In a 5xFAD, five familial AD-related mutations, AD mouse model, mice exhibited markers for lipid peroxidation and ferroptosis along with cognitive decline, which improved with the generation of transgenic 5xFAD mice that overexpress GPX4 [353], displaying the crucial role of GPX4 in the mediation of ferroptosis-induced neurodegeneration. This evidence concerns the gene GPX4 and Alzheimer disease.