Amyloid-β (Aβ42) Peptide Aggregation Rate and Mechanism on Surfaces with Widely Varied Properties: Insights from Brownian Dynamics Simulations.

ABSTRACT: Amyloid-β (Aβ) plaques, which form by aggregation of harmless Aβ peptide monomers into larger fibrils, are characteristic of neurodegenerative disorders such as Alzheimer's disease. Efforts to treat Alzheimer's disease focus on stopping or reversing the aggregation process that leads to fibril formation. However, effective treatments are elusive due to certain unknown aspects of the process. Many hypotheses point to disruption of cell membranes by adsorbed Aβ monomers or oligomers, but how Aβ behaves and aggregates on surfaces of widely varying properties, such as those present in a cell, is unclear. Elucidating the effects of various surfaces on the dynamics of Aβ and the kinetics of the aggregation process from bulk solution to a surface-adsorbed multimer can help identify what drives ag

SUBMITTER: Cholko T 

PROVIDER: S-EPMC7797022 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature