GSK3β has been centrally implicated in AD pathogenesis (Forlenza et al., 2014; Kerr et al., 2018; Hampel et al., 2019), affecting both the overproduction of the amyloid-beta peptide (Aβ) and hyperphosphorylation of microtubule-associated protein Tau, mechanisms that respectively lead to the formation of senile plaques and neurofibrillary tangles—pathological hallmarks of AD (Tan et al., 2010; Forlenza et al., 2014; Kerr et al., 2018; Hampel et al., 2019; Li et al., 2020). This evidence concerns the gene GSK3B and Alzheimer disease.