It is well-accepted that the transcript levels of synaptic plasticity-associated genes such as Grin2b (NR2B), Gria1 (GluR1), Arc, Egr1, Homer-1, c-fos, Camk2β are significantly reduced in the hippocampus of patients at moderate and severe AD stages and of transgenic mouse models of AD, coinciding with extensive amyloid plaque deposition, degeneration and cognitive deficits (Yasuda et al., 1995; Wakabayashi et al., 1999; Sze et al., 2001; Dickey et al., 2003; Hynd et al., 2004; Liang et al., 2008; Wang and Reddy, 2017). This evidence concerns the gene CAMK2B and amyloidosis.