细胞因子风暴诱发脱髓鞘的神经元信号影响的硅学建模。

IF 4.5 3区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Open Biology Pub Date : 2024-09-01 Epub Date: 2024-09-04 DOI:10.1098/rsob.240138
Geoflly L Adonias, Harun Siljak, Sasitharan Balasubramaniam, Michael Taynnan Barros
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引用次数: 0

摘要

在这项研究中,我们建立了一个神经元在细胞因子风暴引起的脱髓鞘作用下行为的硅学模型,以研究病毒感染对大脑的影响。我们使用一个综合模型来测量细胞因子诱导的脱髓鞘如何影响神经元内动作电位(AP)信号的传播。我们运用信息和通信理论分析了不同脱髓鞘水平下神经元-神经元通信的影响。我们的模拟结果表明,病毒引起的变性会对信号功率和尖峰率产生影响,从而损害神经元之间的信息传播和处理。我们提出了一个传递函数来模拟对 AP 的削弱效应。我们的研究结果表明,细胞因子风暴诱发的脱髓鞘不仅会降低信号,还会损害信号在轴突内的传播。我们提出的硅学模型可以分析病毒诱导的神经变性,加深我们对病毒诱导的脱髓鞘的理解。
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In silico modelling of neuron signal impact of cytokine storm-induced demyelination.

In this study, we develop an in silico model of a neuron's behaviour under demyelination caused by a cytokine storm to investigate the effects of viral infections in the brain. We use a comprehensive model to measure how cytokine-induced demyelination affects the propagation of action potential (AP) signals within a neuron. We analysed the effects of neuron-neuron communications by applying information and communication theory at different levels of demyelination. Our simulations demonstrate that virus-induced degeneration can play a role in the signal power and spiking rate, which compromise the propagation and processing of information between neurons. We propose a transfer function to model the weakening effects on the AP. Our results show that demyelination induced by a cytokine storm not only degrades the signal but also impairs its propagation within the axon. Our proposed in silico model can analyse virus-induced neurodegeneration and enhance our understanding of virus-induced demyelination.

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来源期刊
Open Biology
Open Biology BIOCHEMISTRY & MOLECULAR BIOLOGY-
CiteScore
10.00
自引率
1.70%
发文量
136
审稿时长
6-12 weeks
期刊介绍: Open Biology is an online journal that welcomes original, high impact research in cell and developmental biology, molecular and structural biology, biochemistry, neuroscience, immunology, microbiology and genetics.
期刊最新文献
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