Fucosterol from Sargassum horridum as an amyloid-beta (Aβ_1-42) aggregation inhibitor: in vitro and in silico studies

Abstract

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 Aβ_1-42 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 Aβ_1-42, suggesting that fucosterol could affect amyloid-beta (Aβ_1-42) aggregation by preventing the formation of oligomers, preventing the development of AD.

Communicated by Ramaswamy H. Sarma

Keywords:

• Molecular docking
• molecular modeling
• Alzheimer disease
• anti-beta amyloid

Acknowledgements

We also want to thank the support received by Centro de nanociencias y Micro y Nanotecnologías del IPN-México for chemical characterization.

Disclosure statement

There are no conflicts to declare.

Additional information

Funding

This work was supported by CONACYT, Mexico (A1-S-21278, 286653, 254600), and Proyecto Insignia 2015 IPN.