Açaí (Euterpe oleraceae Mart.) berry extract exerts neuroprotective effects against β-amyloid exposure in vitro

- Açaí extract inhibited neurotoxicity following Aβ1-42 exposure in PC12 cells.
- Açaí extract inhibited Aβ1-42 fibril and aggregate formation in vitro.
- Açaí extract did not provide significant protection against oxidative stress.
- Açaí may have neuroprotective potential in Alzheimer's disease.

The 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 (0.5-50 μg/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.