Folia neuropathologica最新文献

Introduction: 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.

Material and methods: 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.

Results: 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.

Conclusions: 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.

Introduction: 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.

Case summary: 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).

Conclusions: 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.

Methylation profiling is one of the diagnostic methods included in the 2021 World Health Organization Classification of Central Nervous System Tumors (WHO CNS5). In the present short study, we performed methylation analysis of 16 archival diffuse gliomas, including seven glioblastomas (GB) with long survival and three GB with early disease presentation. The formalin-fixed paraffin-embedded (FFPE) and freshly frozen (FF) samples were analyzed using Infinium Methylation-EPIC microarrays. The diagnosis was changed in two cases, and two other cases were classified as control tissue due to the low content of neoplastic cells in examined frozen samples. No differences were found between the usefulness of FF and FFPE material for methylation profiling. Copy number variation analysis and comparative immunohistochemical and molecular studies were also performed. The MGMT promoter methylation assessment was consistent between the micro-array and methylation-sensitive high-resolution melting (MS-HRM) testing. The performed analyses did not supply new data according to the unexpected clinical course of the selected cases. Immunohistochemical evaluation with p16 and PTEN antibodies was consistent with the CDKN2A and PTEN status in most cases. In conclusion, the classification of gliomas based on genome-wide methylation profiles increases the precision of histopathological diagnosis but has limitations, and pathological and clinical consistency is always necessary. Furthermore, immunohistochemical surrogates of molecular alterations are suitable and widely available diagnostic tools.

Introduction: The present study explored the effects and possible mechanisms of ZDHHC16 in a model of cerebral apoplexy (CA).

Material and methods: Patients with CA were collected from our hospital. Mice were used to establish an middle cerebral artery occlusion (MCAO) model.

Results: 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.

Conclusions: 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.

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.

Introduction: 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.

Material and methods: 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.

Results: 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.

Conclusions: 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.

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.

Introduction: The incidence of major depressive disorder (MDD) in adults has been associated with dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, leading to elevated secretion of cortisol. However, limited research has been done globally on how the dysregulated HPA axis and changed cortisol levels relate to depression in adolescents and young adults. The objective of this research was to conduct a systematic review and meta-analysis of the association between cortisol level, a marker of HPA axis activity, and depression in adolescents and young adults.

Material and methods: A systematic search was conducted using four electronic databases (PubMed, EMBASE, Scopus, and Cochrane Library) to select publications published in peer-reviewed journals written in English. The odds ratio (OR) and standard mean difference (SMD) were calculated, along with their 95% confidence intervals. We assessed heterogeneity using Cochrane c2 and I2 statistics and the appropriate P-value. The analysis used RevMan 5.3.

Results: The current meta-analysis included 10 cross-sectional studies with a total of 1301 adolescents and young adults across various age cohorts, with 629 depressed and 672 non-depressed individuals. It was found that the likelihood of depression is higher among the included adolescents and young adults, with an OR of 1.62 (95% CI: 0.44-5.92), and depressed individuals have significantly higher cortisol levels (SMD of 0.87 (95% CI 0.43-1.31) and cortisol stress response SMD of 0.68 (95% CI 0.31-1.05)). Furthermore, there was a strong positive linear association ( r = 0.82) between morning and afternoon cortisol levels in adolescents and young adults and depression scores.

Conclusions: The results of our study indicate that an increase in both morning and afternoon cortisol levels is associated with the development of depression in adolescence and young adults. Research has indicated that an increased level of cortisol is considered a risk factor for depression during adolescence and a linear correlation exists between cortisol levels and depression scores.

Activation of the NogoA/NgR/ROCK pathway limits nerve repair after brain ischemia-reperfusion (I/R) injury. Triptolide displays anti-inflammatory, anti-oxidant, and immunosuppressive effects and is derived from the traditional Chinese medicine Tripterygium wilfordii Hook F. This agent can also penetrate the blood-brain barrier, where it has a neuroprotective effect and ameliorates cerebral I/R injury via an as yet unknown mechanism(s). Here, an animal model of middle cerebral artery occlusion and reperfusion (MCAO/R) was employed to assess triptolide's therapeutic impact on brain I/R injury and the possible mechanism of action. The results indicate that triptolide treatment can decrease cerebral infarction and nerve injury after cerebral I/R injury. Importantly, in vivo and in vitro experiments revealed that treatment with triptolide decreased NogoA, NgR, p75NTR and ROCK2 expression, and upregulated the expression of GAP43 and PSD-95, thus suggesting improved synaptic function. These results indicate that triptolide can promote nerve repair following brain I/R injury by inhibiting NogoA/NgR/ROCK signalling.

Introduction: MicroRNA (miR)-485-5p has been linked to regulation of neurological disorders. The current study examined miR-485-5p levels in patients with epilepsy secondary to cerebral infarction and investigated its predictive significance.

Material and methods: The Gene Expression Omnibus (GEO) database was employed to screen differentially expressed miRNAs in cerebral infarction and epilepsy. 168 patients with cerebral infarction were enrolled, including 67 patients with secondary epilepsy and 101 patients without secondary epilepsy. Serum miR-485-5p levels were examined by reverse transcription-quantitative real-time PCR (RT-qPCR). Logistic regression analysis was used to explore risk factors for epilepsy secondary to cerebral infarction. The diagnostic and predictive value of miR-485-5p was evaluated by receiver operating characteristic (ROC) analysis. Bioinformatics predicted miR-485-5p target mRNA and performed Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis.

Results: The GEO database identified differentially expressed miRNAs including miR-485-5p. miR-485-5p levels were poorly expressed in patients with cerebral infarction ( p < 0.05) and negatively correlated with the National Institutes of Health Stroke Scale (NIHSS) score, an indicator of cerebral infarction severity. Additionally, miR-485-5p is a typical indicator for differentiating cerebral infarctions from controls. Serum miR-485-5p was lower in patients with epilepsy secondary to cerebral ischemia compared to non-epilepsy patients and is a potential risk factor for epilepsy secondary to cerebral infarction. The sensitivity and specificity for predicting epilepsy were 74.63% and 80.20%, respectively. KEGG pathway studies revealed miR-485-5p's target mRNA is primarily enriched in the adipocytokine signaling pathway and the AMPK pathway.

Conclusions: miR-485-5p correlates with cerebral infarction severity. Low expression of miR-485-5p is a promising predictive biomarker for epilepsy secondary to cerebral infarction.