Active Constituents from Drynaria fortunei Rhizomes on the Attenuation of Aβ(25-35)-Induced Axonal Atrophy.

Axonal regeneration might contribute to the restoration of damaged neuronal networks and improvement of memory deficits in a murine Alzheimer's disease (AD) model. A search for axonal regenerative drugs was performed to discover novel therapeutic options for AD. In this study, an aqueous extract of Drynaria fortunei rhizomes reversed Aβ25-35-induced axonal atrophy in cultured cortical neurons of mice. Bioassay-guided fractionation of this extract led to the isolation and identification of compounds 1-5. Among them, (2S)-neoeriocitrin (2) and caffeic acid 4-O-glucoside (4) showed significant axonal elongation effects on Aβ25-35-induced atrophy.