Folia neuropathologica最新文献

{"title":"Recovery of nonketotic hyperglycaemic hemichorea -hemiballismus due to acute ischemic stroke in the contralateral supplementary motor area: a case report and literature review.","authors":"Xiuyu Du, Xiaochuan Guo, Xiaobao Zhou","doi":"10.5114/fn.2024.135290","DOIUrl":"10.5114/fn.2024.135290","url":null,"abstract":"<p><strong>Introduction: </strong>There remains uncertainty about the mechanism and specific location of the relative cortex with nonketotic hyperglycaemic hemichorea-hemiballismus (HC-HB). This paper aims to analyse the relationship between the disappearance of HC-HB and the supplementary motor area (SMA) infarction in a patient who recovered following an acute ischemic stroke.</p><p><strong>Case presentation: </strong>An 83-year-old female patient with diabetes mellitus presenting with severe and refractory involuntary movement after hypoglycaemic therapy was referred to an outpatient neurosurgery department for further intervention. Laboratory, magnetic resonance imaging (MRI) and computed tomography (CT) neuroimaging and physical examinations were performed. After a diagnosis of HC-HB was confirmed, the patient received hypoglycaemic therapy and haloperidol; however, there was no significant improvement. Brain MRI T1-weighted images and CT scans showed high signal intensity involving the bilateral putamen nucleus. CT perfusion and CT angiography showed a hypo-perfusion in the SMA of the right hemisphere without significant vascular occlusion. Then, aspirin and clopidogrel were administered, and the patient's left leg presented slight involuntary movement three days later. Interestingly, her involuntary movement disappeared again on the second day after the discontinuation of antiplatelet therapy. She was discharged three days later, and her symptoms did not recur during a follow-up for three months.</p><p><strong>Conclusions: </strong>The SMA dysfunction caused by the acute infarction could terminate or reset the pathological neural path-way of nonketotic hyperglycaemic HC-HB and contribute to the disappearance of the involuntary movement on the contralateral side. The SMA may be a selective intervention target for patients with refractory nonketotic hyperglycaemic HC-HB.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":" ","pages":"100-105"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008507","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":"Suppression of the lncRNA TUG1 alleviates neuropathic pain in rats with chronic contractile injury via the miR-29b-3p/HMGB1 axis.","authors":"Jingjing Dong, Yonghong Ding, Xia Geng, Xiaona Guo, Linkai Jiang, Aiping Ouyang","doi":"10.5114/fn.2024.141512","DOIUrl":"10.5114/fn.2024.141512","url":null,"abstract":"<p><strong>Introduction: </strong>The present research focused on the function of lncRNA taurine upregulated 1 (TUG1) in a rat neuropathic pain (NP) model constructed by chronic contractile injury (CCI).</p><p><strong>Material and methods: </strong>Construction of the NP rat model was performed by CCI surgery. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were applied to examine the NP behavior. RT-qPCR was established to explore the levels of TUG1, microRNA (miR)-29b-3p, and HMGB1. ELISA was carried out to evaluate the concentrations of interleukin (IL)-6, IL-1b, tumor necrosis factor a (TNF-a), IL-4, and IL-6. The underlying mechanisms of TUG1 were explored by RNA-binding protein immunoprecipitation (RIP) and dual-luciferase reporter (DLR) assay.</p><p><strong>Results: </strong>TUG1 and HMGB1 were statistically elevated in the tissue of CCI rats, while miR-29b-3p was reduced. TUG1 competitively binds to miR-29b-3p to upregulate HMGB1 levels. Suppression of TUG1 persistently decreased PWL and PWT along with increased frequency of paw-lifting, whereas this alleviation was typically rescued by the abrogated miR-29b-3p. Analogously, knockdown of TUG1 inhibited CCI-induced overproduction of IL-6, IL-1b, and TNF-a, and reduction of IL-4 and IL-6, but this inhibition was partially abrogated by the reduction of miR-29b-3p.</p><p><strong>Conclusions: </strong>Suppression TUG1 can alleviate NP hypersensitivity and neuroinflammation in CCI rats by competitively binding miR-29b-3p to weaken HMGB1.