Numerous literatures have reported that intra-hippocampal or intra-cerebroventricular injections of Aβ1–42 or Aβ25–35 fragments into rats or mice could induce neuronal death, and alter spatial learning and memory performance. Aβ could induce a variety of injuries, such as oxidative injury and disturbed neuronal ionic homeostasis, which could eventually result in neuronal dysfunction and selective neuronal loss (Lue et al., 1999; Niikura et al., 2002). Excessive neuronal loss can damage brain functions, and the cognitive ability is destroyed firstly. In this study, we established the mice model which was induced by the intra-cerebroventricular injection of Aβ25–35, and found that there were a lot of apoptotic neurons in the hippocampus CA3 region and cortex. The results of MWM test indicated that neuronal apoptosis was accompanied with an obvious failure in spatial learning and memory performance. On the other hand, DNLA treatment could significantly improve the ability of spatial learning and memory, and decreased apoptosis in TUNEL and H&E staining. This result demonstrated that DNLA could improve learning and memory deficits in AD model mice, and the protection may be due to the decreased apoptosis induced by Aβ25–35.