| Literature DB >> 22832776 |
David R Lynch1, Eric C Deutsch, Robert B Wilson, Gihan Tennekoon.
Abstract
During the past 15 years, the pace of research advancement in Friedreich ataxia has been rapid. The abnormal gene has been discovered and its gene product characterized, leading to the development of new evidence-based therapies. Still, various unsettled issues remain that affect clinical trials. These include the level of frataxin deficiency needed to cause disease, the mechanism by which frataxin-deficient mitochondrial dysfunction leads to symptomatology, and the reason selected cells are most affected in Friedreich ataxia. In this review, we summarize these questions and propose testable hypotheses for their resolution.Entities:
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Year: 2012 PMID: 22832776 PMCID: PMC3674553 DOI: 10.1177/0883073812453498
Source DB: PubMed Journal: J Child Neurol ISSN: 0883-0738 Impact factor: 1.987