Jia Feng

This study shows that HTT CAA/CCA-loss variants increase toxicity in Huntington disease models independently of somatic repeat instability.

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.

This study shows that HTT polyQ expansions disrupt motor and adaptor recruitment to vesicles, causing transport defects and altered responses to neuroinflammatory stress.