Molecular nutrition & food research
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Comparative Study
Amyloid-beta (Aβ₁₋₄₂)-induced paralysis in Caenorhabditis elegans is inhibited by the polyphenol quercetin through activation of protein degradation pathways.
Dietary polyphenols are suggested to play a role in the prevention of Alzheimer's disease, of which accumulation of aggregated beta amyloid (Aβ) is a key histopathological hallmark. We used the transgenic Caenorhabditis elegans strain CL2006, which expresses human Aβ₁₋₄₂ under control of a muscle-specific promoter and responds to Aβ₁₋₄₂ aggregation with paralysis, to test effects of the polyphenol quercetin on the phenotype. ⋯ The proteostasis network, including unfolded protein response, defines the aggregation of Aβ₁₋₄₂ and the associated paralysis phenotype in a nematode model for Alzheimer's disease. The polyphenol quercetin, by specifically activating macroautophagy and proteasomal degradation pathways, proved able to prevent Aβ₁₋₄₂ agregation and paralysis.