Effect of goji berry on the formation of extracellular senile plaques of Alzheimer's disease

BACKGROUND: Alzheimer's disease (AD) is the most common neurodegenerative disease and a major source of morbidity and mortality. Currently, no therapy nor drug can cure or modify AD progression, but recent studies suggest that nutritional compounds in certain foods can delay or prevent the onset of AD. Diets with high antioxidants is one of the examples which is believed to influence AD pathogenesis through direct effect on amyloid beta levels. Compared to other fruits and vegetables, goji berry (GB) has high levels of polyphenolic substances with antioxidant activities which have shown some positive effects on cognitive function while its mechanism on neuroprotection is yet to be explored. We investigated whether GB would decrease the quantity of amyloid beta in cell culture model of AD. OBJECTIVE: To assess the protective effects of GB against amyloid beta toxicity in M17 cells using different techniques. METHODS: Goji berry powder (GBP) at different concentrations was treated with 20 μM amyloid beta-induced neuronal cells. MTS assay (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxy-phenyl)-2-(4-sulfophenyl)-2H-tetrazolium), bicinchoninic acid (BCA) assay, Western blot analysis, enzyme-linked immunosorbent assay (ELISA) and atomic force microscopy (AFM) were performed to identify how GB affected amyloid beta. RESULTS: MTS assay indicated that GBP significantly increased cell viability up to 105% when GBP was at 1.2 μg/ mL. Western blot showed significant reduction of amyloid beta up to 20% in cells treated with 1.5 μg/ mL GBP. GBP at 1.5 μg/ mL was the most effective concentration with 17% reduction of amyloid beta in amyloid beta-induced neuronal cells compared to control (amyloid beta only) based on ELISA results. AFM images further confirmed increasing GBP concentration led to decreased aggregation of amyloid beta. CONCLUSION: GB can be a promising anti-aging agent and warrants further investigating due to its effect on reduction of amyloid beta toxicity