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Genetic contribution to sleep homeostasis in early adolescence

The sleep homeostatic process in adults is moderately stable over time and unique to an individual. Work in transgenic mice has suggested a role of genes in sleep homeostasis. The current study quantified the genetic contribution to sleep homeostasis in adolescence. We use slow wave energy (SWE) as...

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Hauptverfasser: Marković, Andjela (VerfasserIn) , Rusterholz, Thomas (VerfasserIn) , Achermann, Peter (VerfasserIn) , Kaess, Michael (VerfasserIn) , Tarokh, Leila (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: November 2024
In: European journal of neuroscience
Year: 2024, Jahrgang: 60, Heft: 10, Pages: 6420-6428
ISSN:1460-9568
DOI:10.1111/ejn.16568
Online-Zugang:Verlag, kostenfrei, Volltext: https://doi.org/10.1111/ejn.16568
Verlag, kostenfrei, Volltext: https://onlinelibrary.wiley.com/doi/abs/10.1111/ejn.16568
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Verfasserangaben:Andjela Markovic, Thomas Rusterholz, Peter Achermann, Michael Kaess, Leila Tarokh

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520 |a The sleep homeostatic process in adults is moderately stable over time and unique to an individual. Work in transgenic mice has suggested a role of genes in sleep homeostasis. The current study quantified the genetic contribution to sleep homeostasis in adolescence. We use slow wave energy (SWE) as a metric for sleep pressure dissipation during sleep. This measure reflects both sleep intensity and duration. High-density (58 derivations) sleep electroencephalogram (EEG) was recorded in 14 monozygotic and 12 dizygotic adolescent twin pairs (mean age = 13.2 years; standard deviation [SD] = 1.1; 20 females). SWE at the end of sleep was quantified as the cumulative delta power (1-4.6 Hz) over the night. We also examined the time constant of the decay and the level of slow wave activity (SWA) at the beginning of the sleep episode. Structural equation modelling was used to quantify the amount of variance in SWE and the dissipation of sleep pressure due to genes. We found that most (mean = 76% across EEG derivations) of the variance in SWE was due to genes. In contrast, genes had a small (mean = 33%) influence on the rate of dissipation of sleep pressure, and this measure was largely (mean = 67%) driven by environmental factors unique to each twin. Our results show that the amount of dissipated sleep pressure is largely under genetic control; however, the rate of sleep pressure dissipation is largely due to unique environmental factors. Our findings are in line with research in animals and suggest that the heritability of the rate of sleep pressure dissipation is limited. 
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