| Seymour Benzer, Ph.D. California Institute of Technology | | Life extension genes in Drosophila
1998 Senior Scholar Award in Aging
Animals with longer lifespan usually have higher resistance to stress. The extended-lifespan Drosophila mutant methuselah resists all three different stresses tested, heat, starvation,
and paraquat, an oxygen free radical generator. This suggests a
molecular approach to identifying genes which are up-regulated by all three stresses, as candidates... (more) |
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| Judith Campisi, Ph.D. Lawrence Berkeley National Laboratory | | Telomeres, Cell Phenotype and Aging
1998 Senior Scholar Award in Aging
Telomeres are structures composed of a specific DNA sequence and specialized proteins that cap the ends of chromosomes. Telomeres stabilize the chromosome, and thus ensure that the genome is maintained in a normal, stable state. Normal human cells lose a small amount of telomeric DNA each time they divide. When the telomeres reach a critically short length,... (more) |
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| Luca Cavalli-Sforza, M.D. Stanford University School of Medicine | | Genes Controlling Longevity in Centenarians
1998 Senior Scholar Award in Aging
Subjects who can comfortably reach very old ages may have an advantageous consatellation of genes, giving them resistance to many causes of stress and disease, or may simply have one or more genes affecting the duration of their life. Such longevity genes have been observed in other organisms. The contribution to the study of aging we are planning aims... (more) |
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| Stephen J. Elledge, Ph.D. Baylor College of Medicine | | Connections Between the Telomere Sensing and DNA Damage Accumulation
1998 Senior Scholar Award in Aging
Dr. Elledge has an interesting hypothesis that could unify the telomere and DNA
damage theories of cell senescence. He will study the regulation of the ARF1
gene over time, and its interaction with DNA damage, to cause cell senescence.
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| Daniel E. Gottschling, Ph.D. Fred Hutchinson Cancer Research Center | | Replicative senescence in S. cerevisia
1998 Senior Scholar Award in Aging
The yeast Saccharomyces cerevisiae has become recognized as a model system for studying replicative senescence in eukaryotes. It permits easy genetic and physiological manipulations of cells, and a chance to examine aging cells in a homogeneous population. However, current methods of aging analysis in yeast are cumbersome and do not take... (more) |
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| Paul Greengard, Ph.D. Rockefeller University | | Novel APP - containing synaptic organelles and Alzheimer's disease
1998 Senior Scholar Award in Aging
Amyloid Precursor Protein (APP) is the precursor of Ab, which appears to be
critical in the initiation of Alzheimer's disease. Dr. Greengard's research will
characterize synaptic organelles that are the major site of APP in nerve terminals.
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| Carol W. Greider, Ph.D. Johns Hopkins University | | The roles of recombination and telomerase in telomere maintenance
1998 Senior Scholar Award in Aging
We are interested in understanding how cells maintain their chromosomes, the structures that transmit genetic information. Specifically, we are interested in the ends of chromosomes, known as telomeres. Telomeres are specialized structures that are essential for the chromosomes maintenance. When chromosomes are not properly... (more) |
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| Leonard Guarente, Ph.D. Massachusetts Institute of Technology | | Molecular analysis of mammalian aging
1998 Senior Scholar Award in Aging
Dr. Guarente is extending his studies of genetic mechanisms of aging in yeast to
mammals. He intends to determine changes in rDNA that accumulate with age in
mice. He will then generate transgenic mice with specific rDNA changes in order
to test whether specific changes cause aging. |
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Thomas E. Johnson, Ph.D. University of Colorado - Boulder | | Identification of gerontogenes in the mouse
1998 Senior Scholar Award in Aging
In previous research, Dr. Johnson identified gerontogenes (genes that specify
length of life) in the nematode worm C. elegans. Dr. Johnson now proposes to
search for such genes in mice using Recombinant Inbred line and by stress
induced mutagenisis. |
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| Cynthia J. Kenyon, Ph.D. University of California - San Francisco | | Analysis of genes that control aging in C. elegans
1998 Senior Scholar Award in Aging
Dr. Kenyon believes that the study of short-lived mutants of C. elegans may lead
to the identification of important life-span regulating genes. She proposes to
identify such genes. She will also import human genes into C. elegans short-lived
mutants in order to see which of theses genes best compensate for the lost worm
gene. |
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Thomas Perls, M.D., M.P.H Boston Medical Center | | Exploring the genetics of extreme longevity
1998 Senior Scholar Award in Aging
Three human families with clusters of extremely long-lived individuals will be
analyzed in order to identify specific genes responsible for extreme longevity. |
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| Gregory A. Petsko, D. Phil. Brandeis University | | How cells die in Alzheimer's and other neurodegenerative diseases
1998 Senior Scholar Award in Aging
Fragments of Alzheimer's polypeptide (APP) are found in senile plaques. Some
fragments ( Ab, 1-40 and 1-42 ) appear to be toxic to the brain. Dr. Petsko
proposes to identify the enzyme (s) that produce these fragments and then, using
Ab, resistant mutants, determine how the Ab, peptides kill nerves. |
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| Gary Ruvkun, Ph.D. Harvard Medical School | | Exploration of the C.elegans insulin-like aging pathway
1998 Senior Scholar Award in Aging
Dr. Ruvkun has previously shown that an insulin-like signaling pathway regulates
longevity and metabolism in C. elegans. The most important output of this
pathway in C. elegans is the transcription factor DAF-16. Dr. Ruvkun now
proposes to search for the downstream targets of DAF-16 in order to identify the
downstream daf-16 genes involved in longevity control.
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| Jerry W Shay, Ph.D. University of Texas Southwest Medical Center | | Role of telomeres and telomerase in human aging
1998 Senior Scholar Award in Aging
Telomere length appears to be critically involved in cellular senescence and in cellular immortality. Telomerase shortening results in cellular senescence, while stabilization of telomere length results in cellular immortality and cancer. Regulation of telomere length is usually, but not always, maintained by levels of the enzyme telomerase. Dr. Shay proposes to clarify alternative mechanisms to maintain telomeres, determine the mechanism by which shortening of telomeres induces cellular senescence, and investigate the genetic mechanism underlying the premature aging syndrome, Hutchinson-Gilford progeria. |
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