DNA repair pathways underlie a common genetic mechanism modulating onset in polyglutamine diseases
Conceição Bettencourt; Davina J. Hensman Moss; Michael Flower; Sarah Wiethoff; Alexis Brice; Cyril Goizet; Giovanni Stévanin; Georgios Koutsis · 2016 · Annals of Neurology
WASTE classifies this as Negative / Null Result Report · AI classification, approximate
The study found no significant effect — useful as a negative control or null benchmark for your own design.
Abstract
OBJECTIVE: The polyglutamine diseases, including Huntington's disease (HD) and multiple spinocerebellar ataxias (SCAs), are among the commonest hereditary neurodegenerative diseases. They are caused by expanded CAG tracts, encoding glutamine, in different genes. Longer CAG repeat tracts are associated with earlier ages at onset, but this does not account for all of the difference, and the existence of additional genetic modifying factors has been suggested in these diseases. A recent genome-wide association study (GWAS) in HD found association between age at onset and genetic variants in DNA r
Abstract by Conceição Bettencourt; Davina J. Hensman Moss; Michael Flower; Sarah Wiethoff; Alexis Brice; Cyril Goizet; Giovanni Stévanin; Georgios Koutsis, Annals of Neurology (2016) — licensed CC BY 4.0.
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Metadata source: OpenAlex · DOI 10.1002/ana.24656