The proposal that GSK3β may play a pivotal role in AD etiology, termed the “GSK3 hypothesis of AD” [90], posits that pathogenesis of sporadic and familial types of AD may involve GSK3β hyperactivity leading to memory impairment, tau hyperphosphorylation, Aβ plaque accumulation, and development of plaque-related microglia-associated inflammation, and other inflammatory processes through activation of transcription factor NF-κB [91,92,93]. Here, NFKB1 is linked to memory impairment.