Rozalyn Anderson is an associate professor of medicine in the division of geriatrics and gerontology and the division of endocrinology, diabetes and metabolism in the department of medicine at the University of Wisconsin-Madison School of Medicine and Public Health. Her research investigates the biology of aging and what creates the age-associated increase in vulnerability to a spectrum of diseases and disorders. A primary focus of her work is on the mechanisms of delayed aging by caloric restriction in mice and monkeys, with a special emphasis on metabolism as a driver in aging and as a target for interventions to prevent age-related functional loss. Her ongoing research on brain aging and the role of metabolism in neuronal health and resilience to disease as a function of age includes primary cell culture, mouse and nonhuman primate studies.
Anderson is the director of the metabolism of aging program, associate director of the biology of aging and age-related diseases T32 training program, and associate director of research at the William S. Middleton Memorial Veterans Hospital Geriatrics Research Education and Clinical Center. She is a fellow and current president of the American Aging Association and a fellow of the Gerontological Society of America. Her awards include the American Federation for Aging Research Breakthroughs in Gerontology Award, the Glenn Award for Research in Biological Mechanisms of Aging, and the Nathan Shock New Investigator Award from the Gerontological Society of America. Funding sources for her work include the National Institutes of Health/National Institute on Aging, the Glenn Foundation for Medical Research, the American Federation for Aging Research, and the U.S. Department of Veterans Affairs. Anderson serves on several NIH special-interest study sections at NIA and the National Institute of General Medical Sciences and is a permanent member of the NIA-B study section. She mentors undergraduate and graduate students, postdoctoral trainees, and fellows.
Project:
Conserved regulatory pathways in age-related loss of plasticity and cognitive function