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Does oxidative stress contribute to the pathology of Friedreich's ataxia? A radical question

Friedreich’s ataxia (FRDA) is a hereditary neurodegenerative disease that frequently culminates in cardiac failure at an early age. FRDA is believed to arise from reduced synthesis of the mitochondrial iron chaperone frataxin due to impaired gene transcription, which leads to mitochondrial iron accumulation, dysfunction of mitochondrial Fe-S containing enzymes, and increased Fenton-mediated free radical production. Recent reports have challenged this generally accepted hypothesis, by suggesting that the oxidative stress component in FRDA is minimal and thereby questioning the benefit of antioxidant therapeutic strategies. 

Does oxidative stress contribute to the pathology of Friedreich's ataxia? A radical question

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