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":" ","pages":"185-197"},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008508","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":"Expression of components involved in cholesterol homeostasis maintenance during experimental autoimmune encephalomyelitis in rat spinal cord.","authors":"Smilja Todorovic, Katarina Milosevic, Ana Milosevic, Marija M Janjic, Srdjan J Sokanovic, Danijela Savic, Irena Lavrnja","doi":"10.5114/fn.2024.141376","DOIUrl":"10.5114/fn.2024.141376","url":null,"abstract":"<p><p>Dysregulations in cholesterol homeostasis contribute to the pathogenesis of multiple sclerosis (MS) and its best described animal model, experimental autoimmune encephalomyelitis (EAE). Cholesterol is an important component of myelin, which is necessary for signal transmission between neurons. Demyelination leads to the formation of oxysterols, degradation products of cholesterol that are ligands for nuclear liver X receptors (LXRs). Genes regulated by LXRs are involved in cholesterol efflux, absorption, transport, and excretion, which we investigated in this study. In this study, we detected changes in gene expression of Srebf1, Ldlr, Soat1, Abca1, Lrp1, and Npc1, all of which are important in the regulation of cholesterol homeostasis, during the course of EAE in male and female rats. In particular, differential expression of Srebf1, Ldlr, and Soat1 was observed in the spinal cord of male and female rats during EAE. Moreover, these genes are altered during EAE. In contrast, the expression of Abca1 and Lrp1 was significantly affected only by sex. In male animals, the expression of Npc1 is conspicuously reduced in EAE pathology. Thus, our study confirms the involvement of enzymes of cholesterol metabolism in the pathophysiology of EAE, with sex and disease progression affecting the expression of these genes. These findings may improve the understanding of neurodegenerative diseases associated with impaired lipid metabolism in the brain, such as MS/EAE.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":" ","pages":"148-156"},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008577","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":"Neuregulin 2 reversed astrocytosis in the spinal cord in a mouse model of Alzheimer's disease.","authors":"Chong Liu, Qing Xie, Jun-Ping Xu, Kai-Ye Hua, Wei-Jiang Zhao","doi":"10.5114/fn.2025.151824","DOIUrl":"https://doi.org/10.5114/fn.2025.151824","url":null,"abstract":"<p><strong>Introduction: </strong>Alzheimer's disease (AD) is classified as a neurodegenerative disorder without efficacious therapeutic interventions. Accumulating evidence has demonstrated the deposition of b-amyloid peptide (Ab) in the spinal cord in several mouse AD models. Neuregulin 2 (Nrg2), structurally homologous to neuregulin 1 (Nrg1), exerts a regulatory influence over various biological processes within the nervous system. However, the neuroprotective role of Nrg2 in the spinal cord in AD remains unclear.</p><p><strong>Material and methods: </strong>Reverse transcription PCR (RT-PCR) was employed to confirm the expression of mutated amyloid precursor protein (APP) in APPswe mice. Immunohistochemical staining was used to compare the differences between wild-type and APPswe mice in APP and GFAP expression. We applied western blot to test the changes of ErbB4, Akt1, and Erk1/2 activation, as well as that of GFAP in response to recombinant Nrg2 (rNrg2) treatment in the spinal cord in APPswe mice.</p><p><strong>Results: </strong>In the current study, we observed that mutated APP mRNA level was upregulated, and astrocytes were activated in the spinal cord of APPswe transgenic mice. rNrg2 treatment down-regulated astrocyte activation, as indicated by the reduced level of GFAP. Meanwhile, Nrg2 treatment enhanced the phosphorylation-mediated activation of ErbB4, Akt1, and Erk1/2 in most of the spinal cord segments.</p><p><strong>Conclusions: </strong>These combined results suggest the involvement of astrocytosis in the spinal cord of APPswe transgenic mice. Neuregulin 2, when administered exogenously, may represent a potential strategy for preventing and treating AD-induced astrocytosis in the spinal cord.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"63 2","pages":"138-147"},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144775013","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":"STAT3 induces amygdala apoptosis by regulating the expression of stathmin in the rat model of posttraumatic stress disorder.","authors":"Wenqiang Liu, Anqi Liu, Shengxue Yu, Yufei Wang, Wei Shan","doi":"10.5114/fn.2024.140830","DOIUrl":"https://doi.org/10.5114/fn.2024.140830","url":null,"abstract":"<p><strong>Introduction: </strong>Stathmin, recognised as the protein associated with the disassembly of microtubules, plays a vital role in the modulation of human fear as well as anxiety responses. However, it is unclear whether stathmin regulates the specific mechanism of disruption of fear-associated memory resulting from posttraumatic stress disorder (PTSD). This study aims to observe the impact of stathmin on deficit in fear-based memory during PTSD and investigate the underlying mechanisms involved, in order to establish an empirical foundation for elucidating the molecular mechanisms underlying the pathogenesis of PTSD.