Sleep Physiology, Circadian Rhythms, Waking Performance and the Development of Sleep-Wake Therapeutics

Dijk, Derk‐Jan; Landolt, Hans‐Peter

doi:10.1007/164_2019_243

Cited by 49 publications

(48 citation statements)

References 243 publications

(273 reference statements)

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“…As the frontal regions are most sensitive to sleep-wake history 34 , SWE was considered over the frontal electrodes (mean over F3, Fz, F4). To deal with the multiple comparison issue, we did not consider SWE over the other parts of the scalp 35 .…”

Section: Eeg Acquisitions and Analysesmentioning

confidence: 99%

Alzheimer’s disease genetic risk and sleep phenotypes in healthy young men: association with more slow waves and daytime sleepiness

Muto

Koshmanova

Ghaemmaghami

et al. 2020

Sleep

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Study Objectives Sleep disturbances and genetic variants have been identified as risk factors for Alzheimer’s disease. Our goal was to assess whether genome-wide polygenic risk scores (PRS) for AD associate with sleep phenotypes in young adults, decades before typical AD symptom onset. Methods We computed whole-genome Polygenic Risk Scores (PRS) for AD and extensively phenotyped sleep under different sleep conditions, including baseline sleep, recovery sleep following sleep deprivation and extended sleep opportunity, in a carefully selected homogenous sample of healthy 363 young men (22.1 y ± 2.7) devoid of sleep and cognitive disorders. Results AD PRS was associated with more slow wave energy, i.e. the cumulated power in the 0.5-4 Hz EEG band, a marker of sleep need, during habitual sleep and following sleep loss, and potentially with large slow wave sleep rebound following sleep deprivation. Furthermore, higher AD PRS was correlated with higher habitual daytime sleepiness. Conclusions These results imply that sleep features may be associated with AD liability in young adults, when current AD biomarkers are typically negative, and the notion that quantifying sleep alterations may be useful in assessing the risk for developing AD.

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Section: Eeg Acquisitions and Analysesmentioning

confidence: 99%

Alzheimer’s disease genetic risk and sleep phenotypes in healthy young men: association with more slow waves and daytime sleepiness

Muto

Koshmanova

Ghaemmaghami

et al. 2020

Sleep

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“…To the best of our knowledge, we explored for the first time the effects of regular daytime caffeine intake on REM sleep promotion and subjective quality of sleep. An 8-hour sleep window scheduled in the early morning hours allowed to investigate REM sleep expression at its circadian maximum (Dijk and Landolt, 2019) in a highly controlled laboratory setting. Indicating a reduced circadian promotion of sleep (Dijk and Landolt, 2019), volunteers in the caffeine condition entered REM sleep later compared to both placebo and withdrawal conditions and the accumulation of REM sleep across the night was slower compared to placebo.…”

Section: Discussionmentioning

confidence: 99%

“…An 8-hour sleep window scheduled in the early morning hours allowed to investigate REM sleep expression at its circadian maximum (Dijk and Landolt, 2019) in a highly controlled laboratory setting. Indicating a reduced circadian promotion of sleep (Dijk and Landolt, 2019), volunteers in the caffeine condition entered REM sleep later compared to both placebo and withdrawal conditions and the accumulation of REM sleep across the night was slower compared to placebo. Thus, the earlier reported REM sleep reductions after caffeine right before bedtime (Carrier et al, 2007;Carrier et al, 2009;Robillard et al, 2015) seem to persist, even if caffeine intake is restricted to daytime and the last intake is 13.5 h apart from lights-off.…”

Section: Discussionmentioning

confidence: 99%

Regular caffeine intake attenuates REM sleep promotion and sleep quality in healthy men

