Folia neuropathologica最新文献

{"title":"The diagnostic value of serum miR-17-92 cluster in ischemic stroke.","authors":"Lihua Dong, Yuanshen Ye, Guiyuan Huang, Hongmiao Tao","doi":"10.5114/fn.2024.138680","DOIUrl":"10.5114/fn.2024.138680","url":null,"abstract":"<p><strong>Introduction: </strong>Ischemic stroke (IS) is a prevalent disease that poses a significant threat to human life and is responsible for a substantial financial burden. Research has established the crucial role of the miR-17-92 cluster in lung cancer, cardiovascular diseases, and traumatic brain injury. Despite this, few research studies had fully detected the potential of the miR-17-92 cluster as a novel circulating marker for diagnosing IS.</p><p><strong>Material and methods: </strong>miR-17-92 cluster expression in IS was investigated using GSE117064 dataset via bioinformatics analysis. Moreover, qRT-PCR was conducted to further verify miR-17-92 cluster expression in 58 IS individuals and 50 healthy controls (HCs). These cluster members were examined regarding their potential for detecting and diagnosing IS using the ROC method.</p><p><strong>Results: </strong>The expression level of serum miR-20a-5p, miR-19a-3p, miR-18a-5p, and miR-19b-3p was considerably lowered in IS in contrast with HC in both the GSE117064 cohort and clinical cohort. Moreover, these four miRNAs had a fair performance in IS detection. Thereafter, a diagnostic model based on these aforementioned four miRNAs was developed by logistic regression, which had an AUC of 0.974 in the ROC curve. This diagnostic module was verified using the GSE117064 dataset. Further analysis demonstrated an increasing level of the aforementioned miRNAs in day-7 IS patients compared with day-1 IS patients.</p><p><strong>Conclusions: </strong>This research verified the downregulation of the miR-17-92 cluster in IS. This diagnostic model enrolling four cluster members may be a promising biomarker for IS detection.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"62 2","pages":"206-214"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008609","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":"An enriched environment promotes cognitive recovery and cerebral blood flow in aged mice under sevoflurane anaesthesia.","authors":"Wenfeng Gao, Wenji Xie, Wenqin Xie, Changcheng Jiang, Zhenming Kang, Naizhen Liu","doi":"10.5114/fn.2024.136017","DOIUrl":"10.5114/fn.2024.136017","url":null,"abstract":"<p><p>Sevoflurane is an inhalation anaesthetic agent widely used in clinical settings. Despite good surgical outcomes using sevoflurane, patients frequently develop postoperative cognitive dysfunction (POCD). An enriched environment (EE), as a rehabilitation technique, could provide objects and tools to facilitate neuromotor and visual stimuli and brain activity, and is reported to improve cognitive functions. We aim to investigate the impairments of sevoflurane inhalation on cognitive function in mice and determine the benefits of EE in ameliorating POCD. Eighteen-month-old mice were exposed to sevoflurane inhalation for 2 h and then placed in standard environment (SE) or EE cages. The mice without sevoflurane exposure in standard or EE cages were used as controls. The behavioural tests include Morris water maze, Y maze and novel object recognition. Magnetic resonance imaging (MRI) was used to determine the blood circulation in the brains. The proangiogenic factors (CD31, angiopoietin-1, vascular endothelial growth factor, and N-cadherin) and neurotrophic (brain-derived neurotrophic factor, post-synaptic density protein 95) expression in hippocampus of aged mice were evaluated by Western blotting and RT-PCR analysis. Sevoflurane-exposed mice demonstrated reduced performance in learning, memory and spatial memory tests. Enriched environment improved the behavioural performance of sevoflurane-exposed animals. Sevoflurane exposure reduced the blood flow in the brains, and these effects were ameliorated by EE habitation. The EE also promoted the expression of angiogenic and neurotropic factors in sevoflurane-exposed animals. In summary, EE is effective in ameliorating the side-effects of sevoflurane exposure in aged mice.