Moreover, GSK-3β overexpression triggers maturation abnormalities in newly generated neurons, including the lengthening of their immaturity period [48] and the acquisition of an aberrant morphological phenotype characterized by the presence of several primary apical dendrites (named the “V-shape” phenotype) [34]—a phenomenon also observed in patients with AD [88] and frontotemporal dementia [35]. Here, GSK3B is linked to Alzheimer disease.