Folia neuropathologica最新文献

{"title":"Comparison of the effectiveness of diclofenac sodium and tenoxicam in the prevention of epidural fibrosis by topical application with an absorbable gelatin sponge on the dura in an experimental laminectomy model.","authors":"Sule Gokturk, Yasin Gokturk, Suat Erol Celik","doi":"10.5114/fn.2024.141373","DOIUrl":"10.5114/fn.2024.141373","url":null,"abstract":"<p><strong>Introduction: </strong>There has been an increasing trend in spinal surgery interventions in recent years. Low back pain is a disorder that is seen at least once in the lifetime of approximately 80% of the general population. Today, neurosurgeons perform operations including laminectomy for various reasons. Epidural fibrosis is a scar tissue that develops after posterior spinal surgery. Various synthetic and organic materials have been used in experimental studies to prevent epidural fibrosis in laminectomy defects. In this study we aimed to investigate and observe histopathologically the effectiveness of cyclooxygenase inhibitor drugs; tenoxicam and diclofenac sodium in the experimental rat laminectomy model in preventing the postoperative spinal epidural fibrosis.</p><p><strong>Material and methods: </strong>In this study, 32 Wistar-Albino female rats were used. 8 mg/kg tenoxicam and 1.5 mg/kg diclofenac sodium were applied on the dura with an absorbable gelatin sponge. After decapitation, L1-L4 laminectomy area was totally removed and histopathological examination was performed.</p><p><strong>Results and conclusions: </strong>It has been shown that the topical application of diclofenac sodium and tenoxicam, which are selective Cox inhibitor drugs, prevents fibroblast migration by forming a local barrier and Cox inhibitors are caused by the inhibition of prostanoids, which are inflammatory mediators.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":" ","pages":"426-431"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008574","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":"S1P receptor modulators affect the toxicity of amyloid β oligomers in microglial and neuronal cells.","authors":"Iga Wieczorek, Robert P Strosznajder","doi":"10.5114/fn.2024.145758","DOIUrl":"https://doi.org/10.5114/fn.2024.145758","url":null,"abstract":"<p><p>A large body of evidence has shown that the amyloid b peptide oligomers (Abo) are predominantly responsible for the neurodegeneration/cognitive impairments in Alzheimer's disease (AD). Abo cause mitochondrial dysfunctions leading to an imbalance between pro- and antiapoptotic proteins and finally to neuronal apoptosis. Further, Abo trigger overactivation of microglia followed by enhanced release of proinflammatory cytokines, which exacerbates neurotoxicity of Abo. The above-mentioned alterations are accompanied by disturbed metabolism of prosurvival bioactive sphingolipid, sphingosine-1-phosphate (S1P), and S1P-dependent signalling via specific receptors (S1PR1-5). In the present study, we investigated for the first time the influence of selective - ponesimod (S1PR1), CYM5541 (S1PR3), CYM50308 (S1PR4), A971432 (S1PR4), siponimod (S1PR1,5) - and nonselective - phosphorylated fingolimod/pFTY720 (S1PR1,3-5) - S1P receptor modulators on cell viability, mitochondrial membrane potential (MMP) and expression of genes encoding S1P receptors, pro- and antiapoptotic proteins and proinflammatory cytokines in hippocampal neuronal (HT22) and in microglial (BV2) cell lines treated with 1 µM Abo for 24 hours. A significant reduction in the MMP, cell viability and mRNA levels of Bcl2 and Il18 together with increased Il6 expression was observed in HT22 cells after Abo administration. CYM50308 and A971432 restored the Bcl2 mRNA level to control values (those of Abo-untreated cells) and pFTY720 markedly reduced the Il6 expression. In BV2 cells, Abo induced a significant decrease in the MMP, cell viability and expression of S1pr1, Bad, Bcl2, Tnf and Il18, which was not counteracted by any of the modulators used. In turn, mRNA levels of Il1b, Il6, were markedly increased in microglia after Abo treatment and the administration of studied compounds tended to exacerbate the proinflammatory effect of Abo. In conclusion, the toxic effect of Abo is more pronounced in microglia. S1P receptor modulators may to some extent mitigate proapoptotic and proinflammatory effects of Abo in HT22 cells. In contrast, the same compounds tend to enhance Abo-induced inflammatory changes in BV2 cells.