In addition, PrPC inihibits GSK3β activity [36], and the kinase is proposed as playing a central role in AD under the GSK3 hypothesis [57] as it is involved in the mechanisms underlying learning and memory, the hyperphosphorylation of tau, the increased production of Aβ, local cerebral inflammatory responses, and finally in tau exon 10 splicing [19,21,43]. This evidence concerns the gene GSK3B and Alzheimer disease.