It has reported that memory disorders in AD patients begin with subtle changes in hippocampal synaptic efficacy earlier than extensive neuronal degeneration. Davies et al. (1987) performed a quantitative morphometric analysis to measure the densities of neurons and synapses in cerebral cortical biopsy tissues collected from AD patients. They found that the numerical density of synapses decreased 25%–35%, and the number of synapses per cortical neuron decreased 15%–35% in AD patients (Davies et al., 1987). Evidence also suggested that synaptic dysfunction is caused by oligomeric assemblies of Aβ (Lacor et al., 2004; Rowan et al., 2007). Even in very mildly impaired patients, the degree of synaptic loss in the cortex showed a significant association with soluble Aβ levels. Our results revealed that Aβ25–35 induced synapse loss in the hippocampus and cortex, and DLNA could dramatically inhibit the loss of synapses and improve synaptic structures, thereby improving the learning and memory abilities of mice.