OXIDATIVE STRESS IN Q175 MOUSE MODEL OF HUNTINGTON'S DISEASE

FEDERICO LÓPEZ COUSELO; JULIETA SABA; JULIETA BRUNO; LILA CARNIGLIA; DANIELA DURAND; MERCEDES LASAGA; CARLA CARUSO

Honolulu

Congreso; ISN-APSN Meeting 2022; 2022

ISN-JNC

Huntington’s disease (HD) is a neurodegenerative disorder that initially affects the striatum and later the cortex resulting in motor, cognitive and psychiatric dysfunction. Oxidative stress, mitochondrial dysfunction, and neurotoxicity are proposed as pathogenic mechanisms. Oxidative stress is generated by high levels of reactive oxygen species (ROS) which can be reduced by antioxidant molecules such as glutathione (GSH) and the activity of the mitochondrial enzymesuperoxide dismutase 2 (SOD2). UCP4 is an uncoupling protein involved in the reduction of mitochondrial ROS levels which dissipates proton gradient. We evaluated motor performance, ROS and GSH levels, as well as SOD2 and UCP4 expression in striatum and cortex of Q175 knock-in HD mice and WT mice at the ages of 4 months (4m) and 8 months (8m). We observed reduced motor performance in Q175 mice in the open field test at 4m and 8m (p