Oral glutathione supplementation is often debated due to its potential effectiveness and absorption challenges, as digestive enzymes may degrade it
This unexpected link between mitochondrial glutathione and m -AAA protease AFG3L2 might lead to new pathophysiological mechanisms under a diverse clinical spectrum of AFG3L2 mutation-associated neurodegenerative disorders that range from ataxia to parkinsonism 29,43
Presented for research literature review only Borvinskaia EV et al
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