The normal amount of deep sleep is highly age-dependent, and few individuals over age 50 spend more than 5% of the night in stage III and stage IV sleep. For a healthy young person, the first progression through the four nonREM sleep stages (ie, stage I through stage IV) typically takes 70 to 100 minutes; the elapsed time from sleep onset until the beginning of the Inhibitors,research,lifescience,medical first REM period is called REM latency. With normal aging, REM latency characteristically grows shorter because of the loss of slow-wave sleep, and with advanced age the entire night may be spent in only three sleep stages (stage I, stage II, and REM). Sleep architecture is somewhat sex-dependent and, as noted

above, Inhibitors,research,lifescience,medical highly influenced by aging. Women tend to have a greater percentage of deep sleep than men, particularly prior to menopause. Across decades of aging, sleep typically becomes lighter, with more awakenings and awake time. There is also a progressive loss of slow-wave sleep with aging, which Inhibitors,research,lifescience,medical typically occurs in men at an earlier age than women. Sleep quality may be further adversely affected by age-dependent increases in

sleepdisordered breathing. Beyond the direct relationship between sleep deprivation and neurobehavioral function, recent research has linked disturbances of sleep to other important health risks. For example, insomnia is associated with an increase in the cascade of cytokines and Inhibitors,research,lifescience,medical other “markers” of inflammatory processes.15 Disturbed sleep also is associated with alterations in glucose metabolism and may

represent a risk factor for development of obesity16 and adult-onset diabetes mellitus.17 It is not surprising, then, that research has established that “healthy” sleep is a reliable correlate of sub jective well-being, overall physical health, and successful aging.18 Neuroimaging and sleep The availability of modern Inhibitors,research,lifescience,medical imaging methods has permitted a more functional characterization of selected aspects of the topography of sleep.8,9,19,20 Although technological limitations in the measurement of cerebral blood flow or regional shifts in metabolic activity have necessitated Selleck Veliparib focusing on key transition Casein kinase 1 points, such as from waking to nonREM sleep or from nonREM to REM sleep, interesting findings are emerging. Consistent with the homeostatic function of sleep, blood flow and glucose metabolism globally decrease with the transition from waking to sleeping, with the greatest decline during deep sleep.8,9,19,20 Conversely, individuals with primary insomnia have been found to have relatively greater cerebral metabolism during nonREM sleep.21 The onset of REM sleep is associated with a sharp increase in blood flow and cerebral metabolism, including – but not limited to – limbic and pontine structures.