Restoring mitophagy flux in AD models reduces Aβ1-42 burden by 40% and suppresses Tau hyperphosphorylation via ULK1/AMPK signaling (Swerdlow, 2023), positioning mitophagy modulators (e.g., FUNDC1-targeted agents) as promising candidates for early intervention. This evidence concerns the gene FUNDC1 and Alzheimer disease.