ArticleNeurotrauma reports2025
Exploring the Impact of Mitoquinone Supplementation on Glycan Profiles in a Repeated Mild Traumatic Brain Injury Mouse Model.
Article in Neurotrauma reports, 2025. 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
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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.
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Who cites it
1 citing paper in PubMed.
- Restoring mitochondrial health after blast-induced traumatic brain injury: modifiable factors and therapeutic opportunities.npj metabolic health and disease · 2026Review
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) represents a significant cause of injury-related deaths and disabilities. Repeated exposure to mechanical impact can lead to metabolic and ionic imbalance, which can cause oxidative stress and worsen the cellular dysfunction initiated by the initial mild TBI (mTBI). Currently, no FDA-approved drug targets repeated mTBI (rmTBI) and its potential sequelae. Mitoquinone (MitoQ) is a mitochondrion-targeted drug that has proven beneficial in different brain-related diseases. We have previously demonstrated the neurotherapeutic effects of MitoQ at a 30-day chronic time point in a similar rmTBI mouse model, where we observed decreased neuroinflammation, enhanced behavioral outcomes, and diminished oxidation. Recently, alterations in glycans have been shown to modulate key roles in the nervous system. Their relevance has been recognized in several neurodegenerative disorders, including TBI, which indicated injury severity and pathobiology. In this study, we aimed to assess brain glycome profiles post MitoQ treatment in experimental rmTBI using liquid chromatography-tandem mass spectrometry. Our findings indicate that there is a correlation between the HexNAc
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