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Latest Mprize Winners

Z Dave Sharp

Special Mprize Lifespan Achievement

On October 8, 2009 Dave Sharp, University of Texas, San Antonio was awarded the Special Mprize Lifespan Achievement. This special recognition was for the first pharmaceutical intervention to successfully extend the life of laboratory mice. The study, published in the journal Nature, showed that when aging mice were given the drug rapamycin, they lived longer than other mice.

Read more about rapamycin in the news and the event.

Andrzej Bartke

Mprize for Longevity

ResearcherAndrzej Bartke
MouseGHR-KO 11C
InterventionGrowth Hormone Receptor Gene Knockout
Treatment BegunGermline (transgenic)
Age at Death1819 days

"...Dwarf mice...lack growth hormone (GH), prolactin (PRL), and thyroid-stimulating hormone (TSH), (and) live much longer than their normal siblings, and exhibit many symptoms of delayed aging."

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Steven Spindler

Mprize for Rejuvenation

ResearcherSteven Spindler
MouseSix mice (from cohort of 60)
InterventionCaloric Restriction
Treatment Begun19 months
Age at Death1356 days (average)

"Caloric restriction (CR), the consumption of fewer calories while avoiding malnutrition, is a robust method of decelerating aging and the development of age-related diseases. The effects of CR are conserved in nearly every species tested, perhaps including humans. CR delays the onset and reduces the incidence and severity of age-related diseases, including cancer."

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Competitor Leonard Guarente

Why do living things age? What genes influence longevity? Is it possible to extend youthfulness by means of genetic manipulation? Our research analyzes these tantalizing questions and others in molecular detail.

The mammalian ortholog Sirt1 has several functions that trigger physiological changes seen during CR. First, Sirt1 makes cells more resistant to oxidative or radiation-induced stress, which is a phenotype of rodent cells from CR animals. Second, Sirt1 promotes mobilization of fat from white adipose tissues, a change triggered by CR that is sufficient to extend the life span. It does this by modulating the activity of the key regulator of white fat, PPARg. Third, Sirt1 mediates the metabolism of energy sources in metabolically active tissues. CR animals are efficient in metabolism rendering them insulin-sensitive. Fourth, Sirt1 regulates the induction of insulin in pancreatic beta cells, an obvious component of energy utilization during CR. In several cases, Sirt1 is activated by starvation or stress to carry out these functions. Molecular mechanisms of Sirt1 activation and its functions in triggering the physiological changes elicited by CR are under study.

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