Biological Aging and the Cellular Pathogenesis of Huntington’s Disease
Author:
Affiliation:
1. University of Central Florida, College of Medicine, Burnett School of Biomedical Sciences, Orlando, FL, USA
Publisher
IOS Press
Subject
Cellular and Molecular Neuroscience,Clinical Neurology
Reference213 articles.
1. A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington’s disease chromosomes. The Huntington’s Disease Collaborative Research Group;MacDonald;Cell,1993
2. Huntington disease;Bates;Nat Rev Dis Primers,2015
3. Length of uninterrupted CAG, independent of polyglutamine size, results in increased somatic instability, hastening onset of Huntington disease;Wright;Am J Hum Genet,2019
4. CAG repeat not polyglutamine length determines timing of Huntington’s disease onset;Genetic Modifiers of Huntington’s Disease (GeM-HD) Consortium;Cell,2019
5. Relationship between trinucleotide repeat expansion and phenotypic variation in Huntington’s disease;Snell;Nat Genet,1993
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