| Abstract
| - β-Amyloid (βA)-induced oxidative toxicity on neuronal cells is a principal route in Alzheimer's disease(AD), and its toxicity occurs after fibril formation. Inhibitory or promoting effects of naturally occurringcompounds on βA fibril formation were evaluated. Among 214 tested compounds, curcuminoids,flavone type flavonoids, and naphthoquinones were shown to be potent inhibitors of βA fibrilization.The addition of the curcuminoids, curcumin, demethoxycurcumin, and bisdemethoxycurcumin stronglyinhibited βA fibril formation. Flavonoids such as quercetin, rhamnetin, and fisetin strongly inhibitedβA fibril formation. Limonoids, cinnamic acids, and catechins enhanced fibril formation in vitro.Anthothecol possessed the most enhancing activity on fibril formation of the compounds tested. Onthe other hand, it was found that curcuminoids showed cytotoxicity with the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide assay and did not protect HT22 murine neuroblastoma cellsfrom βA(25−35) insult. Two flavone type flavonoids, morin and quercetin, exhibited no cytotoxicityand strongly protected HT22 murine neuroblastoma cells from βA(25−35) oxidative attack.Conclusively, morin or quercetin could be a key molecule for the development of therapeutics forAD. Keywords: Curcumioids; flavonoids; Alzheimer's disease; β-amyloid; HT22 murine neuroblastoma cell;bA burden assay
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