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Rafael de Cabo, Ph.D., Senior Investigator
Experimental Gerontology Section
Rafael de Cabo, Ph.D.After receiving his B.S. and M.S. from the University of Cordoba, Spain, Dr. de Cabo earned his Ph.D. in 2000 from the Department of Foods and Nutrition at Purdue University. Upon completion of his graduate education, he received a postdoctoral position in the Laboratory of Neurosciences at the National Institute on Aging in Baltimore, Maryland. In 2004, he was appointed as a tenure track investigator in the Laboratory of Experimental Gerontology, where he now heads the Aging, Metabolism, and Nutrition Unit (AMNU). The AMNU applies both physiological and tissue-specific molecular approaches to investigate effects of nutritional interventions on basic mechanisms of aging and age-related diseases. Research within his unit strives to identify protective mechanisms invoked by caloric restriction and to evaluate the consequences of dietary interventions on lifespan, pathology, and behavioral function. The AMNU balances the exploration of in vivo rodent, as well as in vitro, paradigms of caloric restriction. Dr. de Cabo is an active member of the Board of the American Aging Association.
The Aging, Metabolism, and Nutrition Unit (AMNU) applies whole body physiological and tissue-specific molecular approaches to investigate effects of nutritional interventions on basic mechanisms of aging and age-related diseases. Caloric restriction (CR), without malnutrition, is widely known to extend lifespan and retard a wide variety of aging processes in several short-lived species and is the primary paradigm employed by AMNU scientists. Research within this unit uses both rodent models of CR as well as an in vitro model for CR. CR affects metabolic regulation to induce an overall phenotypic change leading to a decrease in cellular proliferation and growth rates. CR induces measurable changes on circulating levels of several hormones and growth factors that regulate cell growth and proliferation. Serum obtained from CR animals alters growth, proliferation and stress responses of cells in culture. We have demonstrated that it is possible to investigate certain aspects of CR using this in vitro approach. This approach lends itself to a more rapid investigation of possible mechanisms and, perhaps more importantly to the research, development and rapid evaluation of interventions that would be able to induce or promote a phenotype similar to that seen with CR, essentially a CR mimetic.
CR extends lifespan in a variety of animal model systems and reduces oxidative stress during aging. At least in part, the reduction in oxidative stress may be explained by the fact that animals on CR reach a new bioenergetic equilibrium. Two major components in the bioenergetic pathway are the mitochondria electron transport chain and the plasma membrane (PM) redox system (PMRS). Ubiquinone is the central molecule of the PMRS and protects the membrane under different stress conditions. Aging induces general macromolecular damage that can be prevented and reversed by CR. Preliminary data suggest that several components of the PMRS are altered during aging and that several of these changes are modified by CR in rats and mice. Analysis of the bioenergetic balance between mitochondria and PM in rats and mice on CR can provide the information that might explain the enhanced resistance to oxidative stress that CR affords during aging. The role of the PMRS in the prevention of oxidative stress by CR during aging can provide the basis for the design of potential CR mimetics and nutritional interventions.

Contact Information:
Translational Gerontology Branch
Biomedical Research Center, room 09C218
251 Bayview Boulevard, Suite 100
Baltimore, MD 21224

Phone 410-558-8510
Fax 410-558-8302
E mail deCaboRa@mail.nih.gov

For more information about the Translational Gerontology Branch:
http://www.irp.nia.nih.gov/branches/tgb/tgb.htm

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Updated: Wednesday May 15, 2013