4.5 Review

A Mitochondria-Associated Oxidative Stress Perspective on Huntington's Disease

期刊

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fnmol.2018.00329

关键词

Huntington's disease; Huntingtin; neurodegeneration; yeast; oxidative stress

资金

  1. Fund for Scientific Research Flanders (FWO-Vlaanderen)
  2. FWO
  3. Swedish Cancer Society (Cancerfonden) [CAN 2012/601, CAN 2015/406, CAN 2017/643]
  4. Swedish Natural Research Council [VR 2011-5923, VR 2015-04984]
  5. Carl Trygger Foundation (Carl Tryggers Stiftelse for Vetenskaplig Forskning) [CTS 14: 295]
  6. People Programme (Marie Curie Actions) of the European Union's Seventh Framework Programme (FP7/2007-2013) under REA [608743]
  7. Swedish Research Council [2015-04984] Funding Source: Swedish Research Council

向作者/读者索取更多资源

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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