ACO2 and Parkinson disease: According to Kang et al, MitoQ prevented intervertebral deterioration by correcting the mismatch in mitochondrial dynamics and enhancing PINK-mediated mitophagy.90 In Parkinson’s animal studies, MitoQ reduced the amount of caspase-3 activation that was brought on by MPP + and reduced the amount of mitochondrial aconitase deactivation that was caused by MPTP, keeping the TCA functioning normally and reducing oxidative injury.91 In one study, high doses of MitoQ were administered to PD animal models for up to 28 weeks, and the results indicated no evidence of damage to whole-body biology.