Alzheimer's disease(AD)is a neurodegenerative disease characterized by progressive cognitive dysfunction, with its pathogenesis closely associated with mitochondrial dysfunction. The PINK1/Parkin signaling pathway, as a core regulator of mitophagy, plays a key role in clearing damaged mitochondria and maintaining neuronal homeostasis. While dysfunction of this pathway in Parkinson's disease is mainly attributable to genetic mutations,in AD,it is not a primary cause but rather a secondary consequence of core pathological processes such as abnormal amyloid β-protein (Aβ)deposition and tau protein hyperphosphorylation. These pathological changes can lead to impaired function of the PINK1/Parkin pathway, which in turn triggers mitophagy deficits, creating a vicious cycle of neurodegeneration. PINK1 can activate the mitophagy program by phosphorylating Parkin proteins and ubiquitin molecules, a process that is significantly inhibited in AD. Crucially, the abnormal deposition of Aβ and pathological changes of tau in AD not only inhibit the PINK1/Parkin pathway, but also their own production and toxic effects are regulated by this pathway, forming a complex AD-specific bidirectional interactive network, which is significantly different from the pathophysiological mechanism of Parkinson's disease. Notably, pharmacological interventions aimed at activating the PINK1/Parkin pathway have shown potential in improving AD pathology and cognitive function in animal models. In this review, we systematically elucidate the molecular mechanisms and therapeutic implications of PINK1/Parkin-mediated mitophagy in AD, providing a crucial theoretical basis for the development of novel neuroprotective strategies.