ArticleEpilepsia open2026
A two-sample Mendelian randomization study and mediation analysis exploring the link between cathepsins and epilepsy.
Article in Epilepsia open, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
objectiveThis study aims to investigate the causal relationship between cathepsins and epilepsy, using Mendelian randomization (MR) and mediation analysis.
methodsPublicly accessible summary statistics on epilepsy were obtained from FinnGen and the International League Against Epilepsy Consortium. Cathepsin genome-wide association data were provided by the IEU OpenGWAS. To evaluate the causal relationship between epilepsy and cathepsins, we conducted a bidirectional two-sample Mendelian randomization (MR) and mediation analysis.
resultsThe results of the MR analysis revealed that elevated cathepsin E levels correlated with a higher likelihood of developing generalized epilepsy (odds ratio: 1.304, 95% confidence interval: 1.127-1.508, p: 0.0004, p adjusted for false discovery rate: 0.044). The mediation analysis identified a disintegrin and metalloproteinase with thrombospondin motifs 4 as having a notable impact (mediation effect: 23.5%) in the causal link between cathepsin E and generalized epilepsy. SIGNIFICANCE: This study provides evidence of a causal relationship between cathepsin E and generalized epilepsy, suggesting that elevated cathepsin E levels may increase the risk of developing this condition. The identification of a disintegrin and metalloproteinase with thrombospondin motifs 4 as a mediator offers insight into the molecular mechanisms underlying this association, which could guide future research into potential therapeutic targets for epilepsy. PLAIN LANGUAGE SUMMARY: Epilepsy is a common neurological disorder, but some patients do not respond to standard treatments. This study looks at a protein family called cathepsins and how they might be linked to epilepsy. We found that higher levels of cathepsin E are associated with a higher chance of generalized epilepsy. Our results suggest that cathepsin E could play a key role in causing epilepsy, which could lead to new treatment options for patients who do not respond to current therapies.
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.