Alzheimer's disease(AD) is primarily characterized by neurofibrillary tangles, senile plaques, and neurodegeneration. The major component of senile plaques is the beta-amyloid peptide(A β), Which is considered to have a causal role in AD. However, the biological activities of Aβ in AD has not been clearly defined. In this study we have investigated the effects of Aβ 25-35 fragment to neurons using organotypic hippocampal slice culture system which maintained intact hippocampal synaptic circuit and anatomy. Hippocampal slice culture is prepared from rat postnatal 10-old days and after 14 days culture, slices were treated with 10uM Aβ 25-35 fragment. Neuronal death was measured with propidium iodide(PI) uptake and NeuN, neuronal marker, staining. After treatment of Aβ 25-35 fragment for 3days or 7days on hippocampal slice culture, we observed the increased PI uptake and the decreased number of NeuN-stained neuron in CA1 region of hippocampal pyramidal layer or dentate gyrus. These results suggested that Aβ 25-35 fragment exerts the neurotoxicity in hippocampal slice culture.