Previously, we reported the in vitro finding that Plk2 kinase function promotes activity-dependent APP β-processing and Aβ production by directly binding to and phosphorylating threonine (668) and serine (675) of synaptic APP [30], and may be one of multiple kinases that contributes to hyperphosphorylation of APP in human AD brain [31,32]. This evidence concerns the gene PLK2 and Alzheimer disease.