Although Polygala tenuifolia WILLD (PT) was classically mentioned as an anti-dementia drug in Chinese and Japanese traditional medicine, basic research showed only enhancement of the cholinergic function. In Alzheimer's disease, neuritic atrophy and synaptic loss occur prior to neuronal death event, and may be the first trigger of the memory impairment. Therefore, we studied effects of Polygala tenuifolia WILLD (PT) on Aβ(25—35)-induced neuronal damage using rat cortical neurons for characterization of activities of PT under Aβ-induced neuronal damage. Treatment with the water extract of PT enhanced axonal length dose-dependently after Aβ(25—35)-induced axonal atrophy. However, dendritic atrophy and synaptic loss induced by Aβ(25—35) were not recovered by treatment with PT extract. In contrast, Aβ(25—35)-induced cell damage was completely inhibited by PT extract. By characterization of PT effects on neuronal morphological plasticity and cell damage, usefulness as well as an insufficiency of PT as an anti-dementia drug was clarified.