ArticleMetabolic brain disease2025
Mitochondria-targeted antioxidant skq1 reverses functional impairment and histopathological insults in a chronic animal model of multiple sclerosis.
Article in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Neoepitopes at the crossroads of immunometabolism: metabolic remodeling of antigen presentation in type 1 diabetes.Frontiers in immunology · 2026Review
- Mitochondrial dynamics in skin health and disease: energy, aging, and therapeutic perspectives.Burns & trauma · 2026Review
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Authors and funding
3 authors.
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Abstract
Multiple sclerosis (MS) is the most prevalent demyelinating disorder of the central nervous system (CNS), manifested by motor impairments. Due to the critical role of mitochondrial dysfunction, this study investigated the effects of the mitochondria-targeted antioxidant SkQ1 on a mouse model of MS. Animals were categorized into the control group (CONT), the cuprizone group (CPZ), and the group receiving mitochondria-targeted antioxidant SkQ1 following cuprizone (CPZ + SkQ1). After behavioral assessment, the corpus callosum underwent histopathological, biochemical, and molecular evaluations. The behavioral assessment showed a considerable motor improvement in the CPZ + SkQ1 mice compared to the CPZ group. Histopathological investigations revealed significantly higher remyelination in the corpus callosum of CPZ + SkQ1 mice than in the CPZ group. Evaluation of oxidative stress levels showed that SkQ1 administration resulted in a statistical increase in the superoxide dismutase, catalase, and total thiols but a decrease in the malondialdehyde concentration compared to the CPZ group. The relative gene expression level for myelin-related genes significantly increased in the CPZ + SkQ1 group compared to the CPZ group. The findings of this study demonstrate that mitochondria-targeted antioxidant SkQ1 may, through targeting oxidative stress in the mitochondria and consequently myelin gene expression, have induced remyelination enhancement and improved functional performance in chronic cuprizone-intoxicant mice.
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