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"62 4","pages":"348-361"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143440132","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 crosstalk effect of cancer stem cells in the progression of pediatric medulloblastoma through signaling expression of CD133, CD44, and OCT4 with and without Wnt-b-catenin activation.","authors":"Maher Kurdi, Alaa Alkhotani, Motaz Fadul, Huda Alghefari, Awab T Tayyib, Thamer Alsharif, Majid Almansouri, Yazid Maghrabi, Shadi Alkhayyat, Taghreed Alsinani, Ahmed Bamaga, Saleh Baeesa","doi":"10.5114/fn.2024.144903","DOIUrl":"https://doi.org/10.5114/fn.2024.144903","url":null,"abstract":"<p><strong>Introduction: </strong>Cancer stem cells (CSCs) are principal drivers in medulloblastoma (MB) initiation, growth, and progression. Our study aimed to explore the expression of CD133, CD44, and OCT4 signaling markers and their effects on the progression of MB.</p><p><strong>Material and methods: </strong>A retrospective cohort analysis was conducted on brain tissue of 24 pediatric cases of MB from 2016-2020. Protein expression levels of CSC markers CD133, CD44, and OCT4 were evaluated immunohistochemically and their correlation with b-catenin activity was statistically analyzed.</p><p><strong>Results: </strong>The mean age of patients was 10.2 years (range 3-17), with 18 (75%) males and 6 (25%) females. b-catenin was expressed in 20 (83.3%) tumors, and 4 (16.7%) tumors showed no expression. CD133 was minimally expressed in 6 (25%) tumors and 18 tumors (75%) showed no expression. CD44 was highly expressed in 6 (25%) tumors and 18 (75%) tumors showed minimal to no expression. OCT4 was expressed in all tumors. Despite MBs with positive b-catenin expression and absent CD133 expression having longer progression-free survival (PFS), this impact on PFS did not reach statistical significance ( p = 0.76). However, statistically significant differences in PFS were observed in MBs with positively expressed b-catenin and minimal or no CD44 expression, which showed prolonged PFS ( p = 0.0064). MB patients who did not express CD133 and received combined radiotherapy (RTx) and chemotherapy (CTx) showed longer PFS compared to MB patients with minimal CD133 expression. However, this association was statistically insignificant ( p = 0.42). The impact of CD44 expression and chemoradiation on PFS was statistically significant ( p = 0.0035). MB patients with absent or minimal CD44 expression who received RTx and CTx showed the longest PFS.</p><p><strong>Conclusions: </strong>Medulloblastomas not expressing CSC markers (CD133, CD44) are associated with prolonged PFS and less resistance to chemoradiation. However, b-catenin is considered the main predictor for prognosis when compared to CSC markers.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"62 4","pages":"376-385"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143440152","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":"Cytidine does not affect acute toxicity of intravenously administered choline.","authors":"Kamil Synoradzki, Maciej Swiatkiewicz, Paweł Grieb","doi":"10.5114/fn.2024.140501","DOIUrl":"https://doi.org/10.5114/fn.2024.140501","url":null,"abstract":"<p><p>Cytidine-5'-diphosphocholine (CDP-choline) is a key precursor for the intracellular synthesis of phosphatidylcholine and other phospholipids. Following either intravenous or oral application citicoline (CDP-choline of exogenous origin) undergoes quick decomposition to cytidine and choline, and for this reason it is frequently considered a prodrug. However, upon acute intravenous application in mice citicoline is, on a molar basis, 20 times less toxic than choline. To find out whether cytidine may attenuate toxicity of choline, in the present experiments we compared maximum tolerated doses of single intravenous injections of choline and equimolar mixture of choline and cytidine. We assumed that, if after oral intake a substantial part of citicoline is catabolised already in the intestine and its catabolites enter blood separately, intravenously applied equimolar mixture of cytidine and choline will be markedly less toxic than an equivalent molar dose of choline. However, the maximum tolerated single doses determined in our experiment for choline and equimolar mixture of choline and cytidine were similar. These data suggest that citicoline taken orally is not significantly decomposed in the intestinal lumen, but absorbed to blood as the intact molecule.