Prion diseases are neurodegenerative diseases that are transmitted between humans and animals, which cause spongiform brain degeneration and neuronal death. Prion diseases are difficult to treat. Mitochondrial damage and oxidative stress occurring early in disease progression. Reducing oxidative stress is a therapeutic strategy for disease. Idebenone (IDE) is an antioxidant that enhances electron transfer in the mitochondrial respiratory chain. To investigate IDE protection mechanisms in prion neuron models, we examined IDE effects on apoptosis, mitochondrial dysfunction, cellular respiratory chain damage, and oxidative stress in N2a cells treated with the prion toxic peptide PrP