ArticleNeurosurgical review2025
Causal association between cerebral small vessel disease and epilepsy.
Article in Neurosurgical review, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Article
- Whole-genome resequencing identifies adaptive variation associated with complex terrain in southwestern Chinese ducks.Poultry science · 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
No grant is acknowledged in the PubMed record.
Abstract
Cerebral small vessel disease (SVD) is known to increase the risk of epilepsy, but the causal relationship between the two remains unclear. This study utilizes Mendelian Randomization (MR) to assess the genetic link between SVD and epilepsy, incorporating additional analyses including colocalization, gene-set, and pathway analysis to provide further evidence for shared mechanisms. We performed a two-sample MR study using 13 SNPs strongly associated with SVD as instrumental variables to assess their causal relationship with epilepsy. We also conducted colocalization analysis to identify shared genetic variants between SVD and epilepsy, gene-set enrichment analysis to explore common biological pathways, and protein-protein interaction (PPI) network analysis to investigate the molecular mechanisms. The MR analysis revealed a significant causal effect of SVD on epilepsy, with an odds ratio (OR) of 1.29 (95% CI: 1.09-1.53, P < 0.001). Colocalization analysis identified three genomic regions (chr1:100-600 kb, chr3:200-700 kb, and chr5:50-500 kb) with evidence of shared genetic variants. Pathway analysis highlighted endothelial cell signaling, blood-brain barrier function, and neuroinflammatory responses as enriched pathways, linking vascular health to neuronal excitability. The PPI network revealed key proteins involved in both vascular and neuronal processes, including ZNF646, PLEKHG1, and NOTCH3, further supporting shared mechanisms. This study provides strong genetic evidence for an association between SVD and epilepsy, with new insights from colocalization, gene-set, and pathway analyses while recognizing the limitations of Mendelian Randomization in establishing temporal causality. The findings suggest that genetic variants affecting vascular health, neuroinflammation, and blood-brain barrier integrity may contribute to both SVD and the risk of epilepsy. These results strengthen the understanding of the shared biological mechanisms underlying these two conditions and highlight SVD as an important risk factor for epilepsy.
Indexed as
Identifiers
39954159What Socratic 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 Socratic graph.