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":" ","pages":"312-320"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008572","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":"Minimizing hemorrhagic and perioperative complications in deep brain stimulation surgery in a series of 191 patients operated on over 4 years.","authors":"Michał Sobstyl, Angelika Stapińska-Syniec, Wiktor Paskal","doi":"10.5114/fn.2024.143649","DOIUrl":"https://doi.org/10.5114/fn.2024.143649","url":null,"abstract":"<p><strong>Introduction: </strong>Intracranial hemorrhage (ICH) in functional neurosurgery is a relatively rare but serious complication. One of the possible risk factors related to ICH is the number of trajectories made for microelectrode recording (MER). Authors who solely rely on macrostimulation using macroelectrodes argue that the incidence of ICH is much lower while maintaining good clinical efficacy of deep brain stimulation (DBS). The present study aimed to assess the incidence of ICH in DBS procedures by reducing to the minimum the number of brain passes and the diameter of guiding cannulas. For this reason, we used one MER guiding cannula exclusively for track making with subsequent macrostimulation done through the implanted DBS electrode.</p><p><strong>Material and methods: </strong>All DBS procedures performed between January 2018 and January 2022 in the Department of Neurosurgery of the Institute of Psychiatry and Neurology in Warsaw were analyzed for possible ICH and other perioperative complications. The DBS lead was implanted by an MR image-guided and intraprocedural CT-verified approach. No MER was done.</p><p><strong>Results: </strong>During four years 191 patients underwent 267 DBS lead implantations in 252 stereotactic procedures. ICH occurred in 2 patients. Both were symptomatic. Adverse symptoms resolved within a week. Two DBS leads required replacement. There was 1 case of hematoma at the implantable pulse generator (IPG) site and 1 case of pneumothorax due to tunneling of the extension.</p><p><strong>Conclusions: </strong>Our surgical technique has a low incidence of ICH. Symptomatic ICH affected 2 patients. The other perioperative complications mentioned above required repeated surgery or conservative treatment. No patient suffered from permanent deficits.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"62 3","pages":"249-258"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142617403","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":"Ginsenoside Rb1 attenuates mouse cerebral ischemia/reperfusion induced neurological impairments through modulation of microglial polarization.","authors":"Cong Yu, Yisong Zhang, Yijun Guo, Zhiyang Shen, Keqin Li, Wei Chen, Dabin Ren","doi":"10.5114/fn.2024.134300","DOIUrl":"https://doi.org/10.5114/fn.2024.134300","url":null,"abstract":"<p><p>Cerebral ischemia/reperfusion causes high disability, recurrence, and mortality. Ischemic stroke is a powerful stimulus that triggers significant microglia activation. Ginsenoside Rb1 (GS-Rb1) has been demonstrated to have neuroprotective effects in the central nervous system. In this study, the effects of GS-Rb1 against cerebral ischemia/reperfusion were explored. A mouse model of middle cerebral artery occlusion (MCAO) was used to mimic the cerebral ischemia/reperfusion. Mice in MCAO + GS-Rb1 groups received 5, 10, or 20 mg/kg GS-Rb1 through intraperitoneal injection. Modified neurological severity scoring (mNSS) showed neurological function, while the open field test tested the anxiety-like behaviors. Cognitive impairment was evaluated by Morris water maze. Protein levels were evaluated by ELISA and Western blot and mRNA levels were analyzed by qRT-PCR. When compared to the MCAO mice, mice in the MCAO + GS-Rb1 group had significantly lower mNSS scores and less brain water content. GS-Rb1 alleviated both cognitive impairment and anxiety and inhibited microglial activation in the cerebral ischemia/reperfusion model. GS-Rb1 enhanced M2-type microglia polarization while inhibiting M1-type microglia polarization. In summary, we observed that GS-Rb1 had neuro-protective effects in a cerebral ischemia/reperfusion mouse model through regulating the microglia polarization.