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"62 2","pages":"120-126"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008605","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":"Inhibitor of bromodomain and extraterminal domain proteins decreases transcription of Cd33 in the brain of mice subjected to systemic inflammation; a promising strategy for neuroprotection.","authors":"Grzegorz A Czapski, Marta Matuszewska, Magdalena Cieślik, Joanna B Strosznajder","doi":"10.5114/fn.2024.138140","DOIUrl":"10.5114/fn.2024.138140","url":null,"abstract":"<p><p>The neuroinflammation is a crucial component of virtually all neurodegenerative disorders, including Alzheimer's disease (AD). The bacterial lipopolysaccharide (LPS), a potent activator of the innate immune system, was suggested to influence or even trigger the neuropathological alterations in AD. LPS-induced neuroinflammation involves changes in transcription of several genes, thus controlling these molecular processes may be a potentially efficient strategy to attenuate the progression of AD. Since genome-wide association studies showed that the majority of AD-related genetic risk factors (AD-GRF) are connected to the immune system, our aim was to identify AD-GRF affected in the hippocampus by LPS-induced systemic inflammatory response (SIR). Moreover, we analysed the role of bromodomain and extraterminal domain (BET) proteins, the readers of the acetylation code, in controlling the transcription of selected AD-GRF in the brain during neuroinflammation. In our study, we used a mouse model of LPS-induced SIR and mouse microglial BV2 cells. JQ1 was used as an inhibitor of BET proteins. The level of mRNA was analysed using microarrays and qPCR. Our data demonstrated that among the established AD-GRF, only the expression of Cd33 was significantly upregulated in the hippocampus during SIR. In parallel, we observed an increase in the expression of Brd4, a BET family member. JQ1 prevented an LPS-evoked increase in Cd33 expression in the hippocampus of mice. Moreover, JQ1 reduced Cd33 expression in BV2 microglial cells stimulated with blood serum from LPS-treated mice. Our study suggests that LPS-evoked SIR may increase Cd33 gene expression in the brain, and inhibition of BET proteins through suppression of Cd33 expression could be a promising strategy in prevention or in slowing down the progression of neuroinflammation and may potentially affect the pathomechanism of AD.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"62 2","pages":"127-135"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008608","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 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":"The potential contributions of matrix metalloproteinase 8,9 and 13 (MMP-8,9,13) to cerebral vasospasm and the role of doxycycline inhibitors on gene expression after experimental subarachnoid haemorrhage.","authors":"Yasin Göktürk, Sule Gokturk, Suat E Çelik","doi":"10.5114/fn.2024.143698","DOIUrl":"https://doi.org/10.5114/fn.2024.143698","url":null,"abstract":"<p><strong>Introduction: </strong>Vasospasm has been reported as the most important cause of mortality and morbidity in patients with subarachnoid haemorrhage (SAH) who can reach the hospital. Matrix metalloproteinases (MMPs) are a gene family, which are called neutral proteases in the central nervous system (CNS). In this experimental study we studied the upregulation of MMPs (MMP-8, MMP-9, and MMP-13) gene expression and the inhibitor effects of doxycycline after experimental SAH model in rats.</p><p><strong>Material and methods: </strong>After 24 Wistar Albino rats were divided into groups, a SAH model was created by transfusion of autologous blood from the cisterna magna, and then 30 mg/kg doxycycline treatment was applied. In order to observe the efficacy of the treatment, MMP-8, MMP-9 and MMP-13 gene expression levels were examined, and histopathological examinations were made in the sections taken.