Neuroprotective potential of escitalopram against behavioral mitochondrial and oxidative dysfunction induced by 3-nitropropionic acid

摘要

BackgroundHuntington’s disease (HD) is a neurodegenerative syndrome that leads to marked decline in cognitive functioning along with uncharacteristic body movements called chorea. There exists no therapeutic agent to address the disease.3-Nitropropionic acid (3-NP) which is a suicide inhibitor of succinate dehydrogenase and a well-known experimental model to study Huntington’s disease, causes substantial impairment in gait and memory through oxidative and neuronal damage.