@article{uneatlantico656, journal = {Antioxidants}, title = {An Olive-Derived Extract 20\% Rich in Hydroxytyrosol Prevents {\ensuremath{\beta}}-Amyloid Aggregation and Oxidative Stress, Two Features of Alzheimer Disease, via SKN-1/NRF2 and HSP-16.2 in Caenorhabditis elegans}, year = {2022}, number = {4}, volume = {11}, author = {Jose M. Romero-M{\'a}rquez and Mar{\'i}a D. Navarro-Hortal and Victoria Jim{\'e}nez-Trigo and Pedro Mu{\~n}oz-Ollero and Tamara Y. Forbes-Hern{\'a}ndez and Adelaida Esteban-Mu{\~n}oz and Francesca Giampieri and Irene Delgado Noya and Pedro Bull{\'o}n and Laura Vera-Ram{\'i}rez and Maurizio Battino and Cristina S{\'a}nchez-Gonz{\'a}lez and Jos{\'e} L. Quiles}, pages = {629}, month = {Marzo}, keywords = {age-related diseases; antioxidants; HSP-16.2; neuroprotection; Olea europaea; olive by-products; polyphenols; RNAi; tau protein}, url = {http://repositorio.uneatlantico.es/id/eprint/656/}, abstract = {Olive milling produces olive oil and different by-products, all of them very rich in different bioactive compounds like the phenolic alcohol hydroxytyrosol. The aim of the present study was to investigate the effects of an olive fruit extract 20\% rich in hydroxytyrosol on the molecular mechanisms associated with Alzheimer disease features like A{\ensuremath{\beta}}- and tau- induced toxicity, as well as on oxidative stress in Caenorhabditis elegans. Moreover, characterization of the extracts, regarding the profile and content of phenolics, as well as total antioxidant ability, was investigated. The study of lethality, growth, pharyngeal pumping, and longevity in vivo demonstrated the lack of toxicity of the extract. One hundred {\ensuremath{\mu}}g/mL of extract treatment revealed prevention of oxidative stress and a delay in A{\ensuremath{\beta}}-induced paralysis related with a lower presence of A{\ensuremath{\beta}} aggregates. Indeed, the extract showed the ability to avoid a certain degree of proteotoxicity associated with aggregation of the tau protein. According to RNAi tests, SKN-1/NRF2 transcription factor and the overexpression of HSP-16.2 were mechanistically associated in the observed effects} }