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Elevated emotional contagion in a mouse model of Alzheimer’s disease is associated with increased synchronization in the insula and amygdala
Emotional contagion, a primitive form of empathy, is heightened in patients with Alzheimer’s disease (AD); however, the mechanism underlying this attribute has not been thoroughly elucidated. In this study, observational fear conditioning was performed to measure emotional contagion levels in a mous...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5384199/ https://www.ncbi.nlm.nih.gov/pubmed/28387348 http://dx.doi.org/10.1038/srep46262 |
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author | Choi, Jiye Jeong, Yong |
author_facet | Choi, Jiye Jeong, Yong |
author_sort | Choi, Jiye |
collection | PubMed |
description | Emotional contagion, a primitive form of empathy, is heightened in patients with Alzheimer’s disease (AD); however, the mechanism underlying this attribute has not been thoroughly elucidated. In this study, observational fear conditioning was performed to measure emotional contagion levels in a mouse model of AD. Simultaneous recording of local field potentials in the bilateral anterior insula, basolateral amygdala, anterior cingulate cortex, and retrosplenial cortex was also conducted to investigate related brain network changes. Consistent with the results obtained with AD patients, 11-month-old AD model mice exhibited significantly higher freezing levels in observational fear conditioning, indicating elevated emotional contagion compared to age-matched wild-type mice. Furthermore, the left anterior insula and right basolateral amygdala of 11-months-old AD model mice indicated sustained increases in synchronization when they observed the suffering of conspecifics. These changes did not appear in other age groups or wild-type controls. Additionally, the amyloid plaque burden within the anterior insula was significantly correlated with the freezing levels in observational fear conditioning. Taken together, this study reveals increased and sustained network synchrony between the anterior insula and basolateral amygdala, which comprise a salience network in humans, as a potential mechanism for elevated emotional contagion in a mouse model of AD. |
format | Online Article Text |
id | pubmed-5384199 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-53841992017-04-11 Elevated emotional contagion in a mouse model of Alzheimer’s disease is associated with increased synchronization in the insula and amygdala Choi, Jiye Jeong, Yong Sci Rep Article Emotional contagion, a primitive form of empathy, is heightened in patients with Alzheimer’s disease (AD); however, the mechanism underlying this attribute has not been thoroughly elucidated. In this study, observational fear conditioning was performed to measure emotional contagion levels in a mouse model of AD. Simultaneous recording of local field potentials in the bilateral anterior insula, basolateral amygdala, anterior cingulate cortex, and retrosplenial cortex was also conducted to investigate related brain network changes. Consistent with the results obtained with AD patients, 11-month-old AD model mice exhibited significantly higher freezing levels in observational fear conditioning, indicating elevated emotional contagion compared to age-matched wild-type mice. Furthermore, the left anterior insula and right basolateral amygdala of 11-months-old AD model mice indicated sustained increases in synchronization when they observed the suffering of conspecifics. These changes did not appear in other age groups or wild-type controls. Additionally, the amyloid plaque burden within the anterior insula was significantly correlated with the freezing levels in observational fear conditioning. Taken together, this study reveals increased and sustained network synchrony between the anterior insula and basolateral amygdala, which comprise a salience network in humans, as a potential mechanism for elevated emotional contagion in a mouse model of AD. Nature Publishing Group 2017-04-07 /pmc/articles/PMC5384199/ /pubmed/28387348 http://dx.doi.org/10.1038/srep46262 Text en Copyright © 2017, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Choi, Jiye Jeong, Yong Elevated emotional contagion in a mouse model of Alzheimer’s disease is associated with increased synchronization in the insula and amygdala |
title | Elevated emotional contagion in a mouse model of Alzheimer’s disease is associated with increased synchronization in the insula and amygdala |
title_full | Elevated emotional contagion in a mouse model of Alzheimer’s disease is associated with increased synchronization in the insula and amygdala |
title_fullStr | Elevated emotional contagion in a mouse model of Alzheimer’s disease is associated with increased synchronization in the insula and amygdala |
title_full_unstemmed | Elevated emotional contagion in a mouse model of Alzheimer’s disease is associated with increased synchronization in the insula and amygdala |
title_short | Elevated emotional contagion in a mouse model of Alzheimer’s disease is associated with increased synchronization in the insula and amygdala |
title_sort | elevated emotional contagion in a mouse model of alzheimer’s disease is associated with increased synchronization in the insula and amygdala |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5384199/ https://www.ncbi.nlm.nih.gov/pubmed/28387348 http://dx.doi.org/10.1038/srep46262 |
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