Dysfunctional Wnt signaling induced by Aβ toxicity in AD, characterized by reduced β-catenin levels, constitutively active GSK-3β, and increased expression of the Wnt signaling inhibitor DKK-1, suggests that sustained dysfunctional Wnt signaling may be a key event that contributes to the pathology of AD [22, 65]. This evidence concerns the gene GSK3B and Alzheimer disease.