The accumulation of sAβ also closely correlates with cognitive decline in animal models and AD patients and is primarily due to disrupting synaptic plasticity [5], Ca2+ homeostasis [6–8] and signaling pathways such as glycogen synthase kinase 3 beta (GSK-3β) [9], c-Jun [10], Ca2+/calmodulin-dependent protein kinase kinase (CaMKK), AMP-activated protein kinase (AMPK) [11], cytoskeletal networks [12] and axonal transport [13]. This evidence concerns the gene GSK3B and Alzheimer disease.