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      Effects of Anthocyanins on CAG Repeat Instability and Behaviour in Huntington’s Disease R6/1 Mice

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          Abstract

          Background: Huntington’s disease (HD) is a progressive neurodegenerative disorder caused by CAG repeat expansions in the HTT gene. Somatic repeat expansion in the R6/1 mouse model of HD depends on mismatch repair and is worsened by base excision repair initiated by the 7,8-dihydroxy-8-oxoguanine-DNA glycosylase (Ogg1) or Nei-like 1 (Neil1). Ogg1 and Neil1 repairs common oxidative lesions.

          Methods: We investigated whether anthocyanin antioxidants added daily to the drinking water could affect CAG repeat instability in several organs and behaviour in R6/1 HD mice. In addition, anthocyanin-treated and untreated R6/1 HD mice at 22 weeks of age were tested in the open field test and on the rotarod.

          Results: Anthocyanin-treated R6/1 HD mice showed reduced instability index in the ears and in the cortex compared to untreated R6/1 mice, and no difference in liver and kidney. There were no significant differences in any of the parameters tested in the behavioural tests among anthocyanin-treated and untreated R6/1 HD mice.

          Conclusions: Our results indicate that continuous anthocyanin-treatment may have modest effects on CAG repeat instability in the ears and the cortex of R6/1 mice. More studies are required to investigate if anthocyanin-treatment could affect behaviour earlier in the disease course.

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          Author and article information

          Contributors
          Journal
          PLoS Curr
          PLoS Curr
          plos
          PLoS Currents
          Public Library of Science (San Francisco, USA )
          2157-3999
          5 July 2016
          : 8
          Affiliations
          Institute of Medical Microbiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway
          Centre for Rare Disorders, Oslo University Hospital, Rikshospitalet, Oslo, Norway
          Institute of Medical Microbiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway
          Institute of Medical Microbiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway
          Department of Medical Genetics, Oslo University Hospital, Ullevål, Oslo, Norway
          Institute of Medical Microbiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway
          Institute of Medical Microbiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway
          Department of Medical Genetics, Oslo University Hospital, Ullevål, Oslo, Norway
          Article
          10.1371/currents.hd.58d04209ab6d5de0844db7ef5628ff67
          4973517
          27540492
          41d7f937-dc32-4576-a55f-5e5e0e28f7c7
          © 2016 Møllersen, Moldestad, Rowe, Bjølgerud, Holm, Tveterås, Klungland, Retterstøl, et al

          This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

          Funding
          This work was supported by the Norwegian Research Council, the Norwegian Cancer Society, the Centre for Molecular Biology and Neuroscience, the Health Region South-East of Norway, and Oslo University Hospital. The funding sources had no involvement in conduct of the research and/or preparation of the article. The authors declare no conflict of interest.
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