肥胖诱发阿尔茨海默病的反应-扩散模型中全局吸引子的存在及其控制策略

IF 3.4 2区 数学 Q1 MATHEMATICS, APPLIED
Ranjit Kumar Upadhyay , Debasish Pradhan , Rana D. Parshad , Parimita Roy
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引用次数: 0

摘要

有证据表明,肥胖、糖尿病和衰老会明显增加患老年痴呆症(如阿尔茨海默病)等痴呆症相关疾病的易感性。本文探讨了肥胖、糖尿病和老年痴呆症之间的相关性。文章介绍了一个扩散驱动模型,其中包含葡萄糖动态、胰岛素水平、β细胞、小胶质细胞、细胞因子、淀粉样蛋白-β斑块、神经纤维缠结(τ斑块)、神经变性和认知能力下降等变量。该研究包括稳定性分析(局部和全局),通过显示扩散驱动模型存在全局吸引子来检验有界性和长期行为。利用部分等级相关系数(PRCC)进行的全局敏感性分析确定了对 Aβ 斑块生长、τ 斑块和神经退化产生敏感影响的因素。确定性模型解决方案展示了时空动态,揭示了肥胖与阿尔茨海默氏症之间的联系,阿尔茨海默氏症的特征是明显的斑块模式。虽然阿尔茨海默氏症无法治愈,但采用优化控制技术有助于减轻其影响,提高患者的生活质量。研究提出了一个针对阿兹海默症管理的最优控制问题,优化了疾病管理的多个方面。该研究强调了长期健康生活方式和定制的抗淀粉样蛋白疗法在显著延缓肥胖引起的注意力缺失症进展方面的功效。这项研究揭示了肥胖与阿尔茨海默氏症之间的联系,强调了促炎性小胶质细胞对认知能力下降的负面影响,同时提出了控制策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Existence of global attractor in reaction–diffusion model of obesity-induced Alzheimer’s disease and its control strategies
Evidence suggests that obesity, diabetes, and aging notably increase susceptibility to dementia-related conditions such as Alzheimer’s disease (AD). This article explores the correlations between obesity, diabetes, and AD. It introduces a diffusion-driven model encompassing variables like glucose dynamics, insulin levels, beta cells, microglia, cytokines, amyloid-β plaques, neurofibrillary tangles (τ plaques), neurodegeneration, and cognitive decline. The study includes stability analysis (local and global), examining boundedness and long-time behavior via showing the existence of a global attractor for the diffusion-driven model. A global sensitivity analysis, utilizing the Partial Rank Correlation Coefficient (PRCC), identifies factors sensitively impacting Aβ plaque growth, τ plaques, and neurodegeneration. The deterministic model solution illustrates spatiotemporal dynamics, revealing a link between obesity and Alzheimer’s, which is characterized by distinct patchy patterns. While Alzheimer’s has no cure, employing optimal control techniques can help alleviate its effects and enhance affected individuals’ quality of life. An optimal control problem for AD management is developed, optimizing multiple aspects of disease management. The study highlights the efficacy of long-term healthy lifestyle practices and customized anti-amyloid therapy in significantly delaying obesity-induced AD progression. This research sheds light on the connection between obesity and Alzheimer’s, underscoring the negative impact of pro-inflammatory microglia on cognitive decline while proposing control strategies.
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来源期刊
Communications in Nonlinear Science and Numerical Simulation
Communications in Nonlinear Science and Numerical Simulation MATHEMATICS, APPLIED-MATHEMATICS, INTERDISCIPLINARY APPLICATIONS
CiteScore
6.80
自引率
7.70%
发文量
378
审稿时长
78 days
期刊介绍: The journal publishes original research findings on experimental observation, mathematical modeling, theoretical analysis and numerical simulation, for more accurate description, better prediction or novel application, of nonlinear phenomena in science and engineering. It offers a venue for researchers to make rapid exchange of ideas and techniques in nonlinear science and complexity. The submission of manuscripts with cross-disciplinary approaches in nonlinear science and complexity is particularly encouraged. Topics of interest: Nonlinear differential or delay equations, Lie group analysis and asymptotic methods, Discontinuous systems, Fractals, Fractional calculus and dynamics, Nonlinear effects in quantum mechanics, Nonlinear stochastic processes, Experimental nonlinear science, Time-series and signal analysis, Computational methods and simulations in nonlinear science and engineering, Control of dynamical systems, Synchronization, Lyapunov analysis, High-dimensional chaos and turbulence, Chaos in Hamiltonian systems, Integrable systems and solitons, Collective behavior in many-body systems, Biological physics and networks, Nonlinear mechanical systems, Complex systems and complexity. No length limitation for contributions is set, but only concisely written manuscripts are published. Brief papers are published on the basis of Rapid Communications. Discussions of previously published papers are welcome.
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