 Alzheimer's disease, AD, is a progressive and chronic neurodegenerative disorder characterized by cognitive and memory impairment due to the accumulation of abnormal proteins, such as tau and beta amyloid, in the brain. Additionally, mitochondrial dysfunction has been identified as one of the primary causes of AD, leading to impaired mitophagy, the process of removing dead mitochondria through autophagy. Research into pharmaceutical interventions has focused on drugs that can prevent or reduce these protein aggregates and mitochondrial damage. Furthermore, recent studies have shown that defective mitophagy plays a key role in AD pathogenesis, suggesting that targeting mitophagy could be beneficial in treating AD. In this review, we summarize the latest updates on the mechanisms of mitophagy dysfunction in AD and discuss potential therapeutic and nanotherapeutic strategies to target mitophagy in AD. This article was authored by Reem M. Farsi.