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Alpha rhythm slowing in a modified thalamo-cortico-thalamic model related with Alzheimer’s disease

A decrease in alpha band power is defined as a hallmark of electroencephalogram (EEG) in Alzheimer’s disease (AD). This study devotes to understanding the neuronal correlates of alpha rhythm slowing associated with AD from the view of neurocomputation. Firstly, a modified computational model of thal...

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Autores principales: Li, XiaoYuan, Yang, XiaoLi, Sun, ZhongKui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7067465/
https://www.ncbi.nlm.nih.gov/pubmed/32163454
http://dx.doi.org/10.1371/journal.pone.0229950
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author Li, XiaoYuan
Yang, XiaoLi
Sun, ZhongKui
author_facet Li, XiaoYuan
Yang, XiaoLi
Sun, ZhongKui
author_sort Li, XiaoYuan
collection PubMed
description A decrease in alpha band power is defined as a hallmark of electroencephalogram (EEG) in Alzheimer’s disease (AD). This study devotes to understanding the neuronal correlates of alpha rhythm slowing associated with AD from the view of neurocomputation. Firstly, a modified computational model of thalamo-cortico-thalamic (TCT) circuitry is constructed by incorporating two important biologically plausible ingredients. One is the disinhibition property between different inhibitory interneurons in the cortical module. The other is the full relay function of thalamic relay nucleus (TCR) to the cortical module. Then, by decreasing synaptic connectivity parameters to mimic the neuropathological condition of synapse loss in AD, the correlation between neuronal synaptic behavior and abnormal alpha rhythm is simulated by means of power spectral analysis. The results indicate that these decreases of synaptic activity, i.e., not only the excitatory synaptic connections from TCR to fast inhibitory interneurons C(fte) and from excitatory interneurons to pyramidal neurons C(pxe) but also the inhibitory synaptic connections from fast inhibitory interneurons to slow inhibitory interneurons C(lfi) and from inhibitory interneurons to TCR C(tii), can significantly diminish the peak power density over the alpha band of the thalamic output, which implies that there is a slowing of alpha band. Furthermore, the underlying mechanism behind the alpha rhythmic changes is analyzed using nonlinear dynamical technique. The results reveal that decreases of C(fte), C(pxe), C(lfi) and C(tii) can make the thalamic module transfer from a limit cycle mode to a point attractor mode, which may lead to the alpha rhythm slowing in the modified TCT model. We expect this work can be helpful in identifying early biomarkers of AD’s EEG and understanding potential pathogenesis of AD.
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spelling pubmed-70674652020-03-23 Alpha rhythm slowing in a modified thalamo-cortico-thalamic model related with Alzheimer’s disease Li, XiaoYuan Yang, XiaoLi Sun, ZhongKui PLoS One Research Article A decrease in alpha band power is defined as a hallmark of electroencephalogram (EEG) in Alzheimer’s disease (AD). This study devotes to understanding the neuronal correlates of alpha rhythm slowing associated with AD from the view of neurocomputation. Firstly, a modified computational model of thalamo-cortico-thalamic (TCT) circuitry is constructed by incorporating two important biologically plausible ingredients. One is the disinhibition property between different inhibitory interneurons in the cortical module. The other is the full relay function of thalamic relay nucleus (TCR) to the cortical module. Then, by decreasing synaptic connectivity parameters to mimic the neuropathological condition of synapse loss in AD, the correlation between neuronal synaptic behavior and abnormal alpha rhythm is simulated by means of power spectral analysis. The results indicate that these decreases of synaptic activity, i.e., not only the excitatory synaptic connections from TCR to fast inhibitory interneurons C(fte) and from excitatory interneurons to pyramidal neurons C(pxe) but also the inhibitory synaptic connections from fast inhibitory interneurons to slow inhibitory interneurons C(lfi) and from inhibitory interneurons to TCR C(tii), can significantly diminish the peak power density over the alpha band of the thalamic output, which implies that there is a slowing of alpha band. Furthermore, the underlying mechanism behind the alpha rhythmic changes is analyzed using nonlinear dynamical technique. The results reveal that decreases of C(fte), C(pxe), C(lfi) and C(tii) can make the thalamic module transfer from a limit cycle mode to a point attractor mode, which may lead to the alpha rhythm slowing in the modified TCT model. We expect this work can be helpful in identifying early biomarkers of AD’s EEG and understanding potential pathogenesis of AD. Public Library of Science 2020-03-12 /pmc/articles/PMC7067465/ /pubmed/32163454 http://dx.doi.org/10.1371/journal.pone.0229950 Text en © 2020 Li et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Li, XiaoYuan
Yang, XiaoLi
Sun, ZhongKui
Alpha rhythm slowing in a modified thalamo-cortico-thalamic model related with Alzheimer’s disease
title Alpha rhythm slowing in a modified thalamo-cortico-thalamic model related with Alzheimer’s disease
title_full Alpha rhythm slowing in a modified thalamo-cortico-thalamic model related with Alzheimer’s disease
title_fullStr Alpha rhythm slowing in a modified thalamo-cortico-thalamic model related with Alzheimer’s disease
title_full_unstemmed Alpha rhythm slowing in a modified thalamo-cortico-thalamic model related with Alzheimer’s disease
title_short Alpha rhythm slowing in a modified thalamo-cortico-thalamic model related with Alzheimer’s disease
title_sort alpha rhythm slowing in a modified thalamo-cortico-thalamic model related with alzheimer’s disease
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7067465/
https://www.ncbi.nlm.nih.gov/pubmed/32163454
http://dx.doi.org/10.1371/journal.pone.0229950
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