</p><p><strong>Results: </strong>There was a statistically significant increase ( p < 0.05) in MMP-8, MMP-9 and MMP-13 gene expression within the first 6 hours after SAH. The Ct parameter specifies the number of cycles in which the detected fluorescence radiation threshold value is exceeded. The MMP-13 Ct difference in the SAH group was significantly higher ( p = 0.037) than the control group.</p><p><strong>Conclusions: </strong>The pathophysiology of cerebral vasospasm is complex and multifactorial. Many studies are conducted to solve the complex mechanism of cerebral vasospasm. It has been shown that the use of doxycycline causes a statistically significant ( p < 0.05) inhibition at gene expression levels (MMP-8, MMP-9 and MMP-13), even in a single dose of usage and also these results have been confirmed by histopathology examination.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"62 3","pages":"305-311"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142617488","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":"A case report of glioma with cerebral hemorrhage as the first symptom.","authors":"Tao Xie, Xue-Xin He, Qian Sun, Zhuo-Feng Mao, Xiao-Peng Wang","doi":"10.5114/fn.2024.145177","DOIUrl":"https://doi.org/10.5114/fn.2024.145177","url":null,"abstract":"<p><strong>Introduction: </strong>High-grade gliomas are the most common and most lethal primary cancers of the central nervous system. Glioma patients with initial symptoms of cerebral hemorrhage are prone to clinical misdiagnosis and delayed diagnosis.</p><p><strong>Case summary: </strong>This paper reports the clinical data of a 40-year-old man with glioma who initially presented with cerebral hemorrhage. Cerebral computed tomography (CT) revealed left parietal cerebral hemorrhage, while contrast-enhanced magnetic resonance imaging (MRI) revealed abnormal enhancement of the left frontoparietal junction, indicating internal bleeding of metastatic tumor. Pathological examination confirmed a high-grade glioma, with immunohistochemistry indicating positive glial fibrillary acidic protein (GFAP) and 40% Ki-67 positive labeling. Consequently, the patient received a final diagnosis of glioma (WHO grade IV).</p><p><strong>Conclusions: </strong>We report an interesting case in which glioma initially presented with cerebral hemorrhage. Therefore, gliomas should be considered as a possible cause of cerebral hemorrhage in patients without risk factors for hemorrhage.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"62 4","pages":"456-459"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143440515","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":"ZDHHC16 promoted neurocyte ferroptosis by suppression of CREB in a cerebral apoplexy model.","authors":"Dongmei Xu, Hua Liu, Xiaoyu Deng, Jifan Fu","doi":"10.5114/fn.2024.145878","DOIUrl":"https://doi.org/10.5114/fn.2024.145878","url":null,"abstract":"<p><strong>Introduction: </strong>The present study explored the effects and possible mechanisms of ZDHHC16 in a model of cerebral apoplexy (CA).</p><p><strong>Material and methods: </strong>Patients with CA were collected from our hospital. Mice were used to establish an middle cerebral artery occlusion (MCAO) model.</p><p><strong>Results: </strong>ZDHHC16 levels in patients with CA were up-regulated. ZDHHC16 up-regulation promoted inflammation and accelerated mitochondrial damage in the in vitro model. ZDHHC16 gene up-regulation promoted ferroptosis of neurocytes. The inhibition of ZDHHC16 prevented cerebral apoplexy in the mouse model. ZDHHC16 up-regulation suppressed CREB through interlinkage of CREB by promoting CREB ubiquitination. CREB agonists inhibited the effects of ZDHHC16 up-regulation in the in vitro model. CREB inhibitor inhibited the effects of ZDHHC16 down-regulation in the in vitro model.</p><p><strong>Conclusions: </strong>We conclude that ZDHHC16 promoted ferroptosis and inflammation in a model of CA through the suppression of CREB. The findings might be of benefit in the treatment of CA or other nervous system diseases.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"62 4","pages":"386-395"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143440117","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}