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A Mitochondria-Associated Oxidative Stress Perspective on Huntington's Disease
Ju Zheng1,2,3, Joris Winderickx2, Vanessa Franssens2
1Department of Biology, Southern University of Science and Technology, Shenzhen, China.
Insights
Huntington's disease (HD) involves the Huntingtin (HTT) gene. This review explores how oxidative stress contributes to HD pathogenesis and highlights yeast as a model for studying this neurodegenerative disease.
Area of Science:
- Neuroscience
- Genetics
- Biochemistry
Background:
- Huntington's disease (HD) is a genetic neurodegenerative disorder caused by mutations in the Huntingtin (HTT) gene.
- The precise mechanisms of HTT gene defects and HD development are not fully understood.
- Growing evidence links enhanced oxidative stress to HD pathogenesis in patients.
Purpose of the Study:
- To review the role of oxidative stress in Huntington's disease pathogenesis.
- To discuss mediators and mechanisms of mutant HTT-induced oxidative stress.
- To highlight the utility of *Saccharomyces cerevisiae* in studying HD-related oxidative stress.
Main Methods:
- Literature review focusing on oxidative stress in Huntington's disease.
- Analysis of studies investigating mutant Huntingtin (HTT) protein effects.
- Examination of research utilizing *Saccharomyces cerevisiae* as a model organism.
Main Results:
- Oxidative stress is a significant factor in the development and progression of Huntington's disease.
- Specific mediators and pathways contribute to mutant HTT-associated oxidative stress.
- *Saccharomyces cerevisiae* serves as a valuable model for dissecting these mechanisms.
Conclusions:
- Oxidative stress plays a critical role in Huntington's disease pathology.
- Understanding mutant HTT-mediated oxidative stress is key to identifying therapeutic targets.
- Further research using model organisms like yeast can elucidate HD mechanisms and inform treatment strategies.
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.
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