Genetic Basis of Sleep in Healthy Humans

Landolt, Hans‐Peter; Dijk, Derk‐Jan

doi:10.1016/b978-1-4160-6645-3.00015-3

Cited by 8 publications

(5 citation statements)

References 62 publications

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“…Furthermore, the normal distribution of chronotypes indicates a polygenic basis such that multiple genes contribute modest, aggregative effects to this complex phenotype. 16 Given the heritability of circadian typology and prior success in identifying the components of the molecular circadian clock, chronotype is a logical target for genetic studies.…”

Section: Genetics Of Circadian Timingmentioning

confidence: 99%

Genetic Basis of Chronotype in Humans: Insights From Three Landmark GWAS

Kalmbach

Schneider

Cheung

et al. 2016

Sleep

177

102

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Section: Genetics Of Circadian Timingmentioning

confidence: 99%

Genetic Basis of Chronotype in Humans: Insights From Three Landmark GWAS

Kalmbach

Schneider

Cheung

et al. 2016

Sleep

177

102

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“…Not only the waking EEG, but also self-reported and polysomnographically recorded sleep characteristics such as inter-individual variation in diurnal preference, sleep duration, sleep structure, and the EEG in NREM sleep and REM sleep have all been shown to be under strong genetic control (Landolt and Dijk, 2010). Already the first sleep studies in monozygotic twins revealed almost complete concordance in the temporal sequence of sleep stages (Zung and Wilson, 1966).…”

Section: Sleep Architecturementioning

confidence: 99%

Genetic determination of sleep EEG profiles in healthy humans

Landolt

2011

Progress in Brain Research

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The contribution of slow brain oscillations including delta, theta, alpha, and sigma frequencies to the sleep electroencephalography (EEG) is finely regulated by circadian and homeostatic influences, and reflects functional aspects of wakefulness and sleep. Accumulating evidence demonstrates that individual sleep EEG patterns in non-rapid-eye-movement (NREM) sleep and rapid-eye-movement (REM) sleep are heritable traits. More specifically, multiple recordings in the same individuals, as well as studies in monozygotic and dizygotic twins suggest that a very high percentage of the robust interindividual variation and the high intraindividual stability of sleep EEG profiles can be explained by genetic factors (> 90% in distinct frequency bands). Still little is known about which genes contribute to different sleep EEG phenotypes in healthy humans. The genetic variations that have been identified to date include functional polymorphisms of the clock gene PER3 and of genes contributing to signal transduction pathways involving adenosine (ADA, ADORA2A), brain-derived neurotrophic factor (BDNF), dopamine (COMT), and prion protein (PRNP). Some of these polymorphisms profoundly modulate sleep EEG profiles; their effects are reviewed here. It is concluded that the search for genetic contributions to slow sleep EEG oscillations constitutes a promising avenue to identify molecular mechanisms underlying sleep-wake regulation in humans.

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“…In fact, application of qEEG has led to new insights into the homeostatic regulation of sleep, reflected in the sleep-wake dependent changes of EEG slow-wave activity 8,9 . Moreover, among its manifold applications, qEEG during sleep has identified markers that associate with psychiatric disease 6,10,11 , cognitive development and decline 12,13 , memory consolidation 4,14,15 drug responses 16–18 , and genetic variants 19 . An important barrier for further discovery is that qEEG has required labor-intensive annotation and thus has mostly been applied in relatively small studies.…”

Section: Introductionmentioning

confidence: 99%