</p><p><strong>Material and methods: </strong>We used an single prolonged stress (SPS) protocol to induce the PTSD in the rat model. Open field test and forced swimming test were used to examine the anxious and fearful behaviours exhibited by the rats. STAT3/stathmin signalling-related expressions were assessed through immunofluorescence, immunohistochemical, RT-qPCR and Western blotting. Stathmin and STAT3 binding activity was detected by molecular docking. Amygdala apoptosis was detected by TUNEL staining.</p><p><strong>Results: </strong>In this study, while stathmin gene expression in amygdala was significantly downregulated, after 7 days of SPS, activation of STAT3 was observed in the rats' amygdala, accompanied by a notable increase in the apoptosis rate. Consequently, the rats exhibited heightened fear and anxiety responses. However, the above results were reversed after overexpression of the stathmin gene. In addition, following the administration of the STAT3 inhibitor, WP1066, there was a notable reduction in the apoptosis rate, leading to decreased levels of fear and anxiety in rats exposed to SPS. In rats exposed to SPS, administered WP1066, and injected with adenovirus expressing stathmin-targeted siRNA into the amygdala to make the inhibition of stathmin expression partially counteracted the protective effect of WP1066.</p><p><strong>Conclusions: </strong>The findings above suggest that SPS could potentially modulate the stathmin gene's expression by activating the STAT3 pathway, subsequently leading to apoptosis in amygdala cells. This sequence of events ultimately contributes to the PTSD rat model fear memory impairment.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"63 1","pages":"87-99"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143964317","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":"Treatment update for autoimmune/immune-mediated central nervous system diseases.","authors":"Jiayi Wu, Xuewei Li, Jun Peng, Wan Fu, Shuangxi Chen, Heng Wu","doi":"10.5114/fn.2025.149473","DOIUrl":"https://doi.org/10.5114/fn.2025.149473","url":null,"abstract":"<p><p>Autoimmune/immune-mediated central nervous system (CNS) diseases are chronic, inflammatory, autoimmune diseases, such as multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), and autoimmune encephalitis (AE). A common pathological feature of these diseases is the targeting of the host's immune system against autoantigens expressed by the CNS. In recent years, immunomodulatory therapeutic drugs and methods with different targets have emerged. Therefore, obtaining a more comprehensive and in-depth understanding of the characteristics, adverse reactions and indications of existing therapeutic drugs is essential to develop individualized therapies based on each patient's characteristics, delay the progression of disorders and enhance the life quality of these patients. Although MS, NMOSD, and AE are all associated with immune inflammation, there are considerable differences in clinical treatment. Certain drugs may be approved for only one of these diseases, while other drugs may be suitable for all three. This review systematically describes the characteristics and scope of application of various drugs, including potential drugs under development, as well as non-drug therapeutic approaches.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"63 1","pages":"19-29"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143977749","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":"Effect of sequential treatment with butylphthalide on neurological and cognitive functions and collateral circulation in patients with acute cerebral infarction.","authors":"Chao Zhang, Jing Gao, Shuang Tian, Xiao-Feng Li, Xiao-Di Zhang, SuXia Zhao","doi":"10.5114/fn.2025.149381","DOIUrl":"https://doi.org/10.5114/fn.2025.149381","url":null,"abstract":"<p><strong>Introduction: </strong>This study aimed to investigate the effect of sequential treatment with butylphthalide on neurological and cognitive functions and collateral circulation in patients with acute cerebral infarction (ACI).