Pharmacogenetics of Modafinil After Sleep Loss: Catechol-O-Methyltransferase Genotype Modulates Waking Functions But Not Recovery Sleep

Bodenmann, Sereina; Shou, Xu; Luhmann, Ulrich F O; Arand, Michael; Berger, Wolfgang; Jung, Hans H.; Landolt, Hans‐Peter

doi:10.1038/clpt.2008.222

Cited by 78 publications

(86 citation statements)

References 42 publications

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“…2) is present before and after sleep deprivation, and altered by administration of a moderate dose of the stimulant modafinil during prolonged wakefulness. By contrast, the polymorphism, however, profoundly modulates the efficacy of modafinil to improve impaired well-being and cognitive functions after sleep deprivation (Bodenmann et al, 2009b).…”

Section: G>a Polymorphism Of Catechol-o-methyltransferase (Comt) Genementioning

confidence: 98%

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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Section: G>a Polymorphism Of Catechol-o-methyltransferase (Comt) Genementioning

confidence: 98%

Genetic determination of sleep EEG profiles in healthy humans

Landolt

2011

Progress in Brain Research

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“…There are well documented individual differences in sensitivity to caffeine 29,30) . Individual variability has also been reported for the fatigue-mitigating effects of modafinil 31) , which is another wake-promoting substance 32) . There is a scarcity of knowledge about variability among individuals in the effectiveness of napping as a fatigue countermeasure 33) , and in susceptibility to sleep inertia (cognitive performance impairment and grogginess) immediately after a nap.…”

Section: Individual Differences In Vulnerability To Sleep Loss In Occmentioning

confidence: 99%

“…These include polymorphisms involved in the regulation of neurotransmitters (catechol-O-methyltransferase) 31) , brain metabolism (adenosine receptor and adenosine deaminase) 45,46) , and circadian rhythmicity (the clock gene PER3) 47) . Studies of genetic predictors have typically involved comparison of groups selected a priori to differ by the polymorphism under consideration.…”

Section: Predicting Individual Differences In Vulnerability To Sleep mentioning

confidence: 99%

Individual Differences in Vulnerability to Sleep Loss in the Work Environment

Dongen

Belenky

2009

INDUSTRIAL HEALTH

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It has long been recognized that individuals differ markedly in their responses to extended work hours [1][2][3][4][5][6] and shift work schedules [7][8][9] . Research in this area focused initially on demographics, behavioral patterns and external circumstances as factors explaining and predicting these individual differences, but with limited success 10) . More recently, the emphasis shifted to the endogenous neurobiology underlying sleep/wake regulation and 24-h (circadian) rhythm 10,11) . This line of research gained impetus due to a study showing that there are substantial individual differences in performance impairment resulting from sleep deprivation, and demonstrating that these individual differences constitute a trait 12) . In this paper, we discuss the trait individual differences in performance impairment due to sleep loss, and consider their relevance in operational environments. We also examine ways to predict the individual differences in vulnerability to sleep loss, and reflect on the legal and ethical implications of doing so in occupational settings.

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“…[26][27][28][29][30][31] Larger sample sizes and assessment of phenotype-genotype relationships in both homozygous and heterozygous individuals are needed to definitively determine whether such candidate genes involved in regulation of sleep-wake, circadian, and cognitive functions are associated with inter-individual neurobehavioral responses to sleep loss across an entire population. This is particularly critical given that individuals are necessarily categorized into different genotypes, reducing sample sizes in each subgroup.…”

Section: S U P P L E M E N T Prevalence and Consequences Of Sleep Lossmentioning

confidence: 99%

Behavioral and Genetic Markers of Sleepiness

Goel

Dinges

2011

Journal of Clinical Sleep Medicine

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S19Neurobehavioral responses to acute total and chronic partial sleep deprivation occur in healthy adults and are particularly evident in vigilant attention performance. There are large inter-individual differences in the degree of cognitive deficitssuch differences are manifested in proportionality between the mean and variance as sleep loss progresses. It has recently been demonstrated via laboratory experiments that differential neurobehavioral vulnerability to sleep deprivation is not random-but rather is stable and trait-like-strongly suggesting a phenotypic response with possible genotypic involvement. These experiments also showed that vulnerability was not explained by subjects' baseline functioning or a number of other potential predictors. Differential vulnerability has been shown to extend to chronic partial sleep deprivation. One potential genetic biomarker for such differential vulnerability is the human leukocyte antigen (HLA) DQB1*0602, an allele which we recently demonstrated predicts interindividual differences in sleepiness, physiological sleep, and fatigue to chronic partial sleep deprivation in healthy adults. Determination of biomarkers of individual differences to sleep loss will help identify those individuals in the general population who are most in need of prevention of sleep debt and in need of effective countermeasures for sleep loss; will further understanding and management of vulnerability to excessive sleepiness due to common sleep and medical disorders; and will inform public policies pertaining to the need for adequate sleep. S u p p l e M e n t prevalence and Consequences of Sleep lossStudies estimate that 20% to 40% of the adult US population sleep less than 7 hours per night 1 -the minimum sleep duration necessary to prevent cumulative deterioration in performance on a range of cognitive tasks.2,3 The proportion of people curtailing their sleep due to lifestyle is increasing, 1 and is likely higher than surveys indicate, since physiological sleep duration is typically at least one hour less than self-reported sleep duration.4,5 Moreover, sleep loss has become a significant public health concern as population studies have found reduced sleep duration (less than 7 hours) associated with increased risks of obesity, morbidity, and mortality. [6][7][8] Sleep loss, including chronic partial sleep deprivation (PSD)-a condition experienced by millions of people on a consecutive and daily basis-can result from medical conditions, sleep disorders, work demands, stress/emotional distress, and social/domestic responsibilities.1 In addition, for the majority of people, sleep loss directly causes significant risks via increased fatigue and sleep propensity, and via deficits in mood and neurocognitive functions including vigilant and executive attention, cognitive speed and working memory, and executive functions. 1,9,10 Stable trait-like Individual Differences in Response to Sleep lossOur laboratory was the first to experimentally demonstrate that subjects undergoing acute total sleep dep...

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Pharmacogenetics of Modafinil After Sleep Loss: Catechol-O-Methyltransferase Genotype Modulates Waking Functions But Not Recovery Sleep

Cited by 78 publications

References 42 publications

Genetic determination of sleep EEG profiles in healthy humans

Genetic determination of sleep EEG profiles in healthy humans

Individual Differences in Vulnerability to Sleep Loss in the Work Environment

Behavioral and Genetic Markers of Sleepiness

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