Sunday, April 19, 2009

ASBMB Annual Meeting to feature talks on the biochemistry of aging

18 april 2009--Five-hundred years ago, Ponce de Leon combed the swamps of Florida seeking the legendary "fountain of youth." This week, at the 2009 ASBMB Annual Meeting in New Orleans (held in conjunction with Experimental Biology 2009) will feature a range of exciting talks centering on the new molecular "fountain of youth," the genes and pathways that influence lifespan. While the secrets of longevity may still be a long time away, the presentations at ASBMB illustrate that we are at least beginning to understand the intricate connections between diet, metabolism, aging, and disease.
Some of these aging-related presentations include:
Regulation of Obesity, Heart Function, and Lifespan by the Nutrient Sensing TOR Pathway Sean Michael Oldham, Burnham Institute for Medical Research, La Jolla, CA (Sun, April 19 3:30 PM - 5:50 PM, Room: 356)
Metabolic balance is a highly regulated process, and genetic and/or diet-induced imbalances (like a high fat diet, HFD) bring about increased susceptibility to obesity, diabetes, cardiovascular disease, and cancer. Oldham's group has established a fruit fly model to study the genes and environmental factors responsible for mediating HFD induced obesity. They found that inhibiting the Target of Rapamycin (TOR) pathway, involved in nutrient sensing, can block the detrimental effects of a HFD. They also found that reducing the levels of TOR can mimic a calorie-restricted diet and improve metabolism, heart function and longevity. Thus, in addition to potentially linking HFD-obesity to diabetes and heart disease, TOR might be a central mediator of lifespan.
Conserved Links Between Nutrient Signaling, Translation and Aging Brian Kennedy, University of Washington, Seattle (Wed, April 22 8:30 AM - 10:50 AM, Room: 356)
While model organisms like fruit flies have been invaluable in identifying hundreds of genes associated with aging, there is still concern that any increases in fly lifespan simply cannot be expected to work in mammals. Kennedy and his group examined this issue by carefully analyzing age-related genes in yeast and the C. elegans worm, two organisms that diverged over a billion years ago. They found a statistically significant connection in the genes and pathways that affect aging in both organisms, including reduced mTOR signaling. They suggest that the conservation of aging genes across animals exists not because specific genes have evolved to regulate aging, but rather because animals have evolved a similar response to nutrient restriction, and lifespan is tightly linked to this response, providing evidence that efforts in humans just might work.
The Role of Insulin-like Signaling for the Central and Peripheral Regulation of Nutrient Homeostasis and Life Span Morris White, Children's Hospital Boston, MA (Tue, April 21 3:30 PM - 5:50 PM, Room: 356)
White will discuss some of his group's work in manipulating the levels of various insulin receptor substrates in mice. Insulin-like signaling regulates the storage and usage of nutrients, a process best exemplified by insulin's role in keeping blood glucose levels from getting too low or high; therefore proper insulin-like signaling is absolutely critical for growth and development. Interestingly, though, in lower animals like fruit flies and nematodes, reduced insulin secretion can extend lifespan. White will show some interesting studies suggesting that reduced insulin-like signaling in the brain can have a consistent effect in extending mammalian lifespan —just as seen in worms and flies.
Cancer and Aging in DNA Repair Deficiency: Cause and Treatment Laura J. Niedernhofer, University of Pittsburgh, PA (Wed, April 22 12:50 PM - 3:10 PM, Room: 355)
Finding the keys to slow down aging requires a better understanding of the natural aging process. In that regard, progeroid syndromes, characterized by accelerated aging and increased risks of cancer, have been valuable models. Niedernhofer and her lab have developed a mouse model that expresses sub-normal levels of ERCC1-XPF endonuclease, an enzyme that is important in DNA repair. Starting at 8 weeks of life, the mice display progressive symptoms associated with aging including muscle wasting, loss of vision and hearing, urinary incontinence, decreased liver and kidney function, and osteoporosis. These mice offer a great system to identify the mechanisms by which DNA damage can drive the tissue degeneration associated with aging as well as a platform to test anti-aging therapies like stem cells and free radical scavengers.
For more information prior to the meeting, and for any interested parties who cannot attend, please contact Nick Zagorski (301-634-7366,
For more on-site information or to arrange any meetings, please contact Sarah Goodwin, 770-722-0155 before April 18, 504-670-4513 April 18-April 22

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