Alzheimer’s disease (AD) is the most common type of dementia, characterized by progressive cognitive dysfunction as a primary manifestation of neurodegenerative changes. Regulated cell death, an active and orderly form of cell demise determined by genetic factors, is ubiquitous during the development of living organisms and is crucial for maintaining life homeostasis. With extensive research on regulated cell death in AD, increasing evidence reveals that ferroptosis is closely related to the onset, progression, and outcome of AD. This article will review the molecular mechanisms of ferroptosis and its regulatory role in AD, providing insights into potential therapeutic targets for exploring the pathogenesis and treatment of AD.