This study is aimed to investigate the signal transduction pathway of amyloid β peptide (Aβ)-induced neuronal toxicity and the inhibitory effects of epigallocatechin gallate (EGCG), one of the major constituents of green-tea and the potent anti-oxidant, on the nerve cell damage in PC12 cells. Cellular toxicity was estimated by MTT assay and observation of morphological changes in PC12 cells. By using the methods such as measurement of Reactive Oxygen Species (ROS), western blot and RT-PCR, the underlying mechanisms and signal transduction pathway of Aβ-induced neurotoxicity and the inhibitory effects of EGCG were examined. Aβ-induced cellular toxicity was found in a dose dependent manner. This is confirmed by morphological observations of cultured cells such as findings of cell death similar to apoptosis. Aβ-induced neurotoxicity was effectively inhibited by EGCG pretreatment. Moreover, EGCG reduced ROS as same potent as the NAC (N-acetyl cystein), the ROS scavenger. Among the several process of signal transduction for cell death, a intracytoplasmic cytochrome c, the protein associated with the mitochondria-dependent pathway, was increased from 12 hours after Aβ treatment and the increased cytochrome c by Aβ was blocked by EGCG. Expression levels of Bax/Bcl-2 in relation to intracytoplasmic release of cytochrome c were examined by RT-PCR. Aβ up-regulated Bax expression but did not affect Bcl-2 expression. EGCG was found to block the effect of Aβ-induced Bax increase. From these results, it is speculated that Aβ-induced neuronal toxicity may be assumed to be affected by ROS and the mitochondria-dependent pathway of cell death as well. EGCG, besides having the role of anti-oxidant, is found to have a protective effect against Aβ-induced neurotoxicity through the inhibition of the expression of the protein associated with the mitochondria-dependent cell death pathway.