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Age-related changes in sleep and circadian rhythms: impact on cognitive performance and underlying neuroanatomical networks.

Schmidt C, Peigneux P, Cajochen C - Front Neurol (2012)

Bottom Line: Dampening of the circadian alertness signal and attenuated deterioration of psychomotor vigilance in response to elevated sleep pressure with aging change this interaction pattern.As evidenced by neuroimaging studies, both homeostatic sleep pressure and circadian sleep-wake promotion impact on cognition-related cortical and arousal-promoting subcortical brain regions including the thalamus, the anterior hypothalamus, and the brainstem locus coeruleus (LC).In this perspective, we summarize and discuss here the potential neuroanatomical networks underlying age-related changes in circadian and homeostatic modulation of waking performance, ranging from basic arousal to higher order cognitive behaviors.

View Article: PubMed Central - PubMed

Affiliation: Centre for Chronobiology, Psychiatric Hospital of the University of Basel Basel, Switzerland.

ABSTRACT
Circadian and homeostatic sleep-wake regulatory processes interact in a fine tuned manner to modulate human cognitive performance. Dampening of the circadian alertness signal and attenuated deterioration of psychomotor vigilance in response to elevated sleep pressure with aging change this interaction pattern. As evidenced by neuroimaging studies, both homeostatic sleep pressure and circadian sleep-wake promotion impact on cognition-related cortical and arousal-promoting subcortical brain regions including the thalamus, the anterior hypothalamus, and the brainstem locus coeruleus (LC). However, how age-related changes in circadian and homeostatic processes impact on the cerebral activity subtending waking performance remains largely unexplored. Post-mortem studies point to neuronal degeneration in the SCN and age-related modifications in the arousal-promoting LC. Alongside, cortical frontal brain areas are particularly susceptible both to aging and misalignment between circadian and homeostatic processes. In this perspective, we summarize and discuss here the potential neuroanatomical networks underlying age-related changes in circadian and homeostatic modulation of waking performance, ranging from basic arousal to higher order cognitive behaviors.

No MeSH data available.


Related in: MedlinePlus

Schematic illustration of the impact of circadian and homeostatic processes on sleep and wakefulness. The filled gray area illustrates variations in total sleep time during a constant routine protocol with regularly occurring naps (150 min of wakefulness followed by 75 min of naps), aiming at investigating circadian rhythm parameters under low homeostatic sleep pressure conditions. Black lines indicate superimposed subjective sleepiness as assessed by the Karolinska Sleepiness Scale over a similar nap (dashed line) and total sleep deprivation (straight line) protocol. The wake maintenance zone can be identified in the naps scheduled in the subjective evening hours, with minimal total sleep time (expressed in minutes). The sleep-promoting signal in the biological night is accompanied by rapid increases in subjective sleepiness in both the low (naps) and high (sleep deprivation) sleep pressure conditions. Over the course of the second biological day, subjective sleepiness decreases, even when homeostatic sleep pressure increases (in the sleep deprivation protocol, straight line), indicating that circadian wake promotion rises or that circadian sleep promotion diminishes [modified from Cajochen et al. (2001) and Münch et al. (2005)].
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Figure 1: Schematic illustration of the impact of circadian and homeostatic processes on sleep and wakefulness. The filled gray area illustrates variations in total sleep time during a constant routine protocol with regularly occurring naps (150 min of wakefulness followed by 75 min of naps), aiming at investigating circadian rhythm parameters under low homeostatic sleep pressure conditions. Black lines indicate superimposed subjective sleepiness as assessed by the Karolinska Sleepiness Scale over a similar nap (dashed line) and total sleep deprivation (straight line) protocol. The wake maintenance zone can be identified in the naps scheduled in the subjective evening hours, with minimal total sleep time (expressed in minutes). The sleep-promoting signal in the biological night is accompanied by rapid increases in subjective sleepiness in both the low (naps) and high (sleep deprivation) sleep pressure conditions. Over the course of the second biological day, subjective sleepiness decreases, even when homeostatic sleep pressure increases (in the sleep deprivation protocol, straight line), indicating that circadian wake promotion rises or that circadian sleep promotion diminishes [modified from Cajochen et al. (2001) and Münch et al. (2005)].

Mentions: The specific timing and consolidation of sleep and wake episodes within the 24-h light-dark cycle are regulated by a coordinated action of homeostatic and circadian processes (Borbely, 1982; Daan et al., 1984; see also Figure 1). It is assumed that the circadian and homeostatic process represent independent drives on sleep-wake propensity but interact in a non-linear fashion across the 24-h light-dark cycle. Thus, circadian-based wake propensity is at its highest levels during the early evening hours (commonly after 12 h of wakefulness), when homeostatic sleep pressure is rather high, whereas circadian propensity for sleep reaches its maximum during the early morning (∼2 h before habitual wake up time), when homeostatic sleep pressure is low (Dijk and Czeisler, 1994). At any given time, the magnitude of sleepiness, alertness, and fatigue is thus determined by the interacting influences of these two processes (Figure 1). After homeostatic sleep pressure has mostly dissipated over the first hours of the night, it is the high circadian-based propensity for sleep that prevents us from prematurely waking up in the early morning hours. Conversely, it is the very low circadian-based propensity for sleep (i.e., circadian wake-promoting signal) that prevents us from falling asleep in the early evening hours when homeostatic sleep pressure is at its highest level. In both cases, circadian and homeostatic systems ideally work in opposition to ensure a consolidated period of sleep or wakefulness (Dijk and Czeisler, 1994, 1995; Dijk and von Schantz, 2005).


