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• W2126572451 endingPage "3359" @default.
• W2126572451 startingPage "3351" @default.
• W2126572451 abstract "Huntington's disease (HD) and spinocerebellar ataxia type 7 (SCA7) belong to a group of progressive neurodegenerative diseases caused by polyglutamine (polyQ) expansions. SCA7 is the only one to display degeneration in the retina, a tissue usually spared in HD. We previously described a SCA7 transgenic retinal model expressing mutant full length ataxin-7 in rod photoreceptors. These mice develop a severe and characteristic retinopathy. We show here that R6 transgenic mice, which reproduce many features of HD, express mutant huntingtin in the retina leading to strong vision deficiencies and retinal dystrophy. These two different polyQ mouse models exhibit comparable early and progressive retinal degeneration and dysfunction. These abnormalities are reminiscent of other retinal degeneration phenotypes (in particular rd7/rd7 mice) where photoreceptor cell loss occurs. Retinopathy in R6 and R7E models can be monitored in living mice by ERG and fundus examination, which can facilitate in vivo evaluation of therapeutic agents in polyQ disorders." @default.
• W2126572451 created "2016-06-24" @default.
• W2126572451 creator A5030872396 @default.
• W2126572451 date "2002-12-15" @default.
• W2126572451 modified "2023-10-06" @default.
• W2126572451 title "Progressive retinal degeneration and dysfunction in R6 Huntington's disease mice" @default.
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• W2126572451 doi "https://doi.org/10.1093/hmg/11.26.3351" @default.
• W2126572451 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12471061" @default.
• W2126572451 hasPublicationYear "2002" @default.
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