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.
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:
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.
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 Christiaan Leeuwenburgh
Our general research interest is in the area of free radical biology and aging. Aging and several diseases including cardiovascular disease, diabetes, and neurodegenerative diseases are thought to result from increased formations of reactive oxygen species and reactive nitrogen species (aka, free radicals) resulting in oxidative stress. Reactive oxygen species are highly reactive molecules that cause damage to plasma membranes, enzymes, glucose molecules, and DNA. We are particularly interested in the oxidative mechanisms of aging and the effects of these during the aging process (i.e. mitochondrial dysfunction, apoptosis).
Mitochondiral oxidative stress with aging may be liked to apoptosis. Apoptosis is a highly regulated form of cell death characterized by specific morphological, biochemical, and molecular events. However, its role during aging, particularly in post mitotic tissues such as the brain, heart and skeletal muscle has not been studied in depth. Apoptosis appear to increase in post-mitotic tissues with age and it may be a major contributing factor to the observed loss in tissue function with age. The mechanisms by which apoptosis are induced with advancing age and adaptations that may protect against apoptosis remain to be identified, however. Moreover, the adaptations of major regulatory proteins upon the activation of the apoptotic signal transduction pathways during normal aging are unknown. Caloric restriction - an intervention that reduces oxidant production, improves calcium handling, reduces cell loss and extends maximum life span - could be emplyed to further study the anti-apoptotic adaptations. In addition, skeletal and heart muscle function with age could relate to apoptosis and apoptosis may be attenuated by caloric restriction. Further research would allow us to understand the mechanisms of apoptosis in vivo with normal aging, and caloric restriction.