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-Synuclein aggregates can directly inhibit GCase activity and set up a futile feed-forward loop to increase both -synuclein levels and neurotoxicity (Mazzulli et al., 2011)

Frataxin-knockout mouse myoblasts, heart, and skin fibroblasts all showed characteristics of ferroptosis, and Nrf2 was downregulated in Friedreichs Ataxia patients and frataxin-knockout mice, while Nrf2 activators EPI-743 or sulforaphane regulated redox imbalances and rescued ferroptosis in frataxin knockout cells

Preclinical protocols vary widely in dose, species, and tissue target

as well as hypoxia (Warburg effect) with m -Dys (altered ATP synthesis), immune impairment, and FeRD in an infected individual