Based on the relation between the loss of synaptic markers and deficits of hippocampal synaptic plasticity accompanying memory deterioration in different animal models of aging and brain disease (e.g., [60,61,62]), it was surprising to conclude that there was no alteration in the levels of different synaptic markers (SNAP25, syntaxin, synaptophysin, PSD95) in cerebrocortical synapses of female APP/PS1 mice displaying memory deficits. This evidence concerns the gene APP and brain disorder.