In AD mouse models, knockdown of MCU has been shown to enhance memory performance, and this intervention leds to an increase in Beclin-1 levels and a decrease in P62 levels.[80] In addition, an imbalance in calcium homeostasis can affect mitochondrial function, thereby impairing mitophagy, which play a role in AD’s development.[81]. This evidence concerns the gene SQSTM1 and Alzheimer disease.