To study molecular distribution and organization of NR2B, PSD95, synaptophysin, and Aβ42 along synaptic deficit progression, we initially selected an age with no signs of pathology in the triple transgenic mouse model (3xTg-AD) (1 month; Fig. 2E; supplemental Fig S2) and another when Aβ is just emerging (6 months; Fig. 2) [23]. This evidence concerns the gene GRIN2B and Alzheimer disease.