Overall, these findings reflect the disruptive actions of soluble Aβ on synaptic plasticity in AD, provide keys to interpreting the effects of the Aβ1-6A2V(D)—based strategy on AD-related synaptopathy and support the use of PSD-95, AMPA and NMDA receptor levels as indicators of efficacy for therapeutic strategies against AD aimed at preserving synaptic integrity [54]. The gene discussed is DLG4; the disease is Alzheimer disease.