TY - JOUR
T1 - Fucosterol from Sargassum horridum as an amyloid-beta (Aβ1-42) aggregation inhibitor: in vitro and in silico studies
AU - Castro-Silva, Elena Sthephanie
AU - Bello, Martiniano
AU - Rosales-Hernández, Martha Cecilia
AU - Correa-Basurto, José
AU - Hernández-Rodríguez, Maricarmen
AU - Villalobos-Acosta, Daniel
AU - Méndez-Méndez, Juan Vicente
AU - Estrada-Pérez, Alan
AU - Murillo-Álvarez, Jesus
AU - Muñoz-Ochoa, Mauricio
N1 - Publisher Copyright:
© 2020 Informa UK Limited, trading as Taylor & Francis Group.
Copyright:
Copyright 2021 Elsevier B.V., All rights reserved.
PY - 2021
Y1 - 2021
N2 - 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.
AB - 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.
KW - Alzheimer disease
KW - anti-beta amyloid
KW - Molecular docking
KW - molecular modeling
UR - http://www.scopus.com/inward/record.url?scp=85081920300&partnerID=8YFLogxK
U2 - 10.1080/07391102.2020.1729863
DO - 10.1080/07391102.2020.1729863
M3 - Artículo
C2 - 32159448
AN - SCOPUS:85081920300
SN - 0739-1102
VL - 39
SP - 1271
EP - 1283
JO - Journal of Biomolecular Structure and Dynamics
JF - Journal of Biomolecular Structure and Dynamics
IS - 4
ER -