Consistent with previous research conclusions that AD patients exhibit metabolic dysfunction in both the central and peripheral nervous system, as well as damage to the actin cytoskeleton in muscle cells leading to synaptic dysfunction and the MAPK and ErbB pathways have been identified as potential therapeutic targets for AD (Lee and Kim, 2017; Clarke et al., 2018; Pelucchi et al., 2020; Zhang H. et al., 2021). This evidence concerns the gene EGFR and Alzheimer disease.