SPEAKERS
Daniel Gottschling, Ph.D. |
Daniel Gottschling is a Member of the Division of Basic Sciences at the Fred Hutchinson Cancer Research Center. Dr. Gottschling uses the budding yeast Saccharomyces Cerevisiae to explore the molecular basis of the link between age and cancer susceptibility. One of the hallmarks of cancer cells is genomic instability. The Gottschling laboratory demonstrated that yeast switch to a state of high genomic instability as they approach the end of their replicative lifespan. Dr. Gottschling hypothesized that a build up of damaged proteins caused genomic instability. He went on to identify the first protein quality control degradation pathway of the nucleus. Currently, Dr. Gottschling is focused on discovering the mechanisms by which this pathway detects and destroys aberrant nuclear proteins and the role this plays in aging. |
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Carol Greider, Ph.D. |
Carol Greider is the Daniel Nathans Professor and Director of the Department of Molecular Biology and Genetics at the Johns Hopkins University School of Medicine. In 1984, while a graduate student in the laboratory of Elizabeth Blackburn, she discovered telomerase, an enzyme that maintains telomeres, or chromosome ends. Dr. Greider went on to clone and characterize the RNA component of the telomerase enzyme. Together with Calvin Harley, she showed that telomeres shorten progressively in cultured human cells. This work led to the idea that telomere maintenance and telomerase may play important roles in cellular senescence and cancer. Currently, Dr. Greider is exploring the essential role of telomerase in stem cell viability. Dr. Greider is a member of the National Academy of Sciences and a fellow of the American Academy of Arts and Sciences. She received the Albert Lasker Award for Basic Medical Research in 2006. |
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Cynthia Kenyon, Ph.D.
Keynote Speaker |
Cynthia Kenyon is the Herbert Boyer Professor of Biochemistry and Biophysics at the University of California, San Francisco, and director of the Hillblom Center for the Biology of Aging. She is also co-founder of the biotech company Elixir, whose goal is to develop drugs that delay diseases of aging by slowing the aging process. In 1993, her laboratory discovered that mutations in the gene daf-2, which encodes a receptor similar to the human insulin and IGF-1 receptors, could double the lifespan of the nematode C. elegans, thereby demonstrating that aging is controlled hormonally. Since then, insulin/IGF-1 endocrine systems have been shown to regulate the longevity of flies and mice as well, and Dr. Kenyon has demonstrated that the perturbation of insulin/IGF-1 signaling and reproductive cells in the same animal allow it to live up to six times longer than normal while maintaining a healthy life. Her findings have important disease applications: the insulin/IGF-1 pathway mutations not only extend youthfulness and lifespan but also delay the time of onset of protein aggregation in a nematode model of Huntington's disease, while long-lived mice with reduced IGF-1 levels are resistant to carcinogens. Currently, Dr. Kenyon is trying to understand how the insulin/IGF-1, reproductive, and mitochondrial pathways—as well as another perturbation, caloric restriction—influence lifespan at the molecular level. Dr. Kenyon is a member of the National Academy of Sciences and a fellow of the American Academy of Arts and Sciences. |
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George Martin, M.D. |
Dr. Martin is Professor Emeritus of Pathology (Active), Adjunct Professor of Genome Sciences (Retired) and Director Emeritus of the Alzheimer's Disease Research Center—all at the University of Washington. He was the founding director of the Medical Scientist Training Program and the NIA "Genetic Approaches to Aging" training grant at that institution. His research has involved genetic approaches to elucidate the pathobiology of aging and age-related diseases. This has included basic research in somatic cell genetics, the replicative senescence of human somatic cells, and the formal genetic analysis of progeroid syndromes. Highlights have included leadership roles in the discovery of the genetic defect causing the Werner syndrome and certain familial forms of Alzheimer's disease. His laboratory was also the first to demonstrate the rising frequencies, with age, of somatic mutations in human epithelial cells. At a more clinical level, Dr. Martin has systematized our knowledge of human genetic disorders from the point of view of their rich potential to elucidate specific aspects of the senescent phenotype and used this analysis to make inferences concerning the polygenic basis of aging. More recent research has utilized genetic engineering in mice to elucidate mechanisms of aging and Alzheimer's disease. His honors have included election to the Institute of Medicine of the National Academy of Sciences and a Lifetime Achievement Award of the World Alzheimer Congress. National service has included the presidencies of the Tissue Culture Association of America and the Gerontological Society of America. He currently serves as the Scientific Director of the American Federation for Aging Research. |
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Tom Misteli, Ph.D. |
Tom Misteli is a Principle Investigator in the Laboratory of Receptor Biology and Gene Expression at the National Cancer Institute, where he heads the Cell Biology of Gene Expression group. Dr. Misteli uses several differentiation and disease models, specifically progerias, diseases that resemble premature aging, to elucidate how genome organization contributes to normal cell function.
Dr. Misteli discovered that the same molecular mechanism that causes Hutchinson Gilford Progeria Syndrome (HGPS) plays a role in normal aging. He also demonstrated a method to correct the aberrant splicing event that causes HGPS and rescue the disease phenotype in cultured cells. Dr. Misteli is currently exploring the molecular mechanisms that cause these cellular defects and is developing novel therapeutic strategies to eliminate them. |
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Thomas Rando, M.D., Ph.D. |
Thomas Rando is Associate Professor in the Department of Neurology and Neurological Sciences at the Stanford University School of Medicine and Deputy Director of the Stanford Center on Longevity. A practicing physician, Dr. Rando is also Chief of the Neurology Service and Director of the Geriatric Research, Education, and Clinical Center at the VA Palo Alto Health Care System. The regenerative potential of tissues, such as muscle and liver, decreases with age, but the mechanism of this decline is unknown. The Rando laboratory is exploring how stem cell function changes with age and contributes to reduced regenerative potential. In muscle, Dr. Rando discovered that Notch signaling is a key determinant of regenerative potential. Forced activation of Notch in muscle precursor cells (satellite cells) restored regenerative potential to aged muscle. Dr. Rando went on to demonstrate that fusing the circulatory systems of old and young mice (parabiotic pairings) restored Notch signaling and regenerative capacity of aged satellite cells. A similar result was observed in the liver, suggesting that systemic factors that change with age modulate progenitor cell function. Currently, Dr. Rando is working to identify such factors, to characterize changes in stem cell niches with age, and to assess stem cell functionality in mice with accelerated or retarded aging. |
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John Tower, Ph.D. |
John Tower is Associate Professor in the Department of Biological Sciences at the University of Southern California. Dr. Tower uses Drosophila to investigate the basic mechanisms of aging. He demonstrated that overexpression of superoxide dismutase genes, which encode antioxidant enzymes, increases lifespan. Moreover, Dr. Tower developed a new mutagenesis method to identify additional genes that extend lifespan. He also discovered that heat shock genes are upregulated during aging, and that this occurs in characteristic spatial and temporal patterns. Currently, Dr. Tower is performing a detailed analysis of transcriptional and post-transcriptional regulation of two Drosophila heat shock protein genes during aging. He is also using microarrays to analyze changes in gene expression during aging, with a focus on identifying genes that regulate stem cell survival and proliferation during aging. |
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