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Aging and neurodegeneration: Importance of quantifying thermoregulatory stability in a rodent model of aging
Citation:
GORDON, C. J. Aging and neurodegeneration: Importance of quantifying thermoregulatory stability in a rodent model of aging. Presented at Global College for Neuroprotection and Neurodegeneration, Stockholm, SWEDEN, February 28 - March 03, 2010.
Impact/Purpose:
presentation for meeting
Description:
Over our lives, we are exposed to a multitude of insults including heat and cold stress, toxicants, radiation, drugs, oxidative stress, and many others. The cumulative impact of these insults may ultimately be responsible for the etiology of many diseases. Since all life processes directly depend on temperature, as dictated by the principle of the Arrhenius equation, it is hypothesized that subtle changes in body temperature over the life span of an organism could interact with the aforementioned stressors, and ultimately affect overall health and life span. For example, calorie restricted rodents have a prolonged life span compared to ad lib fed subjects. The mild hypothermia associated with caloric restriction is thought to contribute to the lengthening of life span. It follows that the operation of the thermoregulatory system throughout the life span of a homeotherm may ultimately affect its overall health and likelihood of developing neurodegenerative disease. An elevation in body temperature with age would be expected to exacerbate processes that are thought to contribute to neurodegeneration such as oxidative stress and inflammation. To this end, radiotelemetry was used in the current studies to characterize the stability of core temperature and other autonomic processes in the Brown Norway (BN) rat, a popular rodent model of aging. Core temperature(Tc), heart rate(HR), and motor activity(MA) were monitored continuously for 5 days in 4, 12, and 24 month-old male BN rats, representing young, mature, and senescent adult stages, respectively. Age had no effect on HR and MA T, of 4 and 12 month-old rats was essentially identical; however, T, of 24 month-old rats was significantly elevated by ~0.5 DC during the daylight hours. In another study, T, and MA were monitored at 2-3 month intervals in BN rats, beginning at 60 days and ending at 24 months of age. The mean Tc reached a nadir of 37.2 DC at 8 months of age and then began to increase gradually, reaching 37.8 DC by 24 months of age. Metabolism was measured by direct calorimetery in a separate group ofaging BN rats. Metabolic rate decreased from 9.5 to 7.4 W/kg as the rats aged from 4 to 24 months. Thus, aging in the BN rat is associated with a gradual rise in Tc that is apparently not a result of an elevationin tissue metabolism. It is possible that the rise in Tc with age maybe regulatedas a result of a change in the set-point for thermoregulation. Understanding this process gives us a better understanding of the potential interaction between body temperature, life span, and the etiology of neurodegenerative and other diseases.