Abstract
Aging significantly impacts circadian timing in mammals. The amplitude and precision of behavioral, endocrine, and metabolic rhythms decline with age. This is accompanied with an age-related decline in the amplitude of central pacemaker output, although the molecular clock in the suprachiasmatic nucleus exhibit robust oscillation. Peripheral clocks also exhibit robust oscillation during aging, when extensive reprogramming of other genes' expression rhythms occurs in peripheral tissues. The age-related dissociation between the molecular clock and downstream rhythms in both central and peripheral tissues indicates that mechanisms other than the molecular clock are involved in mediating the impact the aging on circadian organization. In this article, findings are reviewed on the impact of aging on circadian timing functions, and the potential role of increased inflammatory response in age-related changes in circadian organization is highlighted.
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