Dietary polyphenols as inhibitors of Β-amyloid-evoked neurotoxicity: implications for the treatment of Alzheimer's disease

Abstract

Many polyphenolic compounds derived from plant products have demonstrated neuroprotective properties in variety of in vitro and in vivo settings. Much of these protective effects are ascribed to an antioxidant capacity, but there are additional properties of some types of polyphenols to afford a more direct form of neuronal protection. With a focus on neurodegenerative conditions such as Alzheimer’s disease (AD), the additional actions of polyphenols have been ascribed to the activation of neuronal protective mechanisms or via direct interaction with the toxic beta-amyloid (Aβ) protein associated with Alzheimer’s pathology, or a combination of both. This review highlights recent findings on the pathways of neuroprotection employed by bioactive polyphenols which may directly interface with Aβ fibril and aggregate formation, such as the green tea flavonoid (–)-epigallocatechin-3-gallate (EGCG) and the phytoalexin resveratrol. Targeted studies on the biomolecular interactions between such polyphenolics and Aβ may enable not just an improved understanding of the role of β- amyloid in neurodegenerative diseases, but also offer a new horizon to the treatment of Alzheimer’s disease and other amyloidoses.