Alzheimer’s disease (AD), which was first identified more than a century ago, has become a pandemic that exacts enormous social burden and economic tolls as no measure of combating devastated AD is currently available. Growing etiopathological, genetic, and biochemical data indicate that AD is a heterogeneous, polygenic, multifactorial, and complex disease. However, its exact etiopathology remains to be determined. Numerous experimental data show that cerebral iron and copper dyshomeostasis contribute to Aβ amyloidosis and tauopathy, two neuropathological hallmarks of AD. Moreover, increasing experimental evidence suggests ferroptosis, an iron-dependent and nonapoptotic form of cell death, may be involved in the neurodegenerative process in the AD brain. Thus, the anti-ferroptosis approach may be an efficacious therapeutic strategy for AD patients. Furthermore, it remains to be further determined whether cuproptosis, a copper-dependent and distinct form of regulated cell death, also plays a contributing role in AD neurodegeneration. We hope this concise review of recent experimental studies of oxidative stress-mediated ferroptosis and cuproptosis in AD may spur further investigations on this timely and essential line of research.