Therefore, our main objective was to explore cognitive processes that are disrupted in SAD and also to investigate the effects of AEA on cognitive impairments induced by icv-STZ administration and alterations of different synaptic markers (syntaxin, synaptophysin and SNAP-25) and p-tau degradation mechanisms in the hippocampus (p-tau, HSP70, and BAG2 levels). The gene discussed is MAPT; the disease is Cognitive impairment.