Sleep in Normal Aging, Homeostatic and Circadian Regulation and Vulnerability to Sleep Deprivation

In the context of geriatric research, a growing body of evidence links normal age-related changes in sleep with many adverse health outcomes, especially a decline in cognition in older adults. The most important sleep alterations that continue to worsen after 60 years involve sleep timing, (especially early wake time, phase advance), sleep maintenance (continuity of sleep interrupted by numerous awakenings) and reduced amount of sigma activity (during non-rapid eye movement (NREM) sleep) associated with modifications of sleep spindle characteristics (density, amplitude, frequency) and spindle–Slow Wave coupling. After 60 years, there is a very clear gender-dependent deterioration in sleep. Even if there are degradations of sleep after 60 years, daytime wake level and especially daytime sleepiness is not modified with age. On the other hand, under sleep deprivation condition, older adults show smaller cognitive impairments than younger adults, suggesting an age-related lower vulnerability to extended wakefulness. These sleep and cognitive age-related modifications would be due to a reduced homeostatic drive and consequently a reduced sleep need, an attenuation of circadian drive (reduction of sleep forbidden zone in late afternoon and wake forbidden zone in early morning), a modification of the interaction of the circadian and homeostatic processes and/or an alteration of subcortical structures involved in generation of circadian and homeostatic drive, or connections to the cerebral cortex with age. The modifications and interactions of these two processes with age are still uncertain, and still require further investigation. The understanding of the respective contribution of circadian and homeostatic processes in the regulation of neurobehavioral function with aging present a challenge for improving health, management of cognitive decline and potential early chronobiological or sleep-wake interventions.