</p><p><strong>Material and methods: </strong>A total of 62 patients with ACI treated in our hospital between March 2021 and May 2021 were selected by convenience sampling and divided into the observation group ( n = 31) and the control group ( n = 31) using a random number table. Patients in the control group received conventional treatment, and those in the observation group received sequential treatment with butylphthalide in addition to conventional treatment. Neurological and cognitive functions and collateral circulation were compared between the two groups.</p><p><strong>Results: </strong>Improvements in the neurological, activities of daily living (ADL) and cognitive functions were better in the sequential treatment group than in the control group, which received conventional treatment. Statistically significant differences in the National Institutes of Health Stroke Scale (NIHSS), Modified Barthel Index (MBI), Lawton Instrumental Activities of Daily Living (Lawton IADL), Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) scores were also noted between the two groups (F NIHSS treatment = 142.414, p < 0.001; F MBI treatment = 143.662; F IADL treatment = 137.624; F MMSE treatment = 87.418, p < 0.001; F MoCA treatment = 122.724, p < 0.001). Collateral circulation assessment showed that the blood flow velocities of the anterior cerebral artery (50.21 ±7.56 vs. 44.96 ±8.33, t = 2.598, p = 0.012), middle cerebral artery (34.52 ±6.29 vs. 21.74 ±4.81, t = 8.986, p < 0.001) and posterior cerebral artery (37.92 ±6.36 vs. 34.44 ±6.74, t = 2.091, p = 0.041) after treatment were statistically significantly higher in the observation group than in the control group.</p><p><strong>Conclusions: </strong>Sequential treatment with butylphthalide improves the neurological and cognitive functions and collateral circulation, as well as the ADL of patients with ACI, with higher efficacy than conventional treatment and without compromising safety.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"63 1","pages":"67-78"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143990871","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":"Effect of the TGF-b signaling pathway on spinal cord ependymoma: A study based on bioinformatics analysis and clinical trials.","authors":"Yan-Dong Fan, Man-Li Zhu, Mamutijiang Muertizha, Jia-Ming Wang, Kun Luo","doi":"10.5114/fn.2025.152514","DOIUrl":"https://doi.org/10.5114/fn.2025.152514","url":null,"abstract":"<p><p>This study aimed to identify potential therapeutic targets for spinal cord ependymoma (SCE) and key signaling pathways associated with the transforming growth factor b (TGF-b) signaling pathway through bioinformatics analysis, molecular biology validation, and clinical characteristics. Differentially expressed genes (DEGs) in SCE were identified using the limma package in R, and a Venn diagram was created to obtain the intersection of TGF-b signaling pathway-related genes and DEGs. Next, the clusterProfiler package was employed for enrichment analysis of Gene Ontology and Kyoto Encyclopedia of Genes and Genomes. Also, a protein-protein interaction network of DEGs was constructed using the Search Tool for the Retrieval of Interacting Genes/Proteins website, and Cytoscape was used to visualize and screen the top 20 key genes. Additionally, quantitative real-time polymerase chain reaction and western blot were used to validate the mRNA and protein expression levels, respectively, of SMAD4, TGFB1, and TGFB receptor 1 (TGFBR1) in clinical samples. A total of 61 differentially expressed TGF-b signaling pathway-related genes were associated with 1) biological processes, such as the transmembrane receptor protein serine/threonine kinase signaling pathway, TGF-b receptor signaling pathway, and pathway-restricted SMAD protein phosphorylation; 2) cell components, such as the plasma membrane signaling receptor complex and collagen-containing extracellular matrix; and 3) molecular function, such as SMAD binding, growth factor binding, and cytokine binding. The protein-protein interaction network consisted of 57 nodes and 339 edges, and three key genes (SMAD4, TGFB1, and TGFBR1) were screened. The TGF-b and Hippo signaling pathways may have potential roles in SCE progression, and SMAD4, TGFB1, and TGFBR1 are potential key genes.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"63 2","pages":"127-137"},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144775003","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 of Buyang Huanwu Decoction in treating acute ischemic stroke based on the neurovascular unit.","authors":"Qingyang Dong","doi":"10.5114/fn.2025.151207","DOIUrl":"https://doi.org/10.5114/fn.2025.151207","url":null,"abstract":"<p><strong>Introduction: </strong>The aim of the study was to investigate the clinical efficacy of Buyang Huanwu Decoction (BHD) in the treatment of patients who had an acute ischemic stroke (AIS).