancing tumor stemness and modulating the immune microenvironment. Targeting MMRN1 May represent a promising therapeutic approach for GBM treatment.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1-16"},"PeriodicalIF":1.7,"publicationDate":"2025-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144476122","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":"ITGA5 drives glioblastoma progression through SLK-mediated activation of the PI3K-Akt pathway.","authors":"Hongkang Hu, Xingfei Fan, Jialiang Wei, Guangming Wang, Ying Li, Chengyin Lu, Ying Lin, Yi Bao, Lei Jiang, Lijun Hou","doi":"10.1080/01616412.2025.2512437","DOIUrl":"https://doi.org/10.1080/01616412.2025.2512437","url":null,"abstract":"<p><p>Glioblastoma (GBM) is the most common type of malignant primary brain tumor and exhibits a rising trend in both incidence and mortality rates. Several studies have shown Integrin Subunit Alpha 5 (ITGA5) has oncogene-promoting functions in GBM, but its underlying mechanisms remain unclear. Based on public high-throughput RNA sequencing data, we found ITGA5 expression is upregulated in GBM tissues and cells, which was correlated with poor prognosis and pathological parameters. Next, the experiments further demonstrated that ITGA5 promotes GBM in vitro and in vivo. The potential mechanism of ITGA5 in GBM was investigated by proteomics and phosphoproteomics sequencing, and the PI3K-Akt signaling pathway were mainly enriched after knockdown of ITGA5. As a downstream gene of the PI3K-Akt pathway, we proved elevated ITGA5promote GBM cell invasion and migration through SLK. Finally, the expression of ITGA5 and SLK in malignant astrocytes of different states in GBM patients showed heterogeneity using single-cell sequencing. Overall, our findings highlight a novel molecular mechanism for the tumorigenesis driven by upregulated ITGA5 in GBM, suggesting that the ITGA5-SLK axis may be a new therapeutic target for the treatment of GBM.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1-11"},"PeriodicalIF":1.7,"publicationDate":"2025-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144476121","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":"Evaluating the therapeutic efficacy of a Benzofuran-Enaminone derivative for the management of Alzheimer's disease (AD)-like pathology in rats through regulating the expression of apoptosis and AD-related genes.","authors":"Hanan F Aly, Ghadha Ibrahim Fouad, Wagdy K B Khalil, Nahla N Kamel, Nagy S El-Rigal, Kawkab A Ahmed, Dalia A Taha, Mohamed B Shalaby, Somaia S Abd El-Karim, Doha H Abou Baker, Maha Z Rizk","doi":"10.1080/01616412.2025.2520021","DOIUrl":"10.1080/01616412.2025.2520021","url":null,"abstract":"<p><strong>Background: </strong>Alzheimer's disease (AD) is a progressive age-related neurodegenerative disorder. There is currently no promising cure for AD; the available treatments can only alleviate the symptoms.</p><p><strong>Objectives: </strong>The Benzofuran-Enaminone derivative '(E)-1-(benzofuran-2-yl)-3-((2-hydroxyphenyl)amino)prop-2-en-1-one (5)' was synthesized as a potential anti-AD candidate in Aluminum chloride (AlCl₃)-induced AD in rats.</p><p><strong>Methods: </strong>In vivo and in vitro acute and chronic studies were conducted to examine the potential toxicity, as well as the antioxidant and anti-acetylcholinesterase (AChE) activities of compound 5. Then, rats were divided into four groups: (1) negative control; (2) AD-induced rats; (3) AD-induced rats treated with compound 5; and (4) AD-induced rats treated with Donepezil. Behavioral, biochemical, and molecular investigations were conducted. The expression of insulin 1 gene, apoptotic genes, and the AD-related genes were estimated.</p><p><strong>Results: </strong>The selected dose of compound 5 (10 mg/kg) was based on an acute toxicity test, then it was applied for a chronic study for 1 month; no toxicological features were stimulated. In vitro, compound 5 demonstrated antioxidant and anti-AChE activities. The expression of apoptotic genes (Bcl-2, Bax, and Caspase-3), AD-related genes (Amyloid precursor protein (APP) and Tau), and the insulin 1 gene were altered in AD-induced rats versus control rats. Treatment of AD rats with compound 5 counteracted the AlCl₃-induced neurotoxicity.</p><p><strong>Conclusion: </strong>This study could be regarded as an initial step in drug discovery for testing this new chemical entity as a potent anti-AD therapeutic agent.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1-15"},"PeriodicalIF":1.7,"publicationDate":"2025-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144340277","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}