ITCH and Alzheimer disease: In AD, Aβ42 can induce Itch hyperphosphorylation by pathologically activating the c-Jun amino-terminal kinase signaling pathway, and the aberrantly modified Itch will further degrade TAp73 in a ubiquitinated form, which alters the expression of neuronal cell-cycle proteins, ultimately leading to neuronal death and accelerating the progression of AD (Chauhan et al., 2020).