Neuron Signal Propagation Analysis of Cytokine-Storm induced Demyelination

TL;DR

This study models how cytokine storm-induced demyelination affects neuron signal propagation, revealing potential impacts on neural communication and proposing a transfer function for virus-related neurodegeneration analysis.

Contribution

It introduces a novel simulation framework and transfer function to analyze virus-induced demyelination effects on neuronal signal transmission.

Findings

Demyelination reduces signal power and spiking rate.

It affects neurotransmitter release probability.

The transfer function models signal attenuation due to demyelination.

Abstract

The COVID-19 pandemic has shaken the world unprecedentedly, where it has affected the vast global population both socially and economically. The pandemic has also opened our eyes to the many threats that novel virus infections can pose for humanity. While numerous unknowns are being investigated in terms of the distributed damage that the virus can do to the human body, recent studies have also shown that the infection can lead to lifelong sequelae that could affect other parts of the body, and one example is the brain. As part of this work, we investigate how viral infection can affect the brain by modelling and simulating a neuron's behaviour under demyelination that is affected by the cytokine storm. We quantify the effects of cytokine-induced demyelination on the propagation of action potential signals within a neuron. We used information and communication theory analysis on the signal propagated through the axonal pathway under different intensity levels of demyelination to analyse these effects. Our simulations demonstrate that virus-induced degeneration can play a role in the signal power and spiking rate and the probability of releasing neurotransmitters and compromising the propagation and processing of information between the neurons. We also propose a transfer function that models these attenuation effects that degenerates the action potential, where this model has the potential to be used as a framework for the analysis of virus-induced neurodegeneration that can pave the way to improved understanding of virus-induced demyelination.