The development of therapeutic approaches to inhibit GSK3β and/or induce Wnt/β-catenin signaling in neural cells can mitigate the toxic effects of Aβ and promote neurogenesis in AD patients [1,2] This is because overactivation of GSK3β accounts for several features of this pathology, such as memory impairment, tau phosphorylation, increased amyloid production, microglia-mediated inflammation, and neuronal death [24]. Here, GSK3B is linked to memory impairment.