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Effects of Anthocyanins on CAG Repeat Instability and Behaviour in Huntington's Disease R6/1 Mice
Linda Møllersen1, Olve Moldestad2, Alexander D Rowe1
1Institute of Medical Microbiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Insights
Anthocyanin antioxidants may reduce CAG repeat instability in the ears and cortex of R6/1 Huntington
Area of Science:
- Neuroscience
- Genetics
- Pharmacology
Background:
- Huntington's disease (HD) is a neurodegenerative disorder caused by CAG repeat expansions in the HTT gene.
- Somatic CAG repeat instability in HD models is influenced by DNA repair pathways, including mismatch repair and base excision repair.
- Oxidative stress-related DNA lesions are repaired by enzymes like 7,8-dihydroxy-8-oxoguanine-DNA glycosylase (Ogg1) and Nei-like 1 (Neil1).
Purpose of the Study:
- To investigate the effect of anthocyanin antioxidants on CAG repeat instability in the R6/1 mouse model of Huntington's disease.
- To assess the impact of anthocyanins on behavior in R6/1 mice.
Main Methods:
- R6/1 HD mice received daily anthocyanin antioxidants in their drinking water.
- CAG repeat instability was measured in various organs (ears, cortex, liver, kidney).
- Behavioral tests, including the open field test and rotarod, were performed at 22 weeks of age.
Main Results:
- Anthocyanin treatment led to a reduced CAG repeat instability index in the ears and cortex of R6/1 mice.
- No significant differences in CAG repeat instability were observed in the liver or kidney.
- No significant behavioral differences were detected between anthocyanin-treated and untreated R6/1 mice.
Conclusions:
- Continuous anthocyanin treatment may exert a modest protective effect against CAG repeat instability in specific brain regions (ears and cortex) in R6/1 mice.
- Further research is needed to explore potential earlier behavioral effects of anthocyanin treatment in HD.
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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