The circadian timing system and circadian clock are altered in senescence. Circadian rhythms of body temperature, melatonin, corticosterone, and serum testosterone all show reduced amplitude in old rats. In addition, changes in the intrinsic period and phase angle of entrainment to light-dark cycles have been observed in rhythms of old hamsters. A dramatic age-related decrease in the amplitude of circadian rhythms has also been observed in a number of animal models. Moreover, the effects of age on activity rhythms can be reversed with SCN grafts from young animals. Because mRNA synthesis in mammals has been demonstrated to decrease with age, altered production of clock proteins may contribute to age-related changes. Aging also appears to alter the response to entraining agents such as light. For example, the light-induced increase in the number of c-Fos and JunB immunor-eactive SCN cells is significantly attenuated in aged animals. More recently, it has also been suggested that reductions in polysialyted neural cell adhesion molecules on the surface of SCN cells may contribute to the aging-related deficits in circadian function.

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