OXIDATIVE STRESS IN ZQ175 MOUSE MODEL OF HUNTINGTON'S DISEASE

FEDERICO LÓPEZ COUSELO; JULIETA SABA; MATEO PALMIERI; DIEGO RIVAS; MARÍA FRISER; LILA CARNIGLIA; DANIELA DURAND; MERCEDES LASAGA; CARLA CARUSO

Mar del Plata

Congreso; LXVIII Reunión Anual de la Sociedad Argentina de Investigación Clínica; 2023

Sociedad Argentina de Investigación Clínica

Huntington's disease (HD) is a progressive neurodegenerative disorder affecting the brain's striatum and cortex, leadingto motor, cognitive, and psychiatric impairments. Proposed pathological mechanisms include oxidative stress,mitochondrial dysfunction, and neurotoxicity. Oxidative stress arises from elevated reactive oxygen species (ROS), thatcan be countered by antioxidants like glutathione (GSH) and mitochondrial enzyme superoxide dismutase 2 (SOD2).Uncoupling proteins UCP2 and UCP4 are proposed to minimize mitochondrial ROS via proton gradient dissipation. Wehave previously shown that ROS levels were unchanged in the zQ175 knock-in mouse model of HD (HD mice), butreduced GSH levels were evident at 4 months (4m) and 8 months (8m) in the striatum of HD mice. Now, we evaluatedUCP2, UCP4 and SOD2 expression by Western blot in the striatum and cortex of WT and HD mice at 4m and 8m. In HDmice’s striatum, UCP2 decreased at 8m (p