Fig. 2.

Interactions between mitophagy and Tau pathology. Abnormal Tau, together with increased free radicals, SOD2 deficiency, impaired glutathione synthesis and other assaults, causes mitochondrial damage by increasing oxidative stress and ROS production, as well as inducing NADH activity and ATP synthesis. Meanwhile, these mitochondrial dysfunctions increase pathological Tau levels, which compromise mitophagy by increasing COX IV and TOMM20 levels, mitochondrial membrane potential, and disrupt PINK1/parkin localization, further aggravating mitochondrial damage and mitophagy disorder. Thus, the damaged mitochondria accumulate in neurons