Alzheimer’s disease (AD) is a common chronic neurodegenerative disorder of the central nervous system characterized by progressive impairments in memory, cognition, and behavior, eventually leading to severe dementia and loss of self-care ability. Despite decades of investigation, the precise molecular mechanisms underlying AD remain incompletely understood, and effective disease-modifying treatments are still lacking. The traditional pathological hallmarks of AD including amyloid β-protein (Aβ) plaques and neurofibrillary tangles (NFTs) composed of hyperphosphorylated Tau fail to account for the complex biochemical and cellular alterations observed in AD brains. Ferroptosis, a distinct iron-dependent form of non-apoptotic programmed cell death, is increasingly recognized as a contributor to AD pathogenesis. Ferroptosis is driven by excessive accumulation of lipid peroxides and reactive oxygen species (ROS), leading to oxidative destruction of cellular membranes. Unlike apoptosis or necrosis, ferroptosis is morphologically characterized by shrunken mitochondria with condensed membrane densities and biochemically defined by the loss of glutathione peroxidase 4 (GPX4) activity. Disruption of iron homeostasis, a central hallmark of ferroptosis, triggers a cascade that inhibits the cystine/glutamate antiporter (System Xc^-), suppresses glutathione (GSH) synthesis, and impairs GPX4-mediated detoxification of lipid peroxides, leading to uncontrolled lipid peroxidation and oxidative stress that ultimately trigger ferroptotic cell death. This iron-driven cell death exhibits distinct morphological and biochemical characteristics compared with other forms of cell death. Ferroptosis contributes to AD pathogenesis through multiple mechanisms and is closely associated with disease onset and progression. Iron overload can affect early amyloid precursor protein processing, accelerate Aβ production and plaque deposition, reduce Tau protein solubility, and promote Tau hyperphosphorylation and aggregation into NFTs. Therapeutic strategies targeting ferroptosis—such as iron chelation with deferoxamine to reduce labile iron levels and inhibit Fenton reaction-driven oxidative damage, supplementation with antioxidants such as α-tocopherol or α-lipoic acid to neutralize ROS and scavenge lipid radicals, and administration of selenium or activators of the Nrf2-SLC7A11-GPX4 axis and the SIRT1/Nrf2 signaling pathway to restore glutathione-GPX4 function—can effectively block lipid peroxidation and suppress iron-dependent cell death. By modulating iron metabolism, enhancing antioxidant defenses, and inhibiting lipid peroxidation, these approaches hold promise for mitigating ferroptosis-related neuronal injury. These interventions collectively aim to modulate iron metabolism, strengthen antioxidant defenses, and suppress lipid peroxidation, thereby mitigating neuronal injury and delaying cognitive deterioration. Ferroptosis represents a pivotal intersection of iron metabolism, oxidative stress, and neurodegeneration in AD. Exploring ferroptotic mechanisms not only deepens our understanding of AD pathophysiology but also opens new avenues for therapeutic intervention. This review aims to comprehensively summarize the molecular basis of ferroptosis, elucidate its pathological roles in AD, and propose ferroptosis-centered therapeutic strategies, thereby providing a theoretical framework for future research and drug development in AD.