The number of patients diagnosed with Alzheimer's disease (AD) increases each year, and there are currently few treatment strategies to decrease the symptoms of AD; furthermore, these strategies are not sufficient to reduce memory loss in AD patients. In this work, in vitro and in silico studies were performed to evaluate the effects of fucosterol, which was extracted from an algal source and characterized by liquid chromatography-mass spectra (LC-MS), as an inhibitor of Aβ1-42 aggregation. Experimental studies, including protein gel electrophoresis, atomic force microscopy and fluorescence studies with thioflavin T (ThT), highlighted that fucosterol can decrease oligomer formation more than galantamine, which was used as a positive control. Docking and molecular dynamics simulations coupled with an MMGBSA approach showed that fucosterol is capable of recognizing the hydrophobic regions of monomeric Aβ1-42, suggesting that fucosterol could affect amyloid-beta (Aβ1-42) aggregation by preventing the formation of oligomers, preventing the development of AD.Communicated by Ramaswamy H. Sarma.
Keywords: Alzheimer disease; Molecular docking; anti-beta amyloid; molecular modeling.