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Human Study on Oxidative Stress-Related Genes and Multiple Sclerosis Risk
Higher genetically predicted expression of the TSFM gene was associated with an increased risk of multiple sclerosis, as determined through a study analyzing the association of oxidative stress-related genes with neurodegenerative diseases.
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This plain-English summary was written by AI from a published abstract and may contain errors. It is not medical advice. Read the original study and talk to your MS team before making decisions about treatment.
Why it matters
This research provides genetic evidence that suggests a role of oxidative stress-related genes in the development of neurodegenerative diseases, potentially leading to new therapeutic targets.
What this does not prove
The study shows associative findings but does not establish causation or specific mechanisms involved.
Next milestone
No next milestone was established from the available source.
Study facts
- Study design
- Observational
- Participants / samples
- Not reported
- Randomised
- Not reported
- Controlled
- Not reported
- Primary endpoint met
- Yes
- Relevant MS type
- Not reported
- Publication date
- 2026-09-18
- Evidence reviewed
- Abstract only
- Regulatory approval
- Not reported
- Research areas
- Other
Original sources
- Primary evidenceMulti-omics Insights into Oxidative Stress-related Genes and Neurodegenerative Diseases: From Epigenetic Regulation to Pathogenic Pathways. ↗DOI: 10.1007/s12031-026-02601-1
Supporting passages (11)
study phaseThis study aims to delineate the putative causal relationships between OS-related genes (OSRGs) and NDDs, along with the potential regulatory and pathogenic mechanisms.
study designSummary-data-based Mendelian randomization (SMR) was conducted to explore the putative causal associations of 936 OSRGs with NDDs, integrating genome-wide association studies (GWAS) data and expression quantitative trait loci (eQTL) data, using a multi-cohort design with blood eQTLs for discovery and replication, followed by brain eQTL validation.
subjectsSummary-data-based Mendelian randomization (SMR) was conducted to explore the putative causal associations of 936 OSRGs with NDDs, integrating genome-wide association studies (GWAS) data and expression quantitative trait loci (eQTL) data, using a multi-cohort design with blood eQTLs for discovery and replication, followed by brain eQTL validation.
speciesThese findings provide genetic evidence supporting a putative causal role of OSRGs on NDDs, offering mechanistic insights and potential therapeutic targets, and substantially advance the pathobiological understanding of NDDs.
sample size basisSummary-data-based Mendelian randomization (SMR) was conducted to explore the putative causal associations of 936 OSRGs with NDDs, integrating genome-wide association studies (GWAS) data and expression quantitative trait loci (eQTL) data, using a multi-cohort design with blood eQTLs for discovery and replication, followed by brain eQTL validation.
primary endpoint metHigher genetically predicted expression of ACE and TP53INP1 was associated with decreased Alzheimer's disease risk, whereas higher TSFM expression was associated with increased multiple sclerosis risk; these associations were consistently supported by replication cohort and brain eQTL validation for ACE and TSFM, while TP53INP1 showed brain-level consistency without replication.
research categoriesThese findings provide genetic evidence supporting a putative causal role of OSRGs on NDDs, offering mechanistic insights and potential therapeutic targets, and substantially advance the pathobiological understanding of NDDs.
primary endpointSummary-data-based Mendelian randomization (SMR) was conducted to explore the putative causal associations of 936 OSRGs with NDDs, integrating genome-wide association studies (GWAS) data and expression quantitative trait loci (eQTL) data, using a multi-cohort design with blood eQTLs for discovery and replication, followed by brain eQTL validation.
findingsThese findings provide genetic evidence supporting a putative causal role of OSRGs on NDDs, offering mechanistic insights and potential therapeutic targets, and substantially advance the pathobiological understanding of NDDs.
publication datePublication date: 2026-09-18
limitationsTitle: Multi-omics Insights into Oxidative Stress-related Genes and Neurodegenerative Diseases: From Epigenetic Regulation to Pathogenic Pathways.
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