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"62 2","pages":"215-222"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008606","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":"Clear cell meningioma of the filum terminale in a 44-year-old woman: case report.","authors":"Piotr Glinka, Michał Sobstyl, Albert Acewicz, Piotr Bojarski","doi":"10.5114/fn.2024.136476","DOIUrl":"10.5114/fn.2024.136476","url":null,"abstract":"<p><p>Clear cell meningioma (CCM) is a rare subtype of meningioma, especially unusual as a neoplasm of the filum terminale. Clear cell meningioma seems to have a more aggressive nature and a higher risk of recurrence than WHO grade I meningiomas. A 44-year-old woman presented with lower back pain radiating to the left leg and mild weakness in the left leg. Magnetic resonance imaging (MRI) showed a well-demarcated, intradural lesion filling the spinal canal at the L3-S1 levels and compressing the cauda equina. The patient underwent laminectomy from L3 to S1. During the operation, the filum terminale was identified as a structure that was disappearing into the tumor. The filum terminale was cut and the tumor was totally removed in one piece. Pathological findings were indicative of the diagnosis of clear cell meningioma, CNS WHO G2. Postoperative magnetic resonance imaging at 6 months showed no residual mass. Total surgical excision of the CCM of the spinal cord should be chosen as the optimal treatment. In addition, radiological follow-up is equally important due to the high risk of recurrence. Our case is unusual in that the tumor's location was the filum terminale.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":" ","pages":"321-328"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008573","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":"Inhibition of AIM2 expression enhance treatment effect of osimertinib in treatment of glioma.","authors":"Hang Wang, Hongzhuang Zhang, Qianqian Wei","doi":"10.5114/fn.2024.140806","DOIUrl":"10.5114/fn.2024.140806","url":null,"abstract":"<p><strong>Introduction: </strong>Glioma is one of the most commonly tumours which occurs in the central nervous system and accounts for nearly 80% of brain tumours, with a significantly high mortality and morbidity. Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are used as EGFR targeted therapy in various types of solid tumours; however, effective treatment for glioma is still limited. Osimertinib is an irreversible, oral third-generation TKI that targets the mutation at T790M, which causes cancer cells to acquire resistance to drugs. Osimertinib could be effective in the treatment of EGFR mutations with minimal effects on the activity of wild-type EGFR. Absent in melanoma 2 (AIM2) is highly expressed in glioma cells, promoting the maturation of pro-cancer cytokines and contributing to progression of glioma. However, the secretion of pro-cancer cytokines of tumour cells has been regarded as the resistance mechanism to EGFR-TKIs, including osimertinib. A high level of these cytokines also indicates a shorter progression-free survival (PFS). As AIM2 regulates the secretion of pro-cancer cytokines, we thought inhibition of AIM2 may contribute to the therapeutic effect of EGFR-TKIs.</p><p><strong>Material and methods: </strong>We first established AIM2 inhibition and overexpression in cells. Then, the viability rate of cells was calculated by cell counting kit-8 (CCK-8) method, and apoptotic ratio of cells were measured by flow cytometry. The expression of inflammatory-related genes was detected using quantitative polymerase chain reaction (qPCR), concentrations of inflammatory-related factors were measured using enzyme-linked immunosorbent assay (ELISA). The expression of Wnt/b-catenin and EGFR/Ras/Mitogen-activated protein kinase kinase 1 (MEK) signalling pathway components was detected using western blotting.</p><p><strong>Results: </strong>We found that inhibition of AIM2 enlarged the effect of osimertinib on the upregulation of inflammatory gene expression and secretion of these genes, increasing apoptosis. In addition, we also found that AIM2 could enhance the effect of osimertinib on reducing the expression of the Wnt/b-catenin and EGFR/Ras/MEK signalling pathways, resulting in the inhibition of cellular proliferation, and exerting an anti-tumour effect. These effects were also observed using in vivo experiments.</p><p><strong>Conclusions: </strong>AIM2 presents a potential therapeutic target in treatment of glioma.