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":"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":"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}

{"title":"Effect of lncRNA SNHG22 targeting miR-27b-3p on regulation of glioma progression and prognosis.","authors":"Jin Feng, Hongzhi Liu","doi":"10.5114/fn.2024.144178","DOIUrl":"https://doi.org/10.5114/fn.2024.144178","url":null,"abstract":"<p><strong>Introduction: </strong>Glioma is a highly aggressive malignant tumor with high mortality, which is prone to metastasis and recurrence. This study investigated the biological function and related mechanism of action of the long non-coding RNA SNHG22 (lncRNA SNHG22; SNHG22) on glioma cells and its prognostic value.</p><p><strong>Material and methods: </strong>The relative expression levels of SNHG22 and miR-27b-3p in the included glioma patients were detected by real-time quantitative PCR (RT-qPCR). The cell counting kit-8 (CCK-8) proliferation assay and Transwell assay confirmed the effect of knockdown of SNHG22 on the biological function of glioma cells. Luciferase activity characterized the mechanism of SNHG22 targeting miR-27b-3p. Additionally, Kaplan-Meier and multivariate Cox analyses were performed to evaluate the effect of SNHG22 on patient survival.</p><p><strong>Results: </strong>In glioma tissues and cells, compared to normal samples as controls, SNHG22 expression was increased and the expression of miR-27b-3p was decreased. Silencing SNHG22 suppressed the proliferation, migration and invasion levels of glioma cells. SNHG22 directly targets miR-27b-3p to regulate tumor progression. Low expression of SNHG22 was more conducive to the survival of patients than high expression of SNHG22.</p><p><strong>Conclusions: </strong>The lncRNA SNHG22 regulated the progression of glioma by targeting miR-27b-3p, which reflected the prognostic potential of SNHG22 and provided a meaningful theoretical reference for the treatment of glioma patients.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"63 1","pages":"79-86"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971010","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":"Correlation of miR-3188 with patient prognosis and mechanistic inhibition of glioma proliferation, invasion, and migration by targeting MAPK1.","authors":"Pengcheng Feng, Cuiming Yan, Yishen Gao, Hao Cui, Tongbo Ning, Liang Chang","doi":"10.5114/fn.2025.149378","DOIUrl":"https://doi.org/10.5114/fn.2025.149378","url":null,"abstract":"<p><strong>Introduction: </strong>Glioma, as the deadliest malignant tumor, is one of the most difficult problems in medicine. This study aims to further elucidate the molecular mechanism of glioma development and explore possible miRNAs as targets for glioma prognosis and molecular therapy.</p><p><strong>Material and methods: </strong>RT-qPCR was used to determine the expression of miR-3188 in glioma tissues and cells. The relationship between miR-3188 and pathological features, as well as its prognostic importance, were examined using the chisquare test and Cox regression analysis. The dual luciferase reporting assay was utilized to confirm the targeting of miR-3188 and MAPK1. Transwell assay and Cell Counting Kit-8 (CCK-8) assays were used to identify the roles that miR-3188 plays in cell metastasis and proliferation, respectively.</p><p><strong>Results: </strong>Research has revealed downregulation of miR-3188 in the tissues and cells of glioma, which is strongly correlated with the tumor size, Karnofsky Performance Status (KPS) score, World Health Organization (WHO) grade, and patients' survival rate in glioma. Four downstream target genes were screened by bioinformatics analysis, among which MAPK1 was abnormally expressed in glioma, and was negatively correlated with miR-3188. When miR-3188 was overexpressed, the malignant behavioral activity of glioma cells was significantly decreased; however, the inhibitory effect was reversed when MAPK1 was overexpressed.</p><p><strong>Conclusions: </strong>miR-3188 is a potential predictor of malignant development and poor prognosis in glioma patients and targets MAPK1 to inhibit the progression of glioma.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"63 1","pages":"39-50"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143989903","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":"Neuropathological findings in essential tremor.","authors":"Ioannis Mavroudis, Foivos Petridis","doi":"10.5114/fn.2024.140569","DOIUrl":"10.5114/fn.2024.140569","url":null,"abstract":"<p><p>Essential tremor (ET) is one of the most common neurological conditions and the most common movement disorder. The pathophysiological mechanisms that underlie this entity have not yet been described. However, recent post-mortem brain studies have provided useful insight into the underlying pathology of ET. Two brain areas have been consistently found to present neuropathological alterations in patients with ET: the brainstem, for presence of Lewy bodies or neuronal depletion, and the cerebellum, regarding Purkinje cells' morphology and density. In the present study we aim to review the literature on the main neuropathological findings in ET brains.