The application of neurotrophic factors could enable the modulation of neuronal survival and synaptic connectivity (Poo, 2001). Neurotrophic factors are synthesized and secreted by the target tissue. After binding with receptors (tyrosine receptor kinase [Trk] and pan-neurotrophin receptot [p75]), these factors are internalized and transported to the cell body in a retrograde manner, where they would affect neuronal survival and differentiation (Poo, 2001; Barker & Shooter, 1994). The loss of neurons in the AD process is at least partly due to the lack of one or more neurotrophic factors. It has been found that the mRNA expression level of BDNF is low in the hippocampus and cortex of AD patients. Christensen et al. (2008) reported that the injection of Aβ1–42 in the hippocampus of rat would lead to learning and memory impairment and reduce cortical BDNF levels. These results indicate that memory deficit induced by Aβ1–42 is associated with the disorder of the expression of BDNF, which is reflected in lower cortical BDNF levels. Another study has shown that secretory vesicles containing BDNF exist within axon terminals, dendrites of pyramidal, and granule cells. BDNF can be secreted into the synaptic gap and binds with TrkB. After binding, BDNF serves as a key regulator in synaptic plasticity and memory, and plays a role in long-term and short-term memory (Lu, Christian & Lu, 2008). The present study proved that intracerebroventricular injection of Aβ25–35 could decrease the expression of BDNF in the hippocampus and cortex. However, DNLA have significantly increased BDNF expression, suggesting that the abilities of DNLA to reduce neuronal apoptosis and synaptic loss in mice may be partly associated with increased BDNF protein level.