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"62 2","pages":"156-170"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008607","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":"Alterations in mRNA level of proteins related to redox state and mitochondria in an Alzheimer's disease animal model: Promising targets in neuroprotection.","authors":"Sylwia Żulińska, Przemysław L Wencel, Kinga Czubowicz, Joanna B Strosznajder","doi":"10.5114/fn.2024.143039","DOIUrl":"https://doi.org/10.5114/fn.2024.143039","url":null,"abstract":"<p><p>Oxidative stress and disturbances of mitochondrial function in the brain play a crucial role in Alzheimer's disease (AD). However, little is known about the dynamics of these changes in different parts of the brain at the early stage of AD. This study aimed to determine the expression of genes encoding superoxide dismutases (SOD1, SOD2), poly(ADP-ribose) polymerases (PARPs) and sirtuins (SIRTs). Moreover, transcription of genes related to mitochondrial electron transport complexes (ETC) and biogenesis in the brain cortex of 4-, 6- and 12-month-old transgenic AD Tg mice was analyzed. We observed significant decreases in mRNA of Sod2, Parp1 and Sirt1 in the 3-month-old AD Tg mice and upregulation of Parp1 in the 6-month-old AD Tg mice by qPCR analysis. Then, mt-CytB and mt-Co1 (complex III and IV) mRNA levels were increased in 12- and 6-month-old AD brains, respectively. These changes were linked to lower cytochrome c oxidase activity in 3- and significantly in 6-month-old AD Tg mice. Moreover, transcription of several genes involved in mitochondria biogenesis, such as Nfe2L2 and Tfam, was upregulated respectively in the 3- and 6-month-old AD Tg mice. Expression of genes encoding PGC1 and NRF2 was significantly downregulated in 12-month-old AD Tg mice. In summary, our data identified significant changes in gene expression of Sod2, Parp1 and Sirt1 at an early age (3-6-month-old AD mice) then Ppargc1, Nfe2L2 and Sirt1 at a later age. Recognizing these alterations may be important in better understanding the complexity of pathology in AD. Moreover, our results could be helpful in consideration of appropriate target(s) in neuroprotection.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"62 3","pages":"237-248"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142617303","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":"LMTK2 inhibits Ab25-35-elicited ferroptosis, oxidative stress and apoptotic damage in PC12 cells through activating Nrf2/ARE signalling pathway.","authors":"Lili Zhang, Fei Shu","doi":"10.5114/fn.2023.133472","DOIUrl":"10.5114/fn.2023.133472","url":null,"abstract":"<p><p>Alzheimer's disease (AD), the most common contributor to dementia, is a growing global health problem. This study aimed to investigate the role of lemur tyrosine kinase 2 (LMTK2) in AD as well as its relevant mechanism. To establish an in vitro cell model, PC12 cells were challenged with 20 µmol/l Ab 25-35 for 24 h. RT-qPCR and western blot examined LMTK2 mRNA and protein expressions. With the application of CCK-8, TUNEL, iron colorimetric assay kit and DCFH-DA, the viability, apoptosis, Fe 2+ and ROS content in PC12 cells were assessed. Besides, the expressions of oxidative stress-, apoptosis-, ferroptosis- and Nrf2/ARE signalling-related proteins were evaluated with western blot. Moreover, commercial kits examined SOD, MDA and CAT contents. The results manifested that LMTK2 expression was noticeably downregulated in Ab 25-35 -treated PC12 cells. Notably, LMTK2 overexpression exhibited inhibitory effects on oxidative stress, apoptosis and ferroptosis in PC12 cells exposed to Ab 25-35 . The upregulated Nrf2, NQO1 and HO-1 expressions in LMTK2 overexpressed-PC12 cells with Ab 25-35 induction revealed that LMTK2 overexpression could activate the Nrf2/ARE signalling pathway. What is more, a series of cellular experiments further testified that ML385, a specific Nrf2 inhibitor, partly hindered the protective role of LMTK2 overexpression against Ab 25-35 -triggered oxidative stress, apoptosis and ferroptosis in PC12 cells. In conclusion, LMTK2 overexpression alleviated the ferroptosis, oxidant damage and apoptosis in PC12 cells exposed to Ab 25-35 through the activation of the Nrf2/ARE signalling pathway, indicating the potential target of LMTK2 in the treatment of AD.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":" ","pages":"47-58"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139086557","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":"Long non-coding RNA LBX2-AS1 activates IL4R to promote glioblastoma metastasis and angiogenesis by binding to the transcription factor NFKB1.","authors":"Qiang Li, Yong Cheng","doi":"10.5114/fn.2024.135983","DOIUrl":"10.5114/fn.2024.135983","url":null,"abstract":"<p><strong>Introduction: </strong>LncRNA LBX2-AS1 drives the development of various cancers, but the exact mechanism whereby LBX2-AS1 affects glioblastoma (GBM) progression is unaddressed. This study intended to delineate the regulatory mechanism of LBX2-AS1 in GBM metastasis and angiogenesis.