Gliomas represent the most predominant primary malignant tumor in central nervous system. Thymine DNA glycosylase (TDG) is a central component in active DNA demethylation. However, the specific mechanisms of TDG-mediated active DNA demethylation in gliomas remain unclear. This research indicates TDG expression is overexpressed in gliomas and correlated with poor prognosis. TDG knockdown suppressed the malignant phenotype of gliomas both in vitro and vivo. Notably, RNA-seq analysis revealed a strong association between TDG and tenascin-C (TNC). ChIP-qPCR and MeDIP-qPCR assays were undertaken to confirm that TDG participates in TNC active DNA demethylation process, revealing decreased DNA methylation levels and elevated TNC expression as a result. Silencing TNC expression also suppressed the tumor malignant phenotype in both in vitro and in vivo experiments. Additionally, simultaneous silencing of TNC reduced or even reversed the glioma promotion caused by TDG overexpression. Based on our findings, we conclude that TDG exerts an indispensable role in TNC active DNA demethylation in gliomas. The DNA demethylation process leads to alternations in TNC methylation levels and promotes its expression, thereby contributing to the development of gliomas. These results suggest a novel epigenetic therapeutic strategy targeting active DNA demethylation in gliomas.

The inhibitor of growth (ING) family of proteins is emerging as a pivotal regulator of epigenetic modifications within the nervous system. These proteins are involved in various cellular processes, including apoptosis, cell cycle control, and DNA repair, through interactions with chromatin-modifying complexes. Recent studies underscore the dual role of ING proteins in both tumor suppression and neuronal differentiation, development, and neuroprotection. This review summarizes the epigenetic functions of ING proteins in neurobiology, with a focus on their involvement in neural development and their relevance to neuro-oncological diseases. We explore the mechanisms by which ING proteins influence chromatin state and gene expression, highlighting their interactions with histone acetyltransferases, deacetylases, histone methyltransferases, DNA modification enzymes, and non-coding RNAs. A deeper understanding of the role of ING proteins in epigenetic regulation in the nervous system may pave the way for novel therapeutic strategies targeting neurological disorders.

Gut-microbiome-combined metabolomics studies in cerebrovascular disease highlight the microbiota-gut-brain axis in neurological disorders. Here, we present a protocol for correlating the gut microbiome and metabolomics in patients with intracranial aneurysms. We describe steps for sample collection, fecal genomic DNA extraction, rRNA PCR amplification, sequencing library construction, and rRNA sequencing. We then detail procedures for metabolite extraction, liquid chromatography-tandem mass spectrometry (LC-MS/MS) non-targeted metabolomics sequencing, and ELISA for cerebrospinal fluid and plasma samples. Finally, we perform combined multi-omics analysis. For complete details on the use and execution of this protocol, please refer to Xu et al.¹.

Background: Ischemic stroke (IS), a major cerebrovascular disease, is associated with high disability and mortality rates. Acute kidney injury (AKI) often complicates IS and increases in-hospital mortality. While antiplatelet agents are commonly used for IS treatment, their effectiveness in IS patients with AKI is unclear. Methods: This study, using data from the MIMIC-IV database, divided patients into non-combination (clopidogrel or ticagrelor alone) and combination (with aspirin) groups. The primary outcome was 28-day mortality, with secondary outcomes including 90-day, 1-year, and in-hospital mortality. Multivariable Cox and logistic regression models were used to analyze the relationship between antiplatelet regimens and mortality. Subgroup analyses and interaction tests were conducted. Results: Results showed the combination group had lower 28-day, 90-day, 1-year, and in-hospital mortality risks than the non-combination group (all p < 0.001). Subgroup analysis revealed an interaction effect by AKI stage, with combination therapy not significantly reducing mortality in severe AKI (stages 2 and 3, p = 0.743, p = 0.244). Conclusions: This study demonstrates that combination antiplatelet therapy significantly reduces 28-day, 90-day, 1-year, and in-hospital mortality risks of IS patients with AKI, suggesting its potential benefits in improving both short- and long-term clinical outcomes. However, this does not apply to patients with severe AKI, indicating heterogeneous survival benefits of combination therapy across AKI severity. Clinical decision-making should incorporate AKI stage stratification to evaluate the applicability of combination antiplatelet therapy. Further research is needed to explore the impact of AKI staging on antiplatelet therapy in IS patients.

Moyamoya disease (MMD) features progressive intracranial artery stenosis and collateralization. Growing evidence implicates a dysregulated gut–brain