Brinda C. Prasad

The paper develops URSA, a method to quantify DNA repair activity at the CAG repeat tract in HD, showing it correlates with somatic instability and can be measured rapidly in blood cells.

The paper develops targeted mass spectrometry assays to quantify DNA repair and handling proteins in Huntington's disease models and finds HTT influences their abundance and interactions.

The paper uses RNAi to identify dose-dependent MMR gene modulators of somatic instability and proteome changes in HD mouse models.

This study identifies a FAN1 mutation linked to faster Huntington's disease progression and shows it disrupts PCNA-mediated FAN1 assembly on DNA.

This study identifies Msh3 and Pms1 as genetic drivers of CAG-repeat migration in HD mice, leading to selective striatal and cortical pathogenesis.