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":" ","pages":"11-18"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008506","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":"Retrospective analysis and comparison of immunohistochemical features of surgically treated primary-metastatic brain tumours.","authors":"Sule Gokturk, Yasin Göktürk, Nihal Kaya, Arzu Erdem Taşdemir","doi":"10.5114/fn.2025.149487","DOIUrl":"https://doi.org/10.5114/fn.2025.149487","url":null,"abstract":"<p><strong>Introduction: </strong>Malignant tumours diagnosed in the central nervous system are among the leading causes of death from cancer. Central nervous system tumours are the 10th most frequent cause of mortality due to cancer. Immunohistochemistry has become an important tool in the diagnosis of brain tumours. Brain tissue and meninges tumours comprise a heterogeneous group with diverse biological behaviour, treatment management, and different prognoses. Although conventional haematoxylin-eosin staining is crucial for diagnosis, diagnostic neuropathology has benefited from the inclusion of immunohistochemistry and recent advances in the field over the past 20 years. GFAP, S100, IDH, OLIG 2, EMA, ATRX, P53 and Ki67 are the most frequently used immunohistochemical markers globally, which we also highlighted in our study.</p><p><strong>Material and methods: </strong>Ninety-seven cases including primary-metastatic intracranial tumours, operated on in the Neurosurgery Clinic and diagnosed in the Medical Pathology Laboratory between 2018 and 2023 years, were examined retrospectively from the archive. Haematoxylin-eosin slides were re-evaluated under the light microscope by 2 double-blind pathologists and immunohistochemical features and characteristics of tumours were examined. Data were analysed using the program SPSS 22. Differences were accepted as statistically significant at p < 0.05.</p><p><strong>Results: </strong>According to the analysis of results, 46 (47.4%) of the 97 included patients were female and 51 (52.6%) were male. The most common tumour types were meningioma with 31 (32%) and high-grade neuroglial tumours with 31 (32%). GFAP, OLIG2, ATRX, and P53 values were found to be significantly higher in high-grade neuroglial tumours. While S 100 and EMA values were especially high in meningiomas, a positive correlation was found with IDH value in low-grade neuroglial tumours. The study showed that the median Ki67 value was significantly higher in high-grade neuroglial tumours and metastatic tumours.</p><p><strong>Conclusions: </strong>Intracranial tumours cause significant morbidity and mortality in patients. Diagnostic, prognostic and predictive biomarkers evaluated in patient biopsy specimens and/or body fluids are important in neuropathological oncology. By regularly updating our biomarkers and following new treatment approaches, we can improve survival with rapid diagnosis and appropriate treatment in central nervous system tumours after surgery.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"63 1","pages":"30-38"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143981663","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":"Dihydromyricetin mitigates epilepsy and cognitive impairment via NLRP3 inhibition in rats.","authors":"Qing Li, Zhenzhen Qu, Zhuofeng Mao, Lijing Jia, Qi Qiao, Yange Zhang, Kaiping Zhou, Liqin Che, Weiping Wang","doi":"10.5114/fn.2025.149520","DOIUrl":"https://doi.org/10.5114/fn.2025.149520","url":null,"abstract":"<p><strong>Introduction: </strong>The nucleotide-binding domain leucine-rich repeat-containing family pyrin domain-containing 3 (NLRP3) inflammasome has been implicated in numerous neurological disorders, including epilepsy, through its role in inflammation and pyroptosis. Dihydromyricetin (DHM) has neuroprotective effects in patients with neurological disorders. However, the impact of DHM on the NLRP3 inflammasome pathway in epilepsy and related cognitive impairment is yet to be fully understood. Herein, we evaluated whether DHM can alleviate pilocarpine-induced neuronal injury and learning and memory disorders in the hippocampal body of rats by regulating the NLRP3 inflammasome.</p><p><strong>Material and methods: </strong>An epileptic rat model was established, and spontaneous recurrent seizure (SRS) frequency and duration were recorded. The function of hippocampal pyramidal neurons was evaluated using Nissl staining. Western blotting, real-time reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assays were used to detect changes in NLRP3 inflammatory pathway-related factors in the hippocampus. Cognitive function was verified using the Morris water maze test, hippocampal late-phase long-term potentiation recording and associated synaptic protein expression assessment.</p><p><strong>Results: </strong>Treatment with DHM after status epilepticus (SE) induction decreases the frequency and length of SRS in rats receiving pilocarpine, suggesting that DHM has the potential to improve long-term potentiation and cognitive deficits after SE induction in rats. Additionally, after inducing SE in rats, DHM raises the expression of synaptic proteins. It may prevent harm to hippocampal pyramidal neurons, and DHM-induced neuroprotection may contribute to the pyroptosis associated with NLRP3 in epileptic rats. DHM guards against harm to hippocampus pyramidal neurons.</p><p><strong>Conclusions: </strong>We found that DHM plays a role in treating epilepsy and its comorbid cognitive impairment by inhibiting pyroptosis and inflammation.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"63 1","pages":"51-66"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143993501","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}