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Deficit of in vivo Mitochondrial ATP Production in Patients with Friedreich Ataxia

✍ Scribed by Raffaele Lodi, J. Mark Cooper, Jane L. Bradley, David Manners, Peter Styles, Doris J. Taylor and Anthony H.V. Schapira


Book ID
123642256
Publisher
National Academy of Sciences
Year
1999
Tongue
English
Weight
708 KB
Volume
96
Category
Article
ISSN
0027-8424

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## Abstract Friedreich ataxia is an inherited, progressive, neurodegenerative disorder that is clinically heterogeneous. It is caused by a trinucleotide (GAA) repeat expansion resulting in frataxin loss and oxidative stress. We assessed clinical features including the development of cardiomyopathy