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Senior Scholar Awards in Aging 1998

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)

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)

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)

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.

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)

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.

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)

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.

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.

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.

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.

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.

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.

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.