Age‐Related Changes of Circadian Rhythms and Sleep‐Wake Cycles

Yoon, Il; Kripke, Daniel F.; Elliott, Jeffrey A.; Youngstedt, Shawn D.; Rex, Katharine M.; Hauger, Richard L.

doi:10.1046/j.1532-5415.2003.51356.x

Cited by 176 publications

(124 citation statements)

References 33 publications

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“…We also identified certain transcripts that had a shift in phase. This is interesting because it is well documented that healthy older individuals tend to experience a shift toward "morningness" where they prefer to wake early in the morning and go to sleep relatively early in the evening (20,46). There are natural variations in chronotype at all ages with some showing morning preference and some showing evening preference.…”

Section: Discussionmentioning

confidence: 96%

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Effects of aging on circadian patterns of gene expression in the human prefrontal cortex

Chen

Logan

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

238

219

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With aging, significant changes in circadian rhythms occur, including a shift in phase toward a “morning” chronotype and a loss of rhythmicity in circulating hormones. However, the effects of aging on molecular rhythms in the human brain have remained elusive. Here, we used a previously described time-of-death analysis to identify transcripts throughout the genome that have a significant circadian rhythm in expression in the human prefrontal cortex [Brodmann’s area 11 (BA11) and BA47]. Expression levels were determined by microarray analysis in 146 individuals. Rhythmicity in expression was found in ∼10% of detected transcripts (P < 0.05). Using a metaanalysis across the two brain areas, we identified a core set of 235 genes (q < 0.05) with significant circadian rhythms of expression. These 235 genes showed 92% concordance in the phase of expression between the two areas. In addition to the canonical core circadian genes, a number of other genes were found to exhibit rhythmic expression in the brain. Notably, we identified more than 1,000 genes (1,186 in BA11; 1,591 in BA47) that exhibited age-dependent rhythmicity or alterations in rhythmicity patterns with aging. Interestingly, a set of transcripts gained rhythmicity in older individuals, which may represent a compensatory mechanism due to a loss of canonical clock function. Thus, we confirm that rhythmic gene expression can be reliably measured in human brain and identified for the first time (to our knowledge) significant changes in molecular rhythms with aging that may contribute to altered cognition, sleep, and mood in later life.

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Section: Discussionmentioning

confidence: 96%

“…Physiological and activity rhythms are generally known to deteriorate with aging and show a phase advance toward early morning wakening (19,20). Daily rhythms in hormones like melatonin and cortisol are decreased as are sleep and body temperature rhythms in older individuals (21).…”

mentioning

confidence: 99%

Effects of aging on circadian patterns of gene expression in the human prefrontal cortex

Chen

Logan

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

238

219

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“…Since the circadian timing system seems to modulate dream recall, age-related changes within this system are a plausible candidate to explain changes in dream recall. Older people exhibit circadian rhythms of core body temperature and melatonin rhythms with attenuated amplitude and/or phase advanced (Dijk et al, 1999;Yoon et al, 2003). Furthermore, an age-related decrease in the amplitude of the circadian signal results in a dampening of the circadian drive for wakefulness in the evening hours and for sleep in the morning hours .…”

Section: An Old Question In Dream Research: Aging and Dream Recallmentioning

confidence: 99%

Ultradian and circadian modulation of dream recall: EEG correlates and age effects

Chellappa

Cajochen

2013

International Journal of Psychophysiology

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a b s t r a c t a r t i c l e i n f oDreaming occurs during non-rapid eye movement (NREM) and rapid eye movement (REM) sleep, which both are regulated by homeostatic, ultradian, and circadian processes. However, the magnitude of how ultradian REM and NREM sleep and its EEG correlates impact onto dream recall remains fairly unknown. In this review, we address three questions: 1. Is there an ultradian NREM-REM sleep modulation in successful dream recall, which is gated by the circadian clock? 2. What are the key electrophysiological correlates that account for dream recall during NREM and REM sleep and 3. Are there age-related changes in the ultradian and circadian regulation in dream recall and its electrophysiological correlates? Knowledge on the specific frequency and topography NREM and REM sleep differences prior to dream recall may pinpoint to the cerebral correlates that account for this cognitive process, and hint to their possible physiological meaning.

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“…These effects of aging on circadian rhythms-diminished circadian amplitude, earlier phase, shorter circadian period, and desynchronization of rhythms in peripheral organs-have been observed widely in several species of mammals (7,13,14). Paradoxically, however, even though the behavioral phase is earlier in aged humans, multiple studies conclude that the free-running period remains unchanged (15)(16)(17)(18). Thus, changes in phase have been ascribed to alterations in overall circadian amplitude and changed sleep architecture.…”

mentioning

confidence: 99%

Serum factors in older individuals change cellular clock properties

Pagani

Schmitt²,

Meier³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Human aging is accompanied by dramatic changes in daily sleepwake behavior: Activity shifts to an earlier phase, and the consolidation of sleep and wake is disturbed. Although this daily circadian rhythm is brain-controlled, its mechanism is encoded by cellautonomous circadian clocks functioning in nearly every cell of the body. In fact, human clock properties measured in peripheral cells such as fibroblasts closely mimic those measured physiologically and behaviorally in the same subjects. To understand better the molecular mechanisms by which human aging affects circadian clocks, we characterized the clock properties of fibroblasts cultivated from dermal biopsies of young and older subjects. Fibroblast period length, amplitude, and phase were identical in the two groups even though behavior was not, thereby suggesting that basic clock properties of peripheral cells do not change during aging. Interestingly, measurement of the same cells in the presence of human serum from older donors shortened period length and advanced the phase of cellular circadian rhythms compared with treatment with serum from young subjects, indicating that a circulating factor might alter human chronotype. Further experiments demonstrated that this effect is caused by a thermolabile factor present in serum of older individuals. Thus, even though the molecular machinery of peripheral circadian clocks does not change with age, some age-related circadian dysfunction observed in vivo might be of hormonal origin and therefore might be pharmacologically remediable.chronobiology | peripheral oscillators | human behavior C ircadian clocks possess an endogenous periodicity of about 24 h and play a key role in physiological adaptation to the solar day for all living organisms, from cyanobacteria and fungi (1) to insects (2) and mammals (3). Circadian clocks influence nearly all aspects of physiology and behavior, including sleepwake cycles, body temperature, and the function of many organs (3). During normal aging, clock function is attenuated, with consequences both for health and quality of life. Older individuals have an earlier phase of everyday activity compared with the young (4). Not only is the consolidation of sleep and wake dramatically reduced (5, 6), but overall circadian amplitude of hormones and body temperature are lower (7,8), and many agingassociated sleep-wake pathologies have been reported (9-11). As a result, one in five healthy older individuals reports taking sleep medications regularly (9). In cases of pathological aging, chronobiological disturbance is even more acute: Huntington disease, Parkinson disease, and Alzheimer's disease are all associated with profound alterations in sleeping patterns (10-12). These effects of aging on circadian rhythms-diminished circadian amplitude, earlier phase, shorter circadian period, and desynchronization of rhythms in peripheral organs-have been observed widely in several species of mammals (7,13,14). Paradoxically, however, even though the behavioral phase is earlier in aged humans, m...

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Age‐Related Changes of Circadian Rhythms and Sleep‐Wake Cycles

Cited by 176 publications

References 33 publications

Effects of aging on circadian patterns of gene expression in the human prefrontal cortex

Effects of aging on circadian patterns of gene expression in the human prefrontal cortex

Ultradian and circadian modulation of dream recall: EEG correlates and age effects

Serum factors in older individuals change cellular clock properties

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