Inhibitory mechanisms of amentoflavone on amyloid-β peptide aggregation revealed by replica exchange molecular dynamics

Abstract Amyloid-β (Aβ) aggregation is a central pathological hallmark of Alzheimer’s disease, with soluble trimers recognized as particularly neurotoxic species. Amentoflavone (AMF), a natural biflavonoid compound, has shown strong inhibitory effects on Aβ aggregation. However, its underlying molec...

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Main Authors: Suxia Wu, Chang Liu, Yang Li, Xiaoyu Zhang, Qianji Han, Heng Zhao, Kun Zhao, Yaru Dang, Ruihan Wang, Shitao Song
Format: Article
Language:English
Published: Nature Portfolio 2025-07-01
Series:Scientific Reports
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Online Access:https://doi.org/10.1038/s41598-025-10623-9
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author Suxia Wu
Chang Liu
Yang Li
Xiaoyu Zhang
Qianji Han
Heng Zhao
Kun Zhao
Yaru Dang
Ruihan Wang
Shitao Song
author_facet Suxia Wu
Chang Liu
Yang Li
Xiaoyu Zhang
Qianji Han
Heng Zhao
Kun Zhao
Yaru Dang
Ruihan Wang
Shitao Song
author_sort Suxia Wu
collection DOAJ
description Abstract Amyloid-β (Aβ) aggregation is a central pathological hallmark of Alzheimer’s disease, with soluble trimers recognized as particularly neurotoxic species. Amentoflavone (AMF), a natural biflavonoid compound, has shown strong inhibitory effects on Aβ aggregation. However, its underlying molecular mechanism remains poorly understood. In this study, we employed replica exchange molecular dynamics (REMD) and molecular mechanics/Poisson–Boltzmann surface area (MM/PBSA) method to elucidate the interaction between AMF and Aβ peptides. Our results reveal that AMF preferentially binds to the 16KLVFFAEDV24 segment, a hydrophobic core that plays a critical role in the initiation of aggregation. It disrupts b-sheet formation through hydrophobic interactions with Leu-17, Phe-20, and Val-24. This binding stabilizes disordered coil conformations and prevents the conformational transitions required for fibril formation. Based on these findings, we performed structure-based virtual screening and identified two natural product-derived candidates with higher predicted affinity. These insights provide an atomic-level understanding of AMF’s inhibitory mechanism and support the rational design of natural product-inspired inhibitors that target Aβ aggregation.
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publishDate 2025-07-01
publisher Nature Portfolio
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spelling doaj-art-d1c895a3d0124aa1a2fec68a75a747bd2025-08-20T03:46:01ZengNature PortfolioScientific Reports2045-23222025-07-0115111410.1038/s41598-025-10623-9Inhibitory mechanisms of amentoflavone on amyloid-β peptide aggregation revealed by replica exchange molecular dynamicsSuxia Wu0Chang Liu1Yang Li2Xiaoyu Zhang3Qianji Han4Heng Zhao5Kun Zhao6Yaru Dang7Ruihan Wang8Shitao Song9Hebei Normal University of Science and TechnologyHebei Normal University of Science and TechnologyHebei Normal University of Science and TechnologyDepartment of Digital Information, Hebei Institute of International Business and EconomicsHebei Normal University of Science and TechnologyHebei Normal University of Science and TechnologyHebei Normal University of Science and TechnologyHebei Normal University of Science and TechnologyHebei Normal University of Science and TechnologyHebei Normal University of Science and TechnologyAbstract Amyloid-β (Aβ) aggregation is a central pathological hallmark of Alzheimer’s disease, with soluble trimers recognized as particularly neurotoxic species. Amentoflavone (AMF), a natural biflavonoid compound, has shown strong inhibitory effects on Aβ aggregation. However, its underlying molecular mechanism remains poorly understood. In this study, we employed replica exchange molecular dynamics (REMD) and molecular mechanics/Poisson–Boltzmann surface area (MM/PBSA) method to elucidate the interaction between AMF and Aβ peptides. Our results reveal that AMF preferentially binds to the 16KLVFFAEDV24 segment, a hydrophobic core that plays a critical role in the initiation of aggregation. It disrupts b-sheet formation through hydrophobic interactions with Leu-17, Phe-20, and Val-24. This binding stabilizes disordered coil conformations and prevents the conformational transitions required for fibril formation. Based on these findings, we performed structure-based virtual screening and identified two natural product-derived candidates with higher predicted affinity. These insights provide an atomic-level understanding of AMF’s inhibitory mechanism and support the rational design of natural product-inspired inhibitors that target Aβ aggregation.https://doi.org/10.1038/s41598-025-10623-9Amyloid-β aggregationAmentoflavoneMolecular dynamics simulationAggregation Inhibition mechanismVirtual screening
spellingShingle Suxia Wu
Chang Liu
Yang Li
Xiaoyu Zhang
Qianji Han
Heng Zhao
Kun Zhao
Yaru Dang
Ruihan Wang
Shitao Song
Inhibitory mechanisms of amentoflavone on amyloid-β peptide aggregation revealed by replica exchange molecular dynamics
Scientific Reports
Amyloid-β aggregation
Amentoflavone
Molecular dynamics simulation
Aggregation Inhibition mechanism
Virtual screening
title Inhibitory mechanisms of amentoflavone on amyloid-β peptide aggregation revealed by replica exchange molecular dynamics
title_full Inhibitory mechanisms of amentoflavone on amyloid-β peptide aggregation revealed by replica exchange molecular dynamics
title_fullStr Inhibitory mechanisms of amentoflavone on amyloid-β peptide aggregation revealed by replica exchange molecular dynamics
title_full_unstemmed Inhibitory mechanisms of amentoflavone on amyloid-β peptide aggregation revealed by replica exchange molecular dynamics
title_short Inhibitory mechanisms of amentoflavone on amyloid-β peptide aggregation revealed by replica exchange molecular dynamics
title_sort inhibitory mechanisms of amentoflavone on amyloid β peptide aggregation revealed by replica exchange molecular dynamics
topic Amyloid-β aggregation
Amentoflavone
Molecular dynamics simulation
Aggregation Inhibition mechanism
Virtual screening
url https://doi.org/10.1038/s41598-025-10623-9
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