The pathogenesis of Alzheimer's disease (AD) has been extensively studied, revealing that impaired mitophagy is one of the critical factors contributing to AD development. In AD, excessive production of reactive oxygen species (ROS) and alterations in mitochondrial membrane potential lead to mitochondrial dysfunction, structural damage, and the accumulation of impaired mitochondria due to defective mitophagy, thereby exacerbating the progression of AD. This review summarizes the relationship between mitophagy and AD, encompassing the hallmarks of AD, the fundamental mechanisms of mitophagy, and the roles of key signaling pathways such as PINK1-Parkin, FUNDC1, and BNIP3/NIX in regulating mitophagy. Additionally, it explores the interactions between mitophagy and pathological hallmarks of AD, including β-amyloid (Aβ) peptides and Tau proteins. By systematically analyzing the interplay between mitophagy and AD, this article aims to provide new insights for early diagnosis and targeted therapy of AD through the enhancement of mitophagy, potentially offering a promising therapeutic strategy for mitigating AD pathology.