Dr. Steven N. AustadDepartment Chair, Biology of Aging and the Evolution of Life Histories
Campbell Hall 464
Dr. Austad joined the Department of Biology in 2014. A multi-award winning researcher, his scientific interests concern many aspects of the biology of aging and the evolution of life histories, from molecular processes to evolutionary demography. He investigates aging in a number of species.
Aging is a major puzzle in biology. It is also arguably the most important health problem facing humans today, underlying all major causes of death and disability in the developed world. Why do animals age at all? Why do some species live short lives, physically decaying rapidly and others live exceptionally long and healthy lives? Attempting to identify the underlying cellular and molecular mechanisms that account for such species differences is the basis of Dr. Austad's research in comparative biogerontology. A second interest of his laboratory is in development methods for the assessment of animal healthspan, so that the impact on health (as well as longevity) of potential senescence-retarding therapies can be investigated. More detail on these general interests is given below.
Current Lab Projects
- Assessment of Animal Healthspan. For too long, the study of aging has focused only on how long animals live rather than how well they live. The laboratory is working on developing and refining physiological and behavioral metrics to define mouse health and quality of life. New assays are under constant development. Assays already in use include 24 hour metabolic rate and activity patterns, muscle strength, motor coordination, nerve conduction velocity, and a variety of cognitive tests.
- Impact of Rapamycin on Mouse Healthspan. In 2009, it was reported that the drug rapamycin, which inhibits the TOR pathway, significantly extends the lifespan of 20-month-old mice (the human equivalent of about 60 years of age). The lab is now investigating how rapamycin begun either late or early in life affects the details of healthspan.
- Mechanisms of Exceptional Longevity in Bivalve Molluscs. No other animal group lives as long as the bivalve mollusks (clams, scallops, oyster). More than 10 species are known to live at least a century, with one species (the ocean quahog) well-documented to live more than 500 years. This project compares mitochondrial function, proteome stability, and stress resistance in seven species of mollusks, ranging in longevity from one year to more than 500 years.
- Comparative Biology of Mammalian Aging. The lifespan of mammals in the wild ranges over more than 100-fold difference. The mammalian comparative aging project uses cells and tissues from a wide variety of mammal species, carefully chosen for their longevity, the evolutionary relationships among one another, and their body size, to evaluate hypotheses concerning the cellular, molecular, and endocrinological pathways that affect mammalian aging rate.
- Hydra: New Invertebrate Model for Aging Research. Hydra, because of their remarkable powers of regeneration, have been studied in the laboratory for more than two centuries. However, two recent findings have made them especially interesting with respect to aging. First, although hydra had previously been reported to avoid aging altogether, under certain environmental conditions, they begin to age rapidly. Thus, by comparing non-aging and rapidly aging forms of the same species, we should be able gain insight into the molecular mechanisms that modify aging rate. Second, DNA sequencing of a related cnidarian species discovered that more than 10% of its genes are shared with mammals, but absent in the two major animal models of aging, the worm C. elegans and the fruitfly Drosophila melanogaster. Thus hydra offer the opportunity to discover novel molecular pathways modulating aging that are not available in current model systems.
Select Recent PublicationsZhang, Y, Bokov A, Gelfond J, Soto V, Ikeno Y, Hubbard G, Diaz V, Sloane L, Maslin K, Treaster S, Rendon S, VanRemmen H, Ward W, Javors M, Richardson A, Austad SN, Fischer KE. (2014). Rapamycin extends life and health in C57BL/6 mice. Journals of Gerontology: Biological Sciences & Medical Science 69, 119-30.
Shi Y, Pulliam DA, Liu Y, Hamilton RT, Jernigan AL, Bhattacharya A, Sloane LB, Qi W, Chaudhuri A, Buffenstein R, Ungvari ZI, Austad SN, Van Remmen H. (2013). Reduced mitochondrial ROS, enhanced antioxidant defense, and distinct age-related changes in oxidative damage in muscles of Peromyscus leucopus. American Journal of Physiology: Regulatory, Integrative, and Comp Physiology 304, R343-55.
Gimenez LED, Ghildyal P, Fischer KE, Hu H, Ja WW, Eaton BA, Wu Y, Austad SN, Ranjan R. (2013). Modulation of methuselah expression targeted to Drosophila insulin-producing cells extends life and enhances oxidative stress resistance. Aging Cell 12, 21-9
Ungvari Z, Sosnowska D, Mason JB, Gruber H, Lee SW, Schwartz TS, Brown MK, Storm NJ, Fortney K, Sowa J, Byrne AB, Kurz T, Levy E, Sonntag WE, Austad SN, Csiszar A, Ridgway I. (2013). Resistance to genotoxic stresses in Arctica islandica, the longest living noncolonial animal: Is extreme longevity associated with a multistress resistance phenotype? Journals of Gerontology Biolical Sciences & Medical Sciences 68, 521-29.
Austad SN. (2012) Ageing: Mixed results for dieting monkeys. Nature. 489, 210-11.
Nussey DH, Froy H, Lemaitre JF, Gaillard JM, Austad SN. (2012) Senescence in natural populations of animals: Widespread evidence and its implications for bio-gerontology. Ageing Research Reviews 12, 214-25.
Halloran J, Hussong SA, Burbank R, Podlutskaya N, Fischer KE, Sloane LB, Austad SN, Strong R, Richardson A, Hart MJ, Galvan V. (2012) Chronic inhibition of mammalian target of rapamycin by rapamycin modulates cognitive and non-cognitive components of behavior throughout lifespan in mice. Neuroscience. 223,102-13.
Finch CE, Austad SN. (2012) Primate aging in the mammalian scheme: the puzzle of extreme variation in brain aging. Age (Dordr). 34(5):1075-91.