Given that AD patients displayed enhanced hippocampal GSK-3β activity, decreased β-catenin levels, heightened GnT-III expression and increased bisecting GlcNAc pools, treatment of Wnt pathway dysfunction, which might be achieved with GLP-1R activation, has been proposed as a therapeutic strategy for AD (Akasaka-Manya et al., 2010; Rios et al., 2014; Palmigiano et al., 2016). This evidence concerns the gene GSK3B and Alzheimer disease.