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.

Analysis of the Information Capacity of Neuronal Molecular Communications Under Demyelination and Remyelination.

Demyelination of neurons can compromise the communication performance between the cells as the absence of myelin attenuates the action potential propagated through the axonal pathway. In this work, we propose a hybrid experimental and simulation model for analyzing the demyelination effects on neuron communication. The experiment involves locally induced demyelination using Lysolecithin and from this, a myelination index is empirically estimated from analysis of cell images. This index is then coupled with a modified Hodgkin-Huxley computational model to simulate the resulting impact that the de/myelination processes has on the signal propagation along the axon. The effects of signal degradation and transfer of neuronal information are simulated and quantified at multiple levels, and this includes (1) compartment per compartment of a single neuron, (2) bipartite synapse and the effects on the excitatory post-synaptic potential, and (3) a small network of neurons to understand how the impact of de/myelination has on the whole network. By using the myelination index in the simulation model, we can determine the level of attenuation of the action potential concerning the myelin quantity, as well as the analysis of internal signalling functions of the neurons and their impact on the overall spike firing rate. We believe that this hybrid experimental and in silico simulation model can result in a new analysis tool that can predict the gravity of the degeneration through the estimation of the spiking activity and vice-versa, which can minimize the need for specialised laboratory equipment needed for single-cell communication analysis.

Reconfigurable Filtering of Neuro-Spike Communications Using Synthetically Engineered Logic Circuits.

High-frequency firing activity can be induced either naturally in a healthy brain as a result of the processing of sensory stimuli or as an uncontrolled synchronous activity characterizing epileptic seizures. As part of this work, we investigate how logic circuits that are engineered in neurons can be used to design spike filters, attenuating high-frequency activity in a neuronal network that can be used to minimize the effects of neurodegenerative disorders such as epilepsy. We propose a reconfigurable filter design built from small neuronal networks that behave as digital logic circuits. We developed a mathematical framework to obtain a transfer function derived from a linearization process of the Hodgkin-Huxley model. Our results suggest that individual gates working as the output of the logic circuits can be used as a reconfigurable filtering technique. Also, as part of the analysis, the analytical model showed similar levels of attenuation in the frequency domain when compared to computational simulations by fine-tuning the synaptic weight. The proposed approach can potentially lead to precise and tunable treatments for neurological conditions that are inspired by communication theory.