Special Issue "Genetics of Sleep, Sleep Loss, and Cognitive Impairment"

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".

Deadline for manuscript submissions: 30 November 2021.

Special Issue Editors

Dr. Jonathan Wisor
E-Mail Website
Guest Editor
1. Elson S. Floyd College of Medicine, Washington State University Health Sciences Spokane, Spokane, WA 99202, USA
2. Sleep and Performance Research Center, Washington State University Health Sciences Spokane, Spokane, WA 99202, USA
Interests: rodent genetic models and human genetic studies on the neurochemical regulation of sleep
Dr. Brieann Satterfield
E-Mail Website
Guest Editor
1. Elson S. Floyd College of Medicine, Washington State University Health Sciences Spokane, Spokane, WA 99202, USA
2. Sleep and Performance Research Center, Washington State University Health Sciences Spokane, Spokane, WA 99202, USA
Interests: human genetics; individual differences; sleep loss; neurobehavioral impairment; endophenotyping

Special Issue Information

Dear Colleagues,

It has been well established that sleep loss degrades several aspects of cognitive performance, including attention, executive functions, and memory. However, there is considerable variability in individual sensitivity to cognitive impairment during sleep loss, which varies in a task-dependent manner. The stable, trait-like nature of these individual differences suggests a strong genetic component. As such, decades of research have used genetic approaches to investigate the neurobiological basis of phenotypic vulnerability to sleep loss and to identify genetic biomarkers for predict impairment across a wide variety of sleep loss paradigms.

However, given the complex nature of cognition and the vast array of sleep and cognition-related genes, challenges still remain in making a direct link between phenotypic cognitive vulnerability to sleep loss and associated genetic mechanisms. Many currently identified gene–behavior associations still require more in-depth studies to fully characterize the underlying mechanisms associated with cognitive vulnerability during sleep loss.  

This Special Issue is a collection of articles showcasing novel research into the genetic underpinnings of sleep loss-induced cognitive impairments in both humans and animal models, bringing together expert insights from the fields of sleep, circadian biology, genetics, and cognition. Manuscripts on the following topics will be considered for publication and are encouraged: genome-wide association studies, genotype–phenotype behavioral research, pharmacogenetic studies, knock-in/out or transgenic paradigms, variant functional characterization, and statistical approaches for assessing genetic data in the context of sleep and sleep loss and their effects on cognition.

Dr. Jonathan Wisor
Dr. Brieann Satterfield
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Genes is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Sleep deprivation
  • Sleep restriction
  • Pharmacogenetics
  • Genotype–phenotype
  • Polymorphisms
  • Cognitive performance
  • Gene expression
  • Individual differences
  • Biomarkers
  • Cognitive processes
  • Circadian rhythms
  • Genomics/transcriptomics

Published Papers (1 paper)

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Review

Review
Genetic Markers of Differential Vulnerability to Sleep Loss in Adults
Genes 2021, 12(9), 1317; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12091317 - 26 Aug 2021
Viewed by 633
Abstract
In this review, we discuss reports of genotype-dependent interindividual differences in phenotypic neurobehavioral responses to total sleep deprivation or sleep restriction. We highlight the importance of using the candidate gene approach to further elucidate differential resilience and vulnerability to sleep deprivation in humans, [...] Read more.
In this review, we discuss reports of genotype-dependent interindividual differences in phenotypic neurobehavioral responses to total sleep deprivation or sleep restriction. We highlight the importance of using the candidate gene approach to further elucidate differential resilience and vulnerability to sleep deprivation in humans, although we acknowledge that other omics techniques and genome-wide association studies can also offer insights into biomarkers of such vulnerability. Specifically, we discuss polymorphisms in adenosinergic genes (ADA and ADORA2A), core circadian clock genes (BHLHE41/DEC2 and PER3), genes related to cognitive development and functioning (BDNF and COMT), dopaminergic genes (DRD2 and DAT), and immune and clearance genes (AQP4, DQB1*0602, and TNFα) as potential genetic indicators of differential vulnerability to deficits induced by sleep loss. Additionally, we review the efficacy of several countermeasures for the neurobehavioral impairments induced by sleep loss, including banking sleep, recovery sleep, caffeine, and naps. The discovery of reliable, novel genetic markers of differential vulnerability to sleep loss has critical implications for future research involving predictors, countermeasures, and treatments in the field of sleep and circadian science. Full article
(This article belongs to the Special Issue Genetics of Sleep, Sleep Loss, and Cognitive Impairment)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Our special issue has 3 planned papers now. One of them is being processed. We welcome your contributions. If you have any questions about how to submit, please contact me ([email protected]).

Planned paper 1. Tentative title and abstract

Title: ARC Genotype Modulates Slow Wave Sleep and EEG Spectral Power Following Total Sleep Deprivation

Abstract: Recent evidence suggests that the activity-regulated cytoskeleton associated protein (ARC) may be involved in sleep homeostasis. Sleep homeostasis is manifested by an increase in slow wave sleep (SWS) following total sleep deprivation (TSD), with large individual differences in the magnitude of this rebound effect and concomitant changes in EEG spectral power. However, little is known about the mechanisms regulating these phenomena. We sought to determine whether a single nucleotide polymorphism of the ARC gene (rs35900184) is associated with individual differences in SWS rebound and EEG spectral power. 50 healthy adults participated in a study with a 10-hour baseline sleep opportunity, 38 hours TSD, and a 10-hour recovery sleep opportunity. The genotype effects on time spent in SWS and log-transformed spectral power were assessed using mixed-effects ANOVA with fixed effects for ARC, night, frequency bin (spectral power only) and their interactions. There was a significant ARC x night interaction on SWS rebound (p=0.012). C/C homozygotes exhibited a 60.4±3.0 minute increase in SWS, whereas T/T homozygotes exhibited a 42.4±7.1 minute increase in SWS during recovery relative to baseline. There was a significant ARC x night interaction on theta (p=0.003) and alpha (p<0.001) power. C/C homozygotes had 18.9% more theta and 8.7% more alpha power, whereas T/T homozygotes had 20.0% more theta and 15.1% more alpha power during recovery compared to baseline. ARC appears to mediate SWS and EEG spectrum responses to sleep loss through two seemingly distinct dynamics, with homozygosity for the T allele being associated with a blunted SWS response and an amplified increase in spectral power in the theta and alpha bands.

 

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