Overview

What is the Mprize?

The Mprize competition is an exciting and viable mid-term strategy to deliver on the Methuselah Foundation's mission of extending healthy human life. It directly accelerates the development of revolutionary new life extension therapies by awarding two cash prizes: one to the research team that breaks the world record for the oldest-ever mouse; and one to the team that develops the most successful late-onset rejuvenation. Previous winners have already proven that healthy life can be extended; each new winner pushes the outer limits of healthy life back even further...and each new winner takes us even further.

Why Prizes?

A well-designed prize is the ONLY method that has shown to be 100% successful in turning the impossible into a near-term reality. Prizes make this kind of ground-breaking change achievable by:

Encouraging new levels of excellence and specific innovations in uncharted territory
Expanding society's perceptions of what is possible
Attracting high levels of investments, donations, and resources
Dramatically increasing the pool of potential solvers by marshalling the most diverse possible group of talent, approaches, and techniques

By throwing out all previous assumptions about aging and offering scientists and researchers a huge (and ever-increasing!) cash prize incentive, the Mprize is guaranteed to create revolutionary solutions...quite possibly within our lifetimes.

A History of Science Prizes

Why Mice?

Mice are genetically similar to humans. They are small and inexpensive to maintain so studying large quantities is feasible. Their short lifespan, about three years, makes it possible to see if interventions result in longer, healthier lives – all in time to be of benefit to our own lives.

Mice are widely considered to be the prime model of inherited human disease and studies have shown that mice share 99% of their genes with humans. The similarities between sections of human and mouse DNA allow researchers working with mouse genes to make incredibly accurate predictions about the location and function of their human counterparts. Mice have been the mainstay of laboratory research on human illness and longevity.

The species Mus musculus is used in the laboratory for experimental work, including the biology of aging. Their long history of captivity has resulted in strong selection for rapid growth and breeding and has resulted in a wide variation in lifespan between different (inbred) laboratory strains. Most useful studies of lifespan are done on strains with a relatively long lifespan. The one most often used is "C57Bl/6", which normally lives about three years without any life-extending intervention.

What You Can Do

What do the end of famine, the discovery of longitude, and private space travel have in common? Each of these world-changing innovations was created by an inventor seeking to win a prize. The Mprize is a multi-million dollar prize to end the diseases of aging. Right now, brilliant minds all around the world are competing for this prize. Your support will help them get there faster.

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.