Primates

Since the major causes of death in humans are cardiovascular, it is not surprising that primate Table 2 Ulcer Management SOURCE: Author models have been used extensively to study cardiovascular disease and related problems such as obesity and diabetes. Some primates develop atherosclerosis spontaneously, while others must be fed special diets to induce this disease. The latter are usually high in cholesterol and fat. William Cefalu and his colleagues at Bowman Gray School of Medicine have examined various aspects of diet and atherosclerosis in monkeys and compared the manifestations of this disease with those in humans. Dietary lipid is important for both species, and similarities also exist with respect to plasma lipoprotein contributions (i.e., "good" cholesterol or high density lipoprotein, termed HDL, is protective, while "bad" cholesterol, or low density lipoprotein/LDL, contributes to cardiovascular disease), genetic and gender specific susceptibility, and pathology.

Obesity is a risk factor for both cardiovascular problems and diabetes in human and nonhuman primates. Although both obesity and diabetes occur without feeding special diets to nonhuman primates, neither are as prevalent as in humans, at least in the populations of most developed countries. As in humans, diabetes in monkeys is characterized by fasting hypoglycemia (low blood sugar), glucose intolerance, and reduced sensitivity to insulin (the hormone responsible for regulating sugar entry into cells).

Also as in humans, monkeys lose bone mass during aging. In its most extreme form, this constitutes the disease osteoporosis. Females of both species suffer more from this malady than their male counterparts. Part of the problem may stem from the senescence of the reproductive system, and a critical factor in this process is loss of estrogen in females. Rhesus monkeys exhibit regular menstrual cycles of approximately monthly duration until very late in life. Menopause, which is similar to that in humans, occurs with reduced concentrations of blood estrogen and increased concentrations of follicle stimulating hormone (necessary for maturation of ova, but increased in most primates when estrogen levels decline). Loss of estrogen has been linked to both bone loss and cardiovascular disease in humans and monkeys.

Estrogens may also protect, to some extent, against memory (cognitive) loss in many primate species. Menopausal monkeys have more difficulty remembering than pre-menopausal counterparts (Roberts et al.). For this and other reasons, nonhuman primates are used to examine both cognitive changes and overall aging of the brain and nervous system. Various memory tests have been devised to measure different aspects of monkey learning and memory, with the general conclusion being that, like older humans, aged nonhuman primates can still learn new tasks but have difficulty in proportion to the complexity of the challenge. Also like older humans, senescent rhesus monkeys exhibit either neuronal (nerve cell) loss or structural deterioration in certain brain regions. One aspect of the latter, the appearance of so-called senile plaques, parallels a similar phenomenon in humans with Alzheimer's disease.

Finally, it should be mentioned that nonhuman primates also provide important models for evaluating the effects of various interventions on aging and the above age-associated diseases. The most robust such manipulation, reduced dietary caloric intake, has been employed in both rhesus and squirrel monkeys since 1987 (Ingram et al.). It should also be noted that, in addition to information about the diseases of aging, monkeys provide much valuable insight into "healthy" aging as well (Ingram et. al.; Short, Williams, and Bowden). This includes normal age changes in hormones, blood chemistry, and blood cells as well as physiological and behavioral processes.