Alzheimer's disease (AD) is a neurodegenerative disease, which accompanied with memory decline and cognitive dysfunction. Aggregated amyloid β formation and accumulation has been suggested to be one of the underlying mechanisms of the pathophysiology of AD. Based on this hypothesis of AD pathophysiology, we had done screening to identify compound, which can ameliorate amyloid β aggregation using library derived from plant compounds. Based on this screening, we found that alkannin has chemical chaperone activity, which may be able to inhibit amyloid β aggregation. In the present study, we investigated pharmacological action of alkannin on amyloid β aggregation and neuronal cell death. Using circular dichroism (CD) spectra analysis, we found that alkannin may be able to inhibit β-sheet structure formation. Electron microscope analysis indicate that alkannin may also inhibit amyloid β fibril formation. Furthermore, alkannin attenuated amyloid β-induced neuronal cell death in PC12 cell line. Finally, alkannin ameliorated chemotaxis of AD model of Caenorhabditis elegans (C. elegans), suggesting that alkannin may be able to inhibit neurodegeneration at the C. elegans of AD model. Overall, these results suggest that alkannin may be able to inhibit amyloid β aggregation and neuronal cell death in AD.