Pharmaceutical agents that maintain or enhance synaptic NMDAR-mediated pro-survival signaling are potential therapeutic strategies for the effective treatment for AD and/or VCI patients not only during, but also after, the overactivation of NMDARs; hence, it will be important to determine the effect of degradation of proteins such as drebrin on synaptic NMDAR-mediated pro-survival signaling. This evidence concerns the gene DBN1 and Alzheimer disease.