The　effects　of　ginsenosides　were　thought　to　prevent　neurodegenerative　processes　associated　with　aging.　The　accumulation　of　beta-amyloid　protein　(A　beta)　within　the　brain　is　one　of　the　pathological　hallmarks　of　Alzheimer＇s　disease　(AD).　There　is　no　one　effective　treatment　of　AD.　To　investigate　the　effects　of　ginsenoside　Rb1　(GRb1)　on　neuronal　damage　induced　by　A　beta　and　potential　mechanisms　of　the　effects　of　GRb1　in　vitro,　morphological　observation　and　biochemical　analysis　combining　primary　cultured　neurons　were　adopted.　A　positive　control　was　pre-treated　with　Trolox.　Neurons　that　were　treated　with　A　beta　1-42　(2　mu　M)　were　shrunken　perikaryon　with　loss　of　neurite　processes;　the　survival　rate　of　neurons　decreased　almost　to　50%　(p　＜　0.01).　Lactate　dehydrogenase　(LDH)　release,　malondialdehyde　(MDA)　product　and　superoxide　dismutase　(SOD)　activity　level　all　increased　obviously　(p　＜　0.01　or　p　＜　0.05).　However,　neurons　pre-treated　with　GRb1　(0.1,　1　and　10　mu　M)　or　Trolox　(10　mM)　had　a　survival　rate　increase　compared　with　neurons　treated　with　A　beta　alone;　LDH　release　and　MDA　product　decreased　distinctly,　and　the　increase　in　SOD　activity　in　A　beta-treated　neurons　was　attenuated　evidently　(p　＜　0.01　or　p　＜　0.05).　Thus,　we　conclude　that　GRb1　exerted　neuroprotection　obviously.　GRb1　protected　neurons　against　the　toxicity　of　A　beta,　most　likely　through　an　antioxidant　pathway.　GRb1　could　be　useful　neuroprotective　agents　of　AD.　[Neurol　Res　2009;　31:　663-667]