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Wednesday, July 8, in the journal Nature, The University of Texas Health Science Center at San Antonio and two collaborating centers reported that the Easter Island compound - called "rapamycin" after the island's Polynesian name, Rapa Nui - extended the expected lifespan of middle-aged mice by 28 percent to 38 percent. In human terms, this would be greater than the predicted increase in extra years of life if cancer and heart disease were both cured and prevented.
The rapamycin was given to the mice at an age equivalent to 60 years old in humans.
The studies are part of the National Institute on Aging (NIA) Interventions Testing Program, which seeks compounds that might help people remain active and disease-free throughout their lives. The other two centers involved are the University of Michigan at Ann Arbor and Jackson Laboratory in Bar Harbor, Maine.
The Texas study was led by scientists at two institutes at the UT Health Science Center: the Institute of Biotechnology (IBT) and the Barshop Institute for Longevity and Aging Studies.
"I've been in aging research for 35 years and there have been many so-called 'anti-aging' interventions over those years that were never successful," said Arlan G. Richardson, Ph.D., director of the Barshop Institute. "I never thought we would find an anti-aging pill for people in my lifetime; however, rapamycin shows a great deal of promise to do just that."
he secret to longevity may lie in an enzyme with the ability to promote a robust immune system into old age by maintaining the function of the thymus throughout life, according to researchers studying an "anti-aging" mouse model that lives longer than a typical mouse.
The study, led by Abbe de Vallejo, Ph.D., associate professor of pediatrics and immunology, University of Pittsburgh School of Medicine, and immunologist at Children's Hospital of Pittsburgh of UPMC, reports that the novel mouse model has a thymus that remains intact throughout its life. In all mammals, the thymus?the organ that produces T cells to fight disease and infection?degenerates with age.
Results of the study are published in this week's issue of the Proceedings of the National Academy of Sciences.
"These findings give us hope that we may one day have the ability to restore the function of the thymus in old age, or perhaps by intervening at an early age, we may be able to delay or even prevent the degeneration of the thymus in order to maintain our immune defenses throughout life," said Dr. de Vallejo.
The mouse model that Dr. de Vallejo's team studied was developed by his colleague Cheryl Conover, Ph.D., an endocrinology researcher at Mayo Clinic. In this "knockout" mouse model, researchers deleted an enzyme known as pregnancy-associated plasma protein A (PAPPA). PAPPA-knockout mice live at least 30 percent longer and have significantly lower occurrence of spontaneous tumors than typical mice.
PAPPA controls the availability in tissues of a hormone known as insulin-like growth factor (IGF) that is a promoter of cell division. Hence, IGF is required for normal embryonic and postnatal growth. But IGF also is associated with tumor growth, inflammation and cardiovascular disease in adults. By deleting PAPPA, the researchers were able to control the availability of IGF in tissues and dampen its many ill effects. In the thymus, deletion of PAPPA maintained just enough IGF to sustain production of T cells without consuming precursor cells, thereby preventing the degeneration of the thymus.
"Controlling the availability of IGF in the thymus by targeted manipulation of PAPPA could be a way to maintain immune protection throughout life," Dr. de Vallejo said. "This study has profound implications for the future study of healthy aging and longevity."
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