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• W2083149478 abstract "A prominent feature of Friedreich's ataxia (FRDA) is the neurodegeneration of the central and peripheral nervous systems, but little information is available about the mechanisms leading to neuronal damage in this pathology. Currently, no treatments delay, prevent, or reverse the inexorable decline that occurs in this condition. Evidence of oxidative damage has been demonstrated in Friedreich's ataxia, and this damage has been proposed as the origin of the disease. Nevertheless, the role of oxidative stress in FRDA remains debatable. The lack of direct evidence of reactive oxygen species overproduction in FRDA cells and tissues and the failure of exogenous antioxidants to rescue FRDA phenotypes questions the role of oxidative stress in this pathology. For example, the antioxidant idebenone ameliorates cardiomyopathy in FRDA patients, but this therapy does not improve neurodegeneration. To date, no known pharmacological treatment with antioxidant properties cures or delays FRDA neuropathology. This review reports and discusses the evidence of oxidative stress in FRDA and focuses on the existing knowledge of the apparent ineffectiveness of antioxidants for the treatment of neuronal damage." @default.
• W2083149478 created "2016-06-24" @default.
• W2083149478 creator A5019662473 @default.
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• W2083149478 date "2014-09-10" @default.
• W2083149478 modified "2023-09-28" @default.
• W2083149478 title "Friedreich’s Ataxia: A Neuronal Point of View on the Oxidative Stress Hypothesis" @default.
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• W2083149478 doi "https://doi.org/10.3390/antiox3030592" @default.
• W2083149478 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4665420" @default.
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