</p><p><strong>Material and methods: </strong>A total of 100 patients who had experienced an AIS were selected as participants and were randomly divided into the control group and the observation group. Patients in the control group received comprehensive treatment using Western medicine, while those in the observation group received BHD internally. Both groups received ongoing treatment for 2 weeks. We examined the effects of BHD on traditional Chinese medicine (TCM) syndrome scores and neurological deficits, as well as on the expression of S100 calcium-binding protein b (S100b), neuron-specific enolase (NSE), matrix metalloproteinase-9 (MMP-9), and vascular endothelial growth factor (VEGF) in brain tissue.</p><p><strong>Results: </strong>By monitoring patients' adverse reactions and laboratory test indicators, it was found that BHD did not significantly increase the safety risk of patients during the treatment process. The TCM evidence score and National Institutes of Health Stroke Scale (NIHSS) score of the observation group were lower compared with the control group after treatment ( p < 0.05). The TCM evidence score and NIHSS reduction of the observation group were decreased compared with those before treatment ( p < 0.05). The serum S100b protein and NSE levels in the observation group were lower than those in the control group before and after treatment ( p < 0.05). The serum MMP-9 level of the observation group was lower compared with the control group, and the serum VEGF level was higher than that of the control group after treatment ( p < 0.05). The serum MMP-9 level in the observation group was decreased and the serum VEGF level was increased compared with those before treatment ( p < 0.05). The overall response rate of the observation group was higher than that of the control group ( p < 0.05). Spearman correlation analysis revealed no correlation between TCM syndrome score and S100 protein, NSE, MMP-9, and VEGF ( p > 0.05). Furthermore, the NIHSS score was negatively correlated with MMP-9 (r s = -0.359, p < 0.05) but not with S100 protein, NSE, and VEGF ( p > 0.05).</p><p><strong>Conclusions: </strong>BHD boasts various benefits in the treatment of AIS patients with Qi deficiency and blood stasis. The mechanism may be associated with the protection of vascular endothelial cell integrity and the promotion of endothelial cell proliferation.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"63 2","pages":"157-165"},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144775004","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 role of TGFb/SMAD signaling in glioblastoma.","authors":"Gulnara Kapanova, Aigul Tulebayeva, Aigul Bazarbayeva, Assiya Turgambayeva, Aida Akhenbekova, Akmaral Abdykulova, Almat Kodasbayev, Aima Adylova","doi":"10.5114/fn.2025.149662","DOIUrl":"https://doi.org/10.5114/fn.2025.149662","url":null,"abstract":"<p><p>Glioblastoma is a multifaceted and therapeutically challenging disease. Despite decades of ground-breaking research work, therapeutic options for the cure of glioblastoma are limited. A substantial amount of knowledge has been added to the complicated web of intertwined protein networks related to glioblastoma. Researchers have dissected a wide variety of signaling cascades, which play fundamental role in disease onset, progression and drug resistance. Recent technological advancements have changed our understanding of the signal specificity and revealed that discrete spatio-temporal activation profiles of the same effectors resulted in diverse physiological responses. Detailed mechanistic insights revealed that deregulated oncogenic pathways played an instrumental role in onset and progression of glioblastoma. Genomic and proteomic studies have unraveled the molecular underpinnings of the TGF/SMAD pathway in glioblastoma. Overall, we hope that this review will enable researchers and clinicians to develop a better understanding of the underlying mechanisms of glioblastoma. Comprehensive interpretation of multi-omics data in glioblastoma will not only enrich our understanding of the heterogeneous nature of glioblastoma but also galvanize the development of personalized clinical approaches.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"63 1","pages":"1-10"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143981977","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}