Background : It is well known that Alzheimer`s disease (AD) is associated with neuronal loss and accumulation of extracellular senile plaque, whose major constituent is β-amyloid peptide (Aβ). In cell cultures, Aβ can directly stimulate neuronal cell death and make neurons susceptible to excitotoxicity which may include glutamate release and N-methyl-D-aspartate (NMDA) receptor activation. There are numerous reports in the literature of Cedrela sinensis (CS) for pro-apoptotic effects. It was hypothesized that CS might protect neurons against neurodegeneration in AD due to its pro-apoptotic effects. The current study aimed to determine the protective effect of ethanol extract from the leave of CS on Aβ (25-35)-induced neuronal cell death in primary cultured rat cortical neurons. Methods and Results : Cerebral neurons were collected from embryonic day 15 SD rat fetuses and were cultured on DMEM with serum. Neurotoxicity experiments were proceeded on cultured neurons after 4-5 days in vitro. Cultured neurons were treated with 10 μM Aβ (25-35) for 24 h or 1 mM NMDA for 20 h to induce neuronal death. CS was applied 20 min before the treatment with Aβ (25-35) or NMDA and also present in the medium during the incubations. Colorimetric MTT assay and Hoechst 33342 staining were used to estimate viability of neurons. Western blot analysis was carried out to examine the expression levels of anti-apoptotic and pro-apoptotic proteins. CS (5 and 10 ㎍/㎖) significantly inhibited Aβ (25-35)-induced apoptotic neuronal cell death in cultured cortical neurons. CS also inhibited Aβ (25-35)-induced change of apoptosis-related protein expression in western blot analysis. Furthermore CS (5 and 10 ㎍/㎖) reuduced NMDA-induced neuronal cell death. This study demonstrated that NMDA glutamate receptor activation is related with Aβ (25-35)-induced neuronal apoptotic death. Conclusion : CS protected culterd neurons against Aβ (25-35)-induced neurotoxicity probably via inhibition of NMDA receptor activation. These results suggest that CS can prevent the progression of neurodegenerative disease such as Alzheimer's disease.