Steven N. Austad, Ph.D., Professor
Purdue University,
1981

STCBM (210) 562-6011
AUSTAD@UTHSCSA.EDU

Dr. Austad joined the Department of Cellular and structural Biology faculty in June 2004. A Fellow of the Gerontological Society of America since 1993, he is a past recipient of the Robert W. Kleemeier Award (2003) for outstanding research and the Geron Corporation-Samuel Goldstein Distinguished Publication Award (1994) from that Society. He received as well the Nathan A. Shock Award (1994) from the Gerontological Research Center of the National Institute on Aging. He currently serves as Section Editor on the Editorial Boards of Neurobiology of Aging and Aging Cell and as Associate Editor of the Journals of Gerontology: Biological Sciences. With Dr. Edward J. Masoro, he co-edited both the 5th (2001) and 6th (2006) Editions of the Handbook of the Biology of Aging. He also serves (since 2001) on the Initial Review Group for aging grants of the Ellison Medical Foundation. He has served on the NIH Cellular Mechanisms of Aging and Development Study Section. In addition, he co-directs (with Dr. Gary Ruvkun, Harvard University) the 3-week summer course on the Molecular Biology of Aging at the Woods Hole Marine Biological Laboratory. Dr. Austad maintains a keen interest in the communication of science to the general public, and in that capacity has served on the Science Advisory Board of National Public Radio (1992-1997) and has been a consultant to the Oregon Museum of Science and Industry and the American Museum of Natural History in New York City. He has written popular science articles for numerous publications including Natural History magazine, Scientific American, National Wildlife, and International Wildlife. His trade book, Why We Age (1997), has been translated into 7 languages.

Visualizing DNA damage. The Comet’s “tail” shows increasing DNA damage with increasing exposure to gamma irradiation

Research Interests: A major puzzle in biology is why some species live short lives with rapid physical decay and others live much longer, senescing slowly. 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. Using cells isolated from multiple short- and long-lived species, including bats (which can live 40+ years in the wild), squirrels, marmosets, baboons, as well as traditional laboratory rats and mice, the Austad lab investigates comparative cellular stress resistance, and mechanisms underlying that stress resistance, in particular how species differ in their resistance to exogenous DNA damage and how quickly they repair that damage. The rationale for these studies is that published work on long-lived mutants of worms, flies, and mice suggests that cellular stress resistance is enhanced in long-lived genotypes. Furthermore, species longevity has been reported to correlate with cellular stress resistance. We note that some cell types may turn out to be more informative than others in elucidating critical aging mechanisms. The laboratory has been focusing on dermal fibroblasts, but we are expanding to investigate neuronal progenitor cells as well. An extension of the lab’s comparative approach is to identify informative new animal species for development as medical models. A second project the lab is involved with is the development of the common marmoset, a short-lived, rat-sized primate, as a valuable model species for the study of cognitive aging, the impact of diet on aging, therapeutic drug response, and the effects of early life events on later life pathology.

Mouse cells (left) are more susceptible to DNA damage caused by irradiation than are cells from the long-lived naked mole-rat (right). Cells exposed to 4 Gy gamma irradiation. The more DNA in comet “tail” compared to the comet “head,” the more strand breaks have occurred. In the mouse cell 49% of the DNA is in the tail compared with 24% for the naked mole-rat cell, indicating that the naked mole-rat genome is better protected.

PUBLICATIONS:
Shupe, JM, Kristan, DM, Austad, SN, Stenkamp, DL. (2006) The eye of the laboratory mouse remains anatomically adapted for natural conditions. Brain Behav Evol. 67(1):39-52. Epub 2005 Oct 10.

Podlutsky, AJ, Khritankov, AM, Ovodov, ND, Austad, SN. (2005) A new field record for bat longevity. J Gerontol A Biol Sci Med Sci. Nov;60(11):1366-8.

Lorenzini, A, Tresini, M, Austad, SN, Cristofalo, VJ. (2005) Cellular replicative capacity correlates primarily with species body mass not longevity. Mech Ageing Dev. Oct;126(10):1130-3.

Austad, SN. (2005) Diverse aging rates in metazoans: targets for functional genomics. Mech Ageing Dev. Jan;126(1):43-9. Review.

Brunet-Rossinni, AK, Austad, SN. (2006) Senescence in natural populations of mammals and birds. In Handbook of the Biology of Aging, 6th Ed. Masoro, EJ & Austad, SN (eds.). Academic Press, San Diego, CA. pp. 243-265. (ISBN 0-12-088387-2)

Miller, RA, Austad, SN. (2006) Growth and aging: why do big dogs die young? In Handbook of the Biology of Aging, 6th Ed. Masoro, EJ & Austad, SN (eds.). Academic Press, San Diego, CA. pp. 512-533. (ISBN 0-12-088387-2)

Austad, SN, Podlutsky, A. (2006) A critical evaluation of nonmammalian models for aging research. In Handbook of the Biology of Aging, 6th Ed. Masoro, EJ & Austad, SN (eds.). Academic Press, San Diego, CA. pp. 449-469. (ISBN 0-12-088387-2)

Austad, SN. (2005) A biologist’s perspective: whence come we, where are we, whither go we? In. Enduring Questions and Changing Perspectives in Gerontology. D.J. Sheets, D.B. Bradley, & J. Hendricks, Eds. New York: Springer Publishing. pp. 29-62. (ISBN 0-8261-6415-3)