ArticleThe journal of physical chemistry. B2011
Molecular dynamics simulations reveal the protective role of cholesterol in β-amyloid protein-induced membrane disruptions in neuronal membrane mimics.
Article in The journal of physical chemistry. B, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 50 citations in OpenAlex.
- Article
- Article
- Recent Advances in the Treatment and Management of Alzheimer's Disease: A Precision Medicine Perspective.Current topics in medicinal chemistry · 2024Review
- Cholesterol as a key player in amyloid β-mediated toxicity in Alzheimer's disease.Frontiers in molecular neuroscience · 2022Review
- β-Amyloid Peptide: the Cell Compartment Multi-faceted Interaction in Alzheimer's Disease.Neurotoxicity research · 2020Review
- Characterization of Lipid-Protein Interactions and Lipid-Mediated Modulation of Membrane Protein Function through Molecular Simulation.Chemical reviews · 2019Review
- Structure of amyloid βScientific reports · 2019Article
- Ion Channel Formation by Amyloid-β42 Oligomers but Not Amyloid-β40 in Cellular Membranes.The Journal of biological chemistry · 2017Article
- Article
- Maximally asymmetric transbilayer distribution of anionic lipids alters the structure and interaction with lipids of an amyloidogenic protein dimer bound to the membrane surface.Chemistry and physics of lipids · 2016Article
- Lipid insertion domain unfolding regulates protein orientational transition behavior in a lipid bilayer.Biophysical chemistry · 2015Article
- Characterization of 3D Voronoi tessellation nearest neighbor lipid shells provides atomistic lipid disruption profile of protein containing lipid membranes.Biophysical chemistry · 2015Article
- Role of membrane biophysics in Alzheimer's-related cell pathways.Frontiers in neuroscience · 2015Review
- Oxidized cholesterol as the driving force behind the development of Alzheimer's disease.Frontiers in aging neuroscience · 2015Review
- Scaling and alpha-helix regulation of protein relaxation in a lipid bilayer.The Journal of chemical physics · 2014Article
- AβP1-42 incorporation and channel formation in planar lipid membranes: the role of cholesterol and its oxidation products.Journal of bioenergetics and biomembranes · 2013Article
- Molecular interactions of Alzheimer amyloid-β oligomers with neutral and negatively charged lipid bilayers.Physical chemistry chemical physics : PCCP · 2013Article
- Binding to the lipid monolayer induces conformational transition in Aβ monomer.Journal of molecular modeling · 2013Article
- Article
- The role of molecular simulations in the development of inhibitors of amyloid β-peptide aggregation for the treatment of Alzheimer's disease.ACS chemical neuroscience · 2012Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Interactions of β-amyloid (Aβ) peptides with neuronal membranes have been associated with the pathogenesis of Alzheimer's disease (AD); however, the molecular details remain unclear. We used atomistic molecular dynamics (MD) simulations to study the interactions of Aβ(40) and Aβ(42) with model neuronal membranes. The differences between cholesterol-enriched and depleted lipid domains were investigated by the use of model phosphatidylcholine (PC) lipid bilayers with and without 40 mol % cholesterol. A total of 16 independent 200 ns simulation replicates were investigated. The surface area per lipid, bilayer thickness, water permeability barrier, and lipid order parameter, which are sensitive indicators of membrane disruption, were significantly altered by the inserted state of the protein. We conclude that cholesterol protects Aβ-induced membrane disruption and inhibits β-sheet formation of Aβ on the lipid bilayer. The latter could represent a two-dimensional (2D) seeding template for the formation of toxic oligomeric Aβ in the pathogenesis of AD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.