Life Span Of Monkeys Research Articles

A Method to Investigate Astrocyte and Microglial Morphological Changes in the Aging Brain of the Rhesus Macaque.

With a rapidly aging population, studies of neuroinflammation and degeneration associated with eugeric aging are becoming critical. Using the unique archive at the Tulane National Primate Research Center as a resource, we have developed tools to quantify morphological changes in astrocytes and microglia across the life span of monkeys. This method can be used for morphometric studies of multiple parameters simultaneously in an unbiased manner.

Caloric restriction, gene expression and aging

Caloric restriction (CR) increases maximum life span in many species. In laboratory rodents, CR started either early in life or in middle-age opposes the development of age-associated biological and pathological changes. Three main questions are being asked by CR investigators. How does CR retard aging and disease processes? There is evidence that CR lowers oxidative stress generated by mitochondrial oxidative energy (i.e., calorie) metabolism. This lowering is most profound in post-mitotic tissues. Using microarrays, we have described the gene expression profile of aging skeletal muscle, heart and brain in mice and its alteration by CR. We observed that CR opposes the development of many age-associated changes while shifting the level of expression for many genes which are stable in expression with aging in normally fed mice. Does CR retard aging in primates? Two ongoing studies in rhesus monkeys on CR plus epidemiological data support the idea of human translatability. Whether CR extends life span in monkeys should become known in ∼15 years. Studies in humans on CR were launched by the NIA in 2002. Can substances be found which mimic the beneficial actions of CR? The search for “CR mimetics” should benefit from genomic and proteomic approaches.

Caloric restriction, gene expression, and aging.

Abstract Caloric restriction (CR) increases maximum life span in many species. In laboratory rodents, CR started either early in life or in middle-age opposes the development of age-associated biological and pathological changes. Three main questions are being asked by CR investigators. How does CR retard aging and disease processes? There is evidence that CR lowers oxidative stress generated by mitochondrial oxidative energy (i.e., calorie) metabolism. This lowering is most profound in post-mitotic tissues. Using microarrays, we have described the gene expression profile of aging skeletal muscle, heart and brain in mice and its alteration by CR. We observed that CR opposes the development of many age-associated changes while shifting the level of expression for many genes which are stable in expression with aging in normally fed mice. Does CR retard aging in primates? Two ongoing studies in rhesus monkeys on CR plus epidemiological data support the idea of human translatability. Whether CR extends life span in monkeys should become known in ∼15 years. Studies in humans on CR were launched by the NIA in 2002. Can substances be found which mimic the beneficial actions of CR? The search for “CR mimetics” should benefit from genomic and proteomic approaches.

The use of interferon for emergency prophylaxis of marburg hemorrhagic fever in monkeys.

The possibility of emergency prophylaxis of Marburg hemorrhagic fever with leukocytic and recombinant interferons was studied in experiments on Cercopithecus aethiops. None of the agents protected monkeys from the action of lethal doses of Marburg virus. Recombinant interferon-alpha(2)administered according to the emergency prophylaxis schedule prolonged the mean life-span of monkeys injected with Marburg virus in doses of 100 and 1000 LD50 by 1.9 and 6.1 days, respectively.