Self-consistent analytical solutions to the kinetics of lipid-induced protein aggregation

The aggregation of proteins into amyloid fibrils is a hallmark of several neurodegenerative disorders, including Parkinson's disease. A growing body of experimental evidence highlights the significant role lipid membranes play in modulating this aggregation process, particularly for proteins such as α-synuclein. Despite this, there has been a lack of quantitative theoretical frameworks capable of describing the kinetics of lipid-induced protein aggregation. In this work, we develop an analytical theoretical model that explicitly incorporates lipid-mediated interactions into the aggregation kinetics. By formulating rate equations in terms of lipid surface coverage and applying a fixed-point analysis, we derive self-consistent solutions for the full timecourse of aggregation. Our model captures both one-step and two-step nucleation mechanisms and enables the prediction of key kinetic observables, including half-times and maximal growth rates. These results provide a quantitative foundation for interpreting experimental data and offer new mechanistic insights into how lipids influence the self-assembly of amyloidogenic proteins.

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Publication Details

Journal
The Journal of Chemical Physics
Published
2025-10-14
DOI
https://doi.org/10.1063/5.0279601
Primary Topic
Alzheimer's disease research and treatments
Type
article
Field-Weighted Citation Impact
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article

Self-consistent analytical solutions to the kinetics of lipid-induced protein aggregation

Thomas C. T. Michaels, Alisdair Stevenson, David Voderholzer
The Journal of Chemical Physics
Alzheimer's disease research and treatments
article

Self-consistent analytical solutions to the kinetics of lipid-induced protein aggregation

Thomas C. T. Michaels, Alisdair Stevenson, David Voderholzer
article en

Abstract

The aggregation of proteins into amyloid fibrils is a hallmark of several neurodegenerative disorders, including Parkinson's disease. A growing body of experimental evidence highlights the significant role lipid membranes play in modulating this aggregation process, particularly for proteins such as α-synuclein. Despite this, there has been a lack of quantitative theoretical frameworks capable of describing the kinetics of lipid-induced protein aggregation. In this work, we develop an analytical theoretical model that explicitly incorporates lipid-mediated interactions into the aggregation kinetics. By formulating rate equations in terms of lipid surface coverage and applying a fixed-point analysis, we derive self-consistent solutions for the full timecourse of aggregation. Our model captures both one-step and two-step nucleation mechanisms and enables the prediction of key kinetic observables, including half-times and maximal growth rates. These results provide a quantitative foundation for interpreting experimental data and offer new mechanistic insights into how lipids influence the self-assembly of amyloidogenic proteins.

The Journal of Chemical PhysicsVol. 163(14)
ETH Zurich (CH), Life Science Zurich (CH)
Openalex Percentile: Top 64%
Alzheimer's disease research and treatments
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