In line with our findings, HSP of excitatory synapses has been shown to be impaired in neurons lacking presinilin 1 (PS1−/−) or neurons expressing a familial AD-linked mutation (PS1M146V), which was not dependent on γ-secretase activity and showed impaired phosphatidylinositol 3-kinase (PI3K)/Akt signaling [46]. The gene discussed is AKT1; the disease is Alzheimer disease.