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对阿尔茨海默病炎症过程的A单体模型的定性分析。

A qualitative analysis of an A-monomer model with inflammation processes for Alzheimer's disease.

作者信息

Ciuperca Ionel, Pujo-Menjouet Laurent, Matar-Tine Leon, Torres Nicolas, Volpert Vitaly

机构信息

CNRS, Ecole Centrale de Lyon, Université Jean Monnet, Universite Claude Bernard Lyon 1, ICJ UMR5208, INSA Lyon, Lyon, Villeurbanne 69622, France.

Departamento de Matemática Aplicada, Universidad de Granada, Granada, Andalusia, Spain.

出版信息

R Soc Open Sci. 2024 May 15;11(5):231536. doi: 10.1098/rsos.231536. eCollection 2024 May.

DOI:10.1098/rsos.231536
PMID:39076807
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11285901/
Abstract

We introduce and study a new model for the progression of Alzheimer's disease (AD) incorporating the interactions of A -monomers, oligomers, microglial cells and interleukins with neurons through different mechanisms such as protein polymerization, inflammation processes and neural stress reactions. To understand the complete interactions between these elements, we study a spatially homogeneous simplified model that allows us to determine the effect of key parameters such as degradation rates in the asymptotic behaviour of the system and the stability of equilibrium. We observe that inflammation appears to be a crucial factor in the initiation and progression of AD through a phenomenon of hysteresis with respect to the oligomer degradation rate . This means that depending on the advanced state of the disease (given by the value of the A -monomer degradation rate : large value for an early stage and low value for an advanced stage) 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 AD. We also present numerical simulations that allow us to observe the effect of initial inflammation and monomer concentration in our model.

摘要

我们引入并研究了一种阿尔茨海默病（AD）进展的新模型，该模型通过蛋白质聚合、炎症过程和神经应激反应等不同机制，纳入了Aβ单体、寡聚体、小胶质细胞和白细胞介素与神经元之间的相互作用。为了理解这些元素之间的完整相互作用，我们研究了一个空间均匀的简化模型，该模型使我们能够确定关键参数（如降解率）对系统渐近行为和平衡稳定性的影响。我们观察到，通过关于寡聚体降解率的滞后现象，炎症似乎是AD起始和进展的关键因素。这意味着，根据疾病的进展状态（由Aβ单体降解率的值给出：早期值大，晚期值小），存在白细胞介素初始浓度的临界阈值，该阈值决定了疾病是否会长期持续。这些结果为可能用于减轻AD进展的抗炎治疗提供了思路。我们还给出了数值模拟，使我们能够观察模型中初始炎症和单体浓度的影响。

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本文引用的文献

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Anti-inflammatories in Alzheimer's disease-potential therapy or spurious correlate?阿尔茨海默病中的抗炎药物——潜在疗法还是虚假关联？
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Inflammation as a central mechanism in Alzheimer's disease.炎症作为阿尔茨海默病的核心机制。
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