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]. Here, DLG4 is linked to Alzheimer disease.