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. 2018 Jul 17;12:188. doi: 10.3389/fncel.2018.00188

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Copyright © 2018 Abeti, Baccaro, Esteras Gallego and Giunti.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Omaveloxolone (Omav) prevents Complex I inhibition in friedreich’s ataxia (FRDA) fibroblasts and neurons. (A) Representative trace of nicotinamide adenine dinucleotide (NADH) autofluorescence where the basal level refers to the NADH redox state and the response to NaCN subtracting the response to carbonyl cyanide-4-(trifluoromethoxy)phenylhydrazone (FCCP) represents the NADH pool. (B–D) The histograms represent the calculation total NADH pool in KIKO, YG8R cerebellar granule neurons (CGNs) and Patients compared to their controls and without/with omav (**p < 0.005; ***p < 0.0005). (E–G) The histograms represent the calculation total NADH redox state in KIKO, YG8R CGNs and Patients compared to their controls and without/with omav (*p < 0.05; ***p < 0.0005).