Aging is associated with sleep disruptions in humans, monkeys, dogs, cats, rats, mice, and flies. In humans, and in the genetic model organism Drosophila melanogaster, sleep deficits begin during middle age and become more pronounced with age. Importantly, sleep duration and insomnia have been linked with an increased risk of all-cause mortality. Moreover, the adverse effects of sleep loss on metabolic processes, endocrine and immunological functions may increase the susceptibility of individuals to serious diseases,including obesity, type II diabetes and coronary heart disease. These data suggest that age-related functional declines in sleep regulatory pathways may alter the time-course of functional senescence in other systems. Unfortunately, the genetic mechanisms that control senescence in sleep regulation and their impact on other organ systems are unknown. In the proposed studies we will: 1) evaluate the relationship between sleep-quality and neuronal plasticity during aging;2) determine the genetic requirements of insulin/TOR signaling in controlling age-related deficits in sleep and neuronal plasticity;3) screen for genetic suppressors of sleep aging.
In humans, sleep deficits begin during middle age and become more pronounced with age. Importantly, sleep duration and insomnia have been linked with an increased risk of all-cause mortality. We propose to use genetics to offset age-related functional declines in sleep regulatory pathways thereby slowing functional aging.
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