Wong, D.Musgrave, I.Harvey, B.Smid, S.2014-01-022014-01-022013Neuroscience Letters, 2013; 556:221-2260304-39401872-7972http://hdl.handle.net/2440/81631The native South American palm açaí berry (Euterpe oleraceae Mart.) has high polyphenolic and antioxidant levels. This study examined whether açaí berry extract afforded protection against β-amyloid (Aβ)-mediated loss of cell viability and oxidative stress associated with anti-fibrillar effects. PC12 cells were exposed to either Aβ1-42, Aβ25-35 or tert butyl hydroperoxide (t-BHP), alone or in the presence of açaí extract (0.5-50μg/ml). Thioflavin T (ThT) binding assay and transmission electron microscopy were used to determine effects of açaí extract on Aβ1-42 fibril morphology and compared to açaí phenolics gallic acid, cyanidin rutinoside and cyanidin glucoside. Exposure to Aβ1-42, Aβ25-35 or t-BHP decreased PC12 cell viability. Pretreatment with açaí extract significantly improved cell viability following Aβ1-42 exposure, however Aβ25-35 or t-BHP-mediated viability loss was unaltered. Açaí extract inhibited ThT fluorescence and disrupted Aβ1-42 fibril and aggregate morphology. In comparison with other phenolics, açaí was most effective at inhibiting Aβ1-42 aggregation. Inhibition of β-amyloid aggregation may underlie a neuroprotective effect of açaí.en© 2013 Elsevier Ireland Ltd.AçaíAmyloid-βCyanidin glucosideCyanidin rutinosideGallic acidOxidative stressJournal article002013298310.1016/j.neulet.2013.10.0270003285209000442-s2.0-8488752167617350Musgrave, I. [0000-0003-1016-0588]Smid, S. [0000-0003-4192-7219]