A Molecular Communication Perspective of Alzheimer’s Disease: Impact of Amyloid Beta Oligomers on Glutamate Diffusion in the Synaptic Cleft

IF 2.4 Q2 ENGINEERING, ELECTRICAL & ELECTRONIC

IEEE Transactions on Molecular, Biological, and Multi-Scale Communications Pub Date : 2025-03-19 DOI:10.1109/TMBMC.2025.3552959

Nayereh FallahBagheri;Özgür B. Akan

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引用次数: 0

Abstract

Molecular communication (MC) within the synaptic cleft is vital for neurotransmitter diffusion, a process critical to cognitive functions. In Alzheimer’s Disease (AD), beta-amyloid oligomers (A

$\beta $

os) disrupt this communication, leading to synaptic dysfunction. This paper investigates the molecular interactions between glutamate, a key neurotransmitter, and A

$\beta $

os within the synaptic cleft, aiming to elucidate the underlying mechanisms of this disruption. Through stochastic modeling, we simulate the dynamics of A

$\beta $

os and their impact on glutamate diffusion. The findings, validated by comparing simulated results with existing experimental data, demonstrate that A

$\beta $

os serve as physical obstacles, hindering glutamate movement and increasing collision frequency. This impairment of synaptic transmission and long-term potentiation (LTP) by binding to receptors on the postsynaptic membrane is further validated against known molecular interaction behaviors observed in similar neurodegenerative contexts. The study also explores potential therapeutic strategies to mitigate these disruptions. By enhancing our understanding of these molecular interactions, this research contributes to the development of more effective treatments for AD, with the ultimate goal of alleviating synaptic impairments associated with the disease.

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阿尔茨海默病的分子通讯视角：β淀粉样蛋白寡聚物对突触间隙中谷氨酸扩散的影响

突触间隙内的分子通讯（MC）对神经递质扩散至关重要，这是认知功能的关键过程。在阿尔茨海默病（AD）中，β -淀粉样蛋白寡聚物（A $\ β $ os）破坏这种通信，导致突触功能障碍。本文研究了谷氨酸（一种重要的神经递质）与突触间隙中a $\ β $ o之间的分子相互作用，旨在阐明这种破坏的潜在机制。通过随机建模，我们模拟了A $\beta $ os的动态及其对谷氨酸扩散的影响。通过将模拟结果与现有实验数据进行比较，验证了这一发现，表明A $\beta $ o作为物理障碍，阻碍了谷氨酸的运动，增加了碰撞频率。通过与突触后膜上的受体结合，这种突触传递和长期增强（LTP）的损伤在类似神经退行性环境中观察到的已知分子相互作用行为中得到进一步验证。该研究还探索了减轻这些干扰的潜在治疗策略。通过加强我们对这些分子相互作用的理解，本研究有助于开发更有效的阿尔茨海默病治疗方法，最终目标是减轻与该疾病相关的突触损伤。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

IEEE Transactions on Molecular, Biological, and Multi-Scale Communications Mathematics-Modeling and Simulation

CiteScore

3.90

自引率

13.60%

发文量

期刊介绍： As a result of recent advances in MEMS/NEMS and systems biology, as well as the emergence of synthetic bacteria and lab/process-on-a-chip techniques, it is now possible to design chemical “circuits”, custom organisms, micro/nanoscale swarms of devices, and a host of other new systems. This success opens up a new frontier for interdisciplinary communications techniques using chemistry, biology, and other principles that have not been considered in the communications literature. The IEEE Transactions on Molecular, Biological, and Multi-Scale Communications (T-MBMSC) is devoted to the principles, design, and analysis of communication systems that use physics beyond classical electromagnetism. This includes molecular, quantum, and other physical, chemical and biological techniques; as well as new communication techniques at small scales or across multiple scales (e.g., nano to micro to macro; note that strictly nanoscale systems, 1-100 nm, are outside the scope of this journal). Original research articles on one or more of the following topics are within scope: mathematical modeling, information/communication and network theoretic analysis, standardization and industrial applications, and analytical or experimental studies on communication processes or networks in biology. Contributions on related topics may also be considered for publication. Contributions from researchers outside the IEEE’s typical audience are encouraged.