OXIDATIVE STRESS IN ZQ175 MOUSE MODEL OF HUNTINGTON'S DISEASE

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

Mar del Plata

Congreso; Reunion conjunta SAIC SAI AAFE Nanormed.ar; 2023

SAIC

Huntington's disease (HD) is a progressive neurodegenerative disorder affecting the brain's striatum and cortex, leading to motor, cognitive, and psychiatric impairments. Proposed pathological mechanisms include oxidative stress, mitochondrial dysfunction, and neurotoxicity. Oxidative stress arises from elevated reactive oxygen species (ROS), that can 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. We have previously shown that ROS levels were unchanged in the zQ175 knock-in mouse model of HD (HD mice), but reduced GSH levels were evident at 4 months (4m) and 8 months (8m) in the striatum of HD mice. Now, we evaluated UCP2, UCP4 and SOD2 expression by Western blot in the striatum and cortex of WT and HD mice at 4m and 8m. In HD mice’s striatum, UCP2 decreased at 8m (p