</p><p><strong>Material and methods: </strong>LBX2-AS1 level in GBM was assessed by bioinformatics methods. The lncRNA-transcription factor (TF)-mRNA trios were predicted using the lncMAP database. Correlation between genes was predicted by Pearson analysis. The binding relationship was predicted by JASPAR. Levels of LBX2-AS1 and its downstream genes were assayed via qRT-PCR. Changes in expressions of VEGF-A, IL4R, and epithelial-mesenchymal transition (EMT)-associated proteins were assessed through western blot. GBM cell proliferation, migration, and invasion were assayed through CCK8, colony formation, and Transwell experiments. In vitro angiogenesis capacity was evaluated via a HUVEC tube formation experiment. The regulatory relationship between various genes was verified through radioimmunoprecipitation (RIP), chromatin immunoprecipitation (ChIP), and dual-luciferase assays.</p><p><strong>Results: </strong>LBX2-AS1 was elevated in GBM, and in vitro experiments demonstrated the stimulatory effect of LBX2-AS1 on GBM cell proliferation, invasion, migration, and angiogenesis. We observed that LBX2-AS1 activated IL4R expression by binding the transcription factor NFKB1, thus promoting the progression of GBM. Rescue experiments illustrated that silencing IL4R or NFKB1 reversed the impact of forced LBX2-AS1 expression on GBM cells.</p><p><strong>Conclusions: </strong>This study revealed the mechanism of the LBX2-AS1/NFKB1/IL4R axis in driving GBM metastasis and angiogenesis, which may help to improve the regulatory network of GBM malignant progression and provide potential targets for GBM treatment.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":" ","pages":"293-304"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141751449","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 neutrophil extracellular traps-related gene signature predicts the prognosis of glioblastoma multiforme.","authors":"Guanghui Sun, Wei Liu","doi":"10.5114/fn.2023.132980","DOIUrl":"10.5114/fn.2023.132980","url":null,"abstract":"<p><strong>Introduction: </strong>This research hoped to explore the molecular mechanism of neutrophil extracellular traps (NETs) on glioblastoma multiforme (GBM) progression, and develop a promising prognostic signature for GBM based on NETs-related genes (NETGs).</p><p><strong>Material and methods: </strong>Gene expression data and clinical data of GBM tumour samples were downloaded from TCGA and CGGA databases. NETs-related molecular subtypes were explored by using ConsensusClusterPlus. The NETGs with a prognostic value were identified, and then a prognostic model was constructed using LASSO Cox regression. The predicted performance of the prognostic model was evaluated using TCGA training and CGGA validation cohorts. Moreover, independent prognostic indicators were identified by univariate and multivariate analysis to generate the nomogram model. The sensitivities for antitumor drugs and immunotherapy were predicted. Finally, hub genes in the prognostic model were validated using qPCR analysis.</p><p><strong>Results: </strong>GBM patients were divided into two molecular subtypes with significant differences in tumour microenvironment (TME) score, survival, and immune infiltration. A NETGs signature was constructed based on seven genes (CPPED1, F3, G0S2, MME, MMP9, MAPK1, and MPO), which had a high value for predicting prognosis. A nomogram was constructed by two independent prognostic factors (age and risk score), which could be used to predict 1-, 2-, and 3-year survival probability of GBM. Patients in the high-risk group were more sensitive to bicalutamide, gefitinib, and dasatinib; patients in the low-risk group were associated with poor response to immunotherapy. The validation of the six genes in the prognostic model was consistent with the results of bioinformatics analysis.</p><p><strong>Conclusions: </strong>The NETs-based prognostic model and nomogram proposed in this study are promising prognostic prediction tools for GBM, which may provide new ideas for the development of precise tumour targeted therapy.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":" ","pages":"59-75"},"PeriodicalIF":2.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139086559","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}