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E-mail: [email protected] Received: April 29, 2026 Accepted: June 16, 2026 Published: June 16, 2026 Abstract Friedreichs ataxia (FRDA) is a rare neurodegenerative condition driven by a severe deficiency of the mitochondrial protein frataxin (FXN)

2C, NLRP3 cysteine residues can be modified by S-glutathionylation, persulfidation, and S-palmitoylation, with S-glutathionylation and S-persulfidation serving to decrease cytokine release and inflammation, while S-palmitoylation promotes inflammasome activity

(2018) demonstrated that quercetin-mediated upregulation of frataxin promotes mitophagy, consequently restoring mitochondrial function and limiting oxidative damage in hepatocytes

Recent advances in a functional deoxy hexose l-fucose: occurrence, physiological effects, and preparation

Monthly maintenance prevents regression and continues L-Carnitine-facilitated oxidation