In brain lysates from AD patients and Aβ-treated neurons, elevated expression of Aβ causes localization and increased expression of NEDD4-1 in dendritic spines, leading to degradation and a resultant decrease in cell surface α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) expression via endocytosis (Lin et al., 2011; Zhang et al., 2018). The gene discussed is NEDD4; the disease is Alzheimer disease.