Specifically, accumulating evidence implies that mitophagy deficit fails to maintain mitochondrial clearance (Kerr et al., 2017), axonal transport (Ashrafi and Schwarz, 2015), and synapse biosynthesis (Pan et al., 2021), which exacerbates neuroinflammation, Aβ and p-Tau deposition, and energy dysfunction, thereby promoting AD pathology and memory loss (Song et al., 2021). The gene discussed is MAPT; the disease is Alzheimer disease.