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Heritability of REM sleep neurophysiology in adolescence

Alterations of rapid eye movement (REM) sleep have long been observed in patients with psychiatric disorders and proposed as an endophenotype—a link between behavior and genes. Recent experimental work has shown that REM sleep plays an important role in the emotional processing of memories, emotion...

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Autores principales: Markovic, Andjela, Kaess, Michael, Tarokh, Leila
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9492899/
https://www.ncbi.nlm.nih.gov/pubmed/36130941
http://dx.doi.org/10.1038/s41398-022-02106-6
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author Markovic, Andjela
Kaess, Michael
Tarokh, Leila
author_facet Markovic, Andjela
Kaess, Michael
Tarokh, Leila
author_sort Markovic, Andjela
collection PubMed
description Alterations of rapid eye movement (REM) sleep have long been observed in patients with psychiatric disorders and proposed as an endophenotype—a link between behavior and genes. Recent experimental work has shown that REM sleep plays an important role in the emotional processing of memories, emotion regulation, and is altered in the presence of stress, suggesting a mechanism by which REM sleep may impact psychiatric illness. REM sleep shows a developmental progression and increases during adolescence—a period of rapid maturation of the emotional centers of the brain. This study uses a behavioral genetics approach to understand the relative contribution of genes, shared environmental and unique environmental factors to REM sleep neurophysiology in adolescents. Eighteen monozygotic (MZ; n = 36; 18 females) and 12 dizygotic (DZ; n = 24; 12 females) same-sex twin pairs (mean age = 12.46; SD = 1.36) underwent whole-night high-density sleep EEG recordings. We find a significant genetic contribution to REM sleep EEG power across frequency bands, explaining, on average, between 75 to 88% of the variance in power, dependent on the frequency band. In the lower frequency bands between delta and sigma, however, we find an additional impact of shared environmental factors over prescribed regions. We hypothesize that these regions may reflect the contribution of familial and environmental stress shared amongst the twins. The observed strong genetic contribution to REM sleep EEG power in early adolescence establish REM sleep neurophysiology as a potentially strong endophenotype, even in adolescence—a period marked by significant brain maturation.
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spelling pubmed-94928992022-09-23 Heritability of REM sleep neurophysiology in adolescence Markovic, Andjela Kaess, Michael Tarokh, Leila Transl Psychiatry Article Alterations of rapid eye movement (REM) sleep have long been observed in patients with psychiatric disorders and proposed as an endophenotype—a link between behavior and genes. Recent experimental work has shown that REM sleep plays an important role in the emotional processing of memories, emotion regulation, and is altered in the presence of stress, suggesting a mechanism by which REM sleep may impact psychiatric illness. REM sleep shows a developmental progression and increases during adolescence—a period of rapid maturation of the emotional centers of the brain. This study uses a behavioral genetics approach to understand the relative contribution of genes, shared environmental and unique environmental factors to REM sleep neurophysiology in adolescents. Eighteen monozygotic (MZ; n = 36; 18 females) and 12 dizygotic (DZ; n = 24; 12 females) same-sex twin pairs (mean age = 12.46; SD = 1.36) underwent whole-night high-density sleep EEG recordings. We find a significant genetic contribution to REM sleep EEG power across frequency bands, explaining, on average, between 75 to 88% of the variance in power, dependent on the frequency band. In the lower frequency bands between delta and sigma, however, we find an additional impact of shared environmental factors over prescribed regions. We hypothesize that these regions may reflect the contribution of familial and environmental stress shared amongst the twins. The observed strong genetic contribution to REM sleep EEG power in early adolescence establish REM sleep neurophysiology as a potentially strong endophenotype, even in adolescence—a period marked by significant brain maturation. Nature Publishing Group UK 2022-09-21 /pmc/articles/PMC9492899/ /pubmed/36130941 http://dx.doi.org/10.1038/s41398-022-02106-6 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Markovic, Andjela
Kaess, Michael
Tarokh, Leila
Heritability of REM sleep neurophysiology in adolescence
title Heritability of REM sleep neurophysiology in adolescence
title_full Heritability of REM sleep neurophysiology in adolescence
title_fullStr Heritability of REM sleep neurophysiology in adolescence
title_full_unstemmed Heritability of REM sleep neurophysiology in adolescence
title_short Heritability of REM sleep neurophysiology in adolescence
title_sort heritability of rem sleep neurophysiology in adolescence
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9492899/
https://www.ncbi.nlm.nih.gov/pubmed/36130941
http://dx.doi.org/10.1038/s41398-022-02106-6
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