ArticleMolecular brain2025
Multi-omics integration reveals the role of N6-methyladenosine in epilepsy, ischemic stroke, and vascular dementia.
Article in Molecular brain, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Decoding causal m6A: a bioinformatics roadmap for psychiatric disorders.Briefings in bioinformatics · 2026Review
- Identification of Mitochondrial Dysfunction Genes as Diagnostic Biomarkers for Ischemic Stroke by Integrated Bioinformatics Analysis and Machine Learning.Journal of molecular neuroscience : MN · 2026Article
- The Role and Diagnostic Efficacy of the METTL14/GADD45B mCellular and molecular neurobiology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundN6-methyladenosine (m6A) methylation is an essential epigenetic modification that regulates mRNA stability, splicing, and translation. Its role in neurological diseases, including epilepsy, ischemic stroke, and vascular dementia (VaD), remains poorly understood.
methodsWe integrated multi-omics data, including GWAS, m6A quantitative trait loci (QTL), expression QTL (eQTL), and protein QTL (pQTL), and using FUSION to assess the association of m6A with these diseases. Transcriptome-wide association studies (TWAS) and Mendelian Randomization (MR) were performed to identify causal relationships between m6A sites, gene expression, and disease. Differentially expressed genes (DEGs) were analyzed via RNA sequencing and enriched for biological pathways. Protein-protein interaction (PPI) networks and m6A-related gene-disease associations were constructed to reveal regulatory mechanisms.
resultsWe identified 218 m6A sites significantly associated with the three diseases, highlighting 3,430 associations between m6A sites and gene expression. Functional enrichment analysis revealed key pathways, including base excision repair and chemokine-mediated signaling. MR analysis identified causal relationships, such as NBL1 in epilepsy, TPGS2 in ischemic stroke, and SERINC2 in VaD. PPI analysis revealed interactions involving critical proteins like PARP1, MCL1, and CD40, underscoring their role in neuroinflammation and apoptosis.
conclusionOur findings elucidate the genetic and epigenetic roles of m6A in epilepsy, ischemic stroke, and VaD, uncovering potential mechanisms by which m6A modulates gene and protein expression to influence disease outcomes. These insights highlight m6A as a promising biomarker and therapeutic target for neurological diseases.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.