Pharmacogenetics of modafinil after sleep loss: catechol-O-methyltransferase genotype modulates waking functions but not recovery sleep
Open accessAbstract
Sleep loss impairs waking functions and is homeostatically compensated in recovery sleep. The mechanisms underlying the consequences of prolonged wakefulness are unknown. The stimulant modafinil may promote primarily dopaminergic neurotransmission. Catechol-O-methyltransferase (COMT) catalyzes the breakdown of cerebral dopamine. A functional Val158Met polymorphism reduces COMT activity, and Val/Val homozygous individuals presumably have lower dopaminergic signaling in the prefrontal cortex than do Met/Met homozygotes. We quantified the contribution of this polymorphism to the effects of sleep deprivation and modafinil on subjective state, cognitive performance, and recovery sleep in healthy volunteers. Two-time 100 mg modafinil potently improved vigor and well-being, and maintained baseline performance with respect to executive functioning and vigilant attention throughout sleep deprivation in Val/Val genotype subjects but was hardly effective in subjects with the Met/Met genotype. Neither modafinil nor the Val158Met polymorphism affected distinct markers of sleep homeostasis in recovery sleep. In conclusion, dopaminergic mechanisms contribute to impaired waking functions after sleep loss.
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Prediction of individual differences in sleep homeostatic responses by the catechol-O-methyltransferase Val158Met polymorphism has not been shown for acute total sleep deprivation.
“but such prediction has not been shown to acute total sleep deprivation.185”
From Circadian rhythms, sleep deprivation, and human performance (2013) · cites this paper as [185]
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SLEEP-WAKE RHYTHMS AND COGNITION
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- Authors
- Bodenmann, S., Xu, S., Luhmann, U., Arand, M., Berger, W., Jung, H., & Landolt, H.
- Affiliations
- University of Zurich (CH)
- University Hospital Zurich (CH)
- Venue
- Clinical Pharmacology & Therapeutics
- Publisher
- Wiley
- Published
- 2008-11-26
- Volume
- 85
- Issue
- 3
- Pages
- 296-304
- ISSN
- 0009-9236 (ISSN-L)
- 1532-6535
- OpenAlex
- W2045857372
- Cited by
- 85
- References
- 55
- Citations by year
- 2025: 3 · 2024: 3 · 2021: 4 · 2020: 4 · 2019: 6 · 2018: 4 · 2017: 7 · 2016: 1 · 2015: 3 · 2014: 7 · 2013: 8 · 2012: 8
- FWCI
- 12.25
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Clinical Pharmacology & Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, other-oa)
- UCL Discovery (University College London) (submittedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, other-oa)
- Zurich Open Repository and Archive (University of Zurich)
- Funders
- National Science Foundation
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (107874, 120377, 3100A0)
- Topics
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
- Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- modafinil, sleep deprivation, catechol-O-methyltransferase, COMT Val158Met polymorphism, dopamine signaling, recovery sleep, sleep homeostasis, executive function, sustained attention, cognitive performance, pharmacogenetics, stimulants
- MeSH terms
- Modafinil, Benzhydryl Compounds, Catechol O-Methyltransferase, Double-Blind Method, Genotype, Humans, Male, Pharmacogenetics, Polymorphism, Genetic, Prospective Studies, Saliva, Sleep, Sleep Deprivation, Wakefulness, Cross-Over Studies, Young Adult
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