Abstract
Huntington’s disease (HD) is genetically caused by mutation of the Huntingtin (HTT) gene. At present, the mechanisms underlying the defect of HTT and the development of HD remain largely unclear. However, increasing evidence shows the presence of enhanced oxidative stress in HD patients. In this review article, we focus on the role of oxidative stress in the pathogenesis of HD and discuss mediators and potential mechanisms involved in mutant HTT-mediated oxidative stress generation and progression. Furthermore, we emphasize the role of the unicellular organism Saccharomyces cerevisiae in investigating mutant HTT-induced oxidative stress. Overall, this review article provides an overview of the latest findings regarding oxidative stress in HD and potential therapeutic targets for HD.
Highlights
Huntington’s DiseaseHuntington’s disease (HD) is a neurodegenerative disorder inherited in an autosomal dominant pattern
More than two decades have passed since the first identification of the HTT gene, and mutation of this gene is responsible for HD pathogenesis
Given the core role of mitochondria in respiration and energy production, mitochondrial DNA (mtDNA) damage or depletion leads to increased levels of oxidative stress
Summary
Reviewed by: Johannes Herrmann, Technische Universität Kaiserslautern, Germany Martin Lothar Duennwald, University of Western Ontario, Canada. Huntington’s disease (HD) is genetically caused by mutation of the Huntingtin (HTT) gene. The mechanisms underlying the defect of HTT and the development of HD remain largely unclear. Increasing evidence shows the presence of enhanced oxidative stress in HD patients. We focus on the role of oxidative stress in the pathogenesis of HD and discuss mediators and potential mechanisms involved in mutant HTT-mediated oxidative stress generation and progression. We emphasize the role of the unicellular organism Saccharomyces cerevisiae in investigating mutant HTT-induced oxidative stress.
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