The BDNF Val66Met Polymorphism Modulates Sleep Intensity: EEG Frequency- and State-Specificity
Author(s) -
Valérie Bachmann,
Carina Klein,
Sereina Bodenmann,
Nikolaus Schäfer,
Wolfgang Berger,
Peter Brugger,
HansPeter Landolt
Publication year - 2012
Publication title -
sleep
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.222
H-Index - 207
eISSN - 1550-9109
pISSN - 0161-8105
DOI - 10.5665/sleep.1690
Subject(s) - non rapid eye movement sleep , wakefulness , sleep deprivation , slow wave sleep , psychology , electroencephalography , sleep spindle , neuroscience of sleep , sleep (system call) , medicine , k complex , sleep stages , rapid eye movement sleep , endocrinology , polysomnography , neuroscience , circadian rhythm , computer science , operating system
EEG slow waves are the hallmark of deep NREM sleep and may reflect the restorative functions of sleep. Evidence suggests that increased sleep slow waves after sleep deprivation reflect plastic synaptic processes, and that brain-derived neurotrophic factor (BDNF) is causally involved in their homeostatic regulation. The functional Val66Met polymorphism of the gene encoding pro-BDNF causes impaired activity-dependent secretion of mature BDNF protein. We investigated whether this polymorphism contributes to the pronounced inter-individual variation in sleep slow wave activity (SWA) in humans.
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