Age-related changes in sleep and circadian rhythms: impact on cognitive performance and underlying neuroanatomical networks.

Schmidt C, Peigneux P, Cajochen C - Front Neurol (2012)

Schematic illustration of the impact of circadian and homeostatic processes on sleep and wakefulness. The filled gray area illustrates variations in total sleep time during a constant routine protocol with regularly occurring naps (150 min of wakefulness followed by 75 min of naps), aiming at investigating circadian rhythm parameters under low homeostatic sleep pressure conditions. Black lines indicate superimposed subjective sleepiness as assessed by the Karolinska Sleepiness Scale over a similar nap (dashed line) and total sleep deprivation (straight line) protocol. The wake maintenance zone can be identified in the naps scheduled in the subjective evening hours, with minimal total sleep time (expressed in minutes). The sleep-promoting signal in the biological night is accompanied by rapid increases in subjective sleepiness in both the low (naps) and high (sleep deprivation) sleep pressure conditions. Over the course of the second biological day, subjective sleepiness decreases, even when homeostatic sleep pressure increases (in the sleep deprivation protocol, straight line), indicating that circadian wake promotion rises or that circadian sleep promotion diminishes [modified from Cajochen et al. (2001) and Münch et al. (2005)].
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3405459&req=5

Figure 1: Schematic illustration of the impact of circadian and homeostatic processes on sleep and wakefulness. The filled gray area illustrates variations in total sleep time during a constant routine protocol with regularly occurring naps (150 min of wakefulness followed by 75 min of naps), aiming at investigating circadian rhythm parameters under low homeostatic sleep pressure conditions. Black lines indicate superimposed subjective sleepiness as assessed by the Karolinska Sleepiness Scale over a similar nap (dashed line) and total sleep deprivation (straight line) protocol. The wake maintenance zone can be identified in the naps scheduled in the subjective evening hours, with minimal total sleep time (expressed in minutes). The sleep-promoting signal in the biological night is accompanied by rapid increases in subjective sleepiness in both the low (naps) and high (sleep deprivation) sleep pressure conditions. Over the course of the second biological day, subjective sleepiness decreases, even when homeostatic sleep pressure increases (in the sleep deprivation protocol, straight line), indicating that circadian wake promotion rises or that circadian sleep promotion diminishes [modified from Cajochen et al. (2001) and Münch et al. (2005)].
Mentions: The specific timing and consolidation of sleep and wake episodes within the 24-h light-dark cycle are regulated by a coordinated action of homeostatic and circadian processes (Borbely, 1982; Daan et al., 1984; see also Figure 1). It is assumed that the circadian and homeostatic process represent independent drives on sleep-wake propensity but interact in a non-linear fashion across the 24-h light-dark cycle. Thus, circadian-based wake propensity is at its highest levels during the early evening hours (commonly after 12 h of wakefulness), when homeostatic sleep pressure is rather high, whereas circadian propensity for sleep reaches its maximum during the early morning (∼2 h before habitual wake up time), when homeostatic sleep pressure is low (Dijk and Czeisler, 1994). At any given time, the magnitude of sleepiness, alertness, and fatigue is thus determined by the interacting influences of these two processes (Figure 1). After homeostatic sleep pressure has mostly dissipated over the first hours of the night, it is the high circadian-based propensity for sleep that prevents us from prematurely waking up in the early morning hours. Conversely, it is the very low circadian-based propensity for sleep (i.e., circadian wake-promoting signal) that prevents us from falling asleep in the early evening hours when homeostatic sleep pressure is at its highest level. In both cases, circadian and homeostatic systems ideally work in opposition to ensure a consolidated period of sleep or wakefulness (Dijk and Czeisler, 1994, 1995; Dijk and von Schantz, 2005).

Bottom Line: Dampening of the circadian alertness signal and attenuated deterioration of psychomotor vigilance in response to elevated sleep pressure with aging change this interaction pattern.As evidenced by neuroimaging studies, both homeostatic sleep pressure and circadian sleep-wake promotion impact on cognition-related cortical and arousal-promoting subcortical brain regions including the thalamus, the anterior hypothalamus, and the brainstem locus coeruleus (LC).In this perspective, we summarize and discuss here the potential neuroanatomical networks underlying age-related changes in circadian and homeostatic modulation of waking performance, ranging from basic arousal to higher order cognitive behaviors.

View Article: PubMed Central - PubMed

Affiliation: Centre for Chronobiology, Psychiatric Hospital of the University of Basel Basel, Switzerland.

ABSTRACT
Circadian and homeostatic sleep-wake regulatory processes interact in a fine tuned manner to modulate human cognitive performance. Dampening of the circadian alertness signal and attenuated deterioration of psychomotor vigilance in response to elevated sleep pressure with aging change this interaction pattern. As evidenced by neuroimaging studies, both homeostatic sleep pressure and circadian sleep-wake promotion impact on cognition-related cortical and arousal-promoting subcortical brain regions including the thalamus, the anterior hypothalamus, and the brainstem locus coeruleus (LC). However, how age-related changes in circadian and homeostatic processes impact on the cerebral activity subtending waking performance remains largely unexplored. Post-mortem studies point to neuronal degeneration in the SCN and age-related modifications in the arousal-promoting LC. Alongside, cortical frontal brain areas are particularly susceptible both to aging and misalignment between circadian and homeostatic processes. In this perspective, we summarize and discuss here the potential neuroanatomical networks underlying age-related changes in circadian and homeostatic modulation of waking performance, ranging from basic arousal to higher order cognitive behaviors.

No MeSH data available.


Related in: MedlinePlus