Weibel

Lin

Landolt

et al. 2020

Preprint

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Acute caffeine intake can attenuate homeostatic sleep pressure and worsen sleep quality. Besides, caffeine intake – particularly in high doses and close to bedtime – may also affect circadian-regulated REM sleep promotion, an important determinant of subjective sleep quality. However, it is not known whether such changes persist under chronic caffeine consumption during daytime. Twenty male caffeine consumers (26.4 ± 4 years old, habitual caffeine intake 478.1 ± 102.8 mg/day) participated in a double-blind crossover study. Each volunteer completed a caffeine (3 × 150 mg caffeine daily), a withdrawal (3 × 150 mg caffeine for eight days then placebo), and a placebo condition. After ten days of controlled intake and a fixed sleep-wake cycle, we recorded 8 h of electroencephalography starting 5 h after habitual bedtime (i.e., start on average at 04:22 am which is around the peak of circadian REM sleep promotion). A 60 min evening nap preceded each sleep episode and reduced high sleep pressure levels. While total sleep time and sleep architecture did not significantly differ between the three conditions, REM latency was longer after daily caffeine intake compared to both placebo and withdrawal. Moreover, the accumulation of REM sleep proportion was slower, and volunteers reported more difficulties at awakening after sleep and feeling more tired upon wake-up in the caffeine condition compared to placebo. Our data indicate that besides acute also regular daytime caffeine intake affects REM sleep regulation in men. We have evidence that regular caffeine intake during daytime weakens circadian sleep promotion when compared to placebo. Moreover, the observed caffeine-induced deterioration in the quality of awakening may suggest a potential motive to reinstate caffeine intake after sleep.

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“…Results indicated that extension night SWE was not significantly linked to AD PRS. This may be because sleep timing for this particular night affects sleep quality (31,34) ( Figure 3A). In contrast to baseline and recuperation sleep periods which were initiated at habitual sleep time, sleep extension started 2 hours before habitual sleep time, covering the end of a period known as the evening "wake-maintenance zone" corresponding to the time at which the circadian system maximally promotes wakefulness (31).…”

Section: Recovery Sleep Slow Wave Sleep Rebound and Extension Nightmentioning

confidence: 99%

“…In contrast to baseline and recuperation sleep periods which were initiated at habitual sleep time, sleep extension started 2 hours before habitual sleep time, covering the end of a period known as the evening "wake-maintenance zone" corresponding to the time at which the circadian system maximally promotes wakefulness (31). In addition, the circadian system is known to affect the relative content in Non-REM and REM sleep as well as in different EEG frequencies (31,34). Therefore, the imposed 2h advance of sleep time during the extension night affected sleep quality, which may have reduced the association between SWE and AD PRS found with baseline and recovery nights.…”

Section: Recovery Sleep Slow Wave Sleep Rebound and Extension Nightmentioning

confidence: 99%

Alzheimer’s disease genetic risk and sleep phenotypes: association with more slow-waves and daytime sleepiness

Muto

Koshmanova

Ghaemmaghami

et al. 2020

Preprint

Self Cite

View full text Add to dashboard Cite

Study Objectives. Sleep disturbances and genetic variants have been identified as risk factors for Alzheimer s disease. Our goal was to assess whether genome-wide polygenic risk scores (PRS) for AD associate with sleep phenotypes in young adults, decades before typical AD symptom onset. Methods. We computed whole-genome Polygenic Risk Scores (PRS) for AD and extensively phenotyped sleep under different sleep conditions, including baseline sleep, recovery sleep following sleep deprivation and extended sleep opportunity, in a carefully selected homogenous sample of healthy 363 young men (22.1 y +/- 2.7) devoid of sleep and cognitive disorders. Results. AD PRS was associated with more slow wave energy, i.e. the cumulated power in the 0.5-4 Hz EEG band, a marker of sleep need, during habitual sleep and following sleep loss, and potentially with large slow wave sleep rebound following sleep deprivation. Furthermore, higher AD PRS was correlated with higher habitual daytime sleepiness. Conclusions. These results imply that sleep features may be associated with AD liability in young adults, when current AD biomarkers are typically negative, and the notion that quantifying sleep alterations may be useful in assessing the risk for developing AD.

show abstract

Sleep Physiology, Circadian Rhythms, Waking Performance and the Development of Sleep-Wake Therapeutics

Cited by 49 publications

References 243 publications

Alzheimer’s disease genetic risk and sleep phenotypes in healthy young men: association with more slow waves and daytime sleepiness

Alzheimer’s disease genetic risk and sleep phenotypes in healthy young men: association with more slow waves and daytime sleepiness

Regular caffeine intake attenuates REM sleep promotion and sleep quality in healthy men

Alzheimer’s disease genetic risk and sleep phenotypes: association with more slow-waves and daytime sleepiness

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