A qualitative analysis of a A$\beta$-monomer model with inflammation processes for Alzheimer's disease

TL;DR

This paper introduces a new mathematical model for Alzheimer's disease that incorporates inflammation and protein interactions, revealing critical thresholds for disease progression and potential treatment strategies.

Contribution

The study develops a simplified spatially-homogeneous model capturing key interactions and identifies inflammation as a crucial factor with hysteresis effects influencing disease persistence.

Findings

Inflammation acts as a critical threshold for disease progression.

Hysteresis indicates long-term effects of initial inflammation levels.

Numerical simulations demonstrate the impact of initial conditions on disease outcome.

Abstract

We introduce and study a new model for the progression of Alzheimer's disease incorporating the interactions of A$\beta$-monomers, oligomers, microglial cells and interleukins with neurons through different mechanisms such as protein polymerization, inflammation processes and neural stress reactions. In order to understand the complete interactions between these elements, we study a spatially-homogeneous simplified model that allows to determine the effect of key parameters such as degradation rates in the asymptotic behavior of the system and the stability of equilibriums. We observe that inflammation appears to be a crucial factor in the initiation and progression of Alzheimer's disease through a phenomenon of hysteresis, which means that there exists a critical threshold of initial concentration of interleukins that determines if the disease persists or not in the long term. These results give perspectives on possible anti-inflammatory treatments that could be applied to mitigate the progression of Alzheimer's disease. We also present numerical simulations that allow to observe the effect of initial inflammation and concentration of monomers in our model.