What is the Mprize?
The Mprize consists of two separate prize competitions, both of which are judged by our scientific advisory board:
In the competition for the Longevity Prize, money is awarded to the producer of the world's oldest-ever mouse. This is restricted to the species used in virtually all laboratory work, Mus musculus, but no other restrictions should be placed on the way in which the mouse's lifespan is extended, provided that the methods used maintain cognitive and physical wellbeing.
The amount won by a winner of the Longevity Prize is in proportion to the size of the fund at that time, but also in proportion to the margin by which the previous record is broken.
The Rejuvenation Prize rewards successful late-onset interventions performed on an aged mouse and has been instituted to satisfy two shortcomings of the Longevity Prize: first, it is of limited scientific value to focus on a single mouse (a statistical outlier); and second, it is very likely that interventions applied throughout life (as they are during Longevity Prize research) will always be ahead of those initiated late, and thus would have an ongoing advantage in a simple competition structure. Our most important end goal is not merely to extend life, but to promote the development of interventions that restore youthful physiology. By seeking interventions that are effective when initiated at a late age, this prize encourages scientific research that is most likely to benefit those reading these guidelines today.
The Rejuvenation Prize is not awarded for the life extension of an individual mouse but for a published, peer-reviewed study. The study must satisfy the following criteria:
The amount won by a successful new Rejuvenation Prize record is calculated in the same way as for the Longevity Prize, but is only awarded upon publication of the study in question.
Competitor Stephen Spindler
The rate of animal aging is strongly influenced by diet. The more calories consumed, the faster it ages. Well-fed animals not only age faster, they have higher mortality from cancer, heart disease, and diabetes. And the reverse is true, the fewer calories eaten (provided malnutrition is avoided) the slower an animal ages, the lower the death rate from cancer, and the lower the rate of heart disease and diabetes. CR has been viewed as less effective in older animals and as acting incrementally to slow or prevent age-related changes in gene expression. However, we found that mice who begin CR in late middle-age reap its benefits almost immediately.
We also have performed other genome-wide gene-expression studies in mice with disrupted growth hormone-insulin-like growth factor-1 signaling (DF) that were either CR or given free access to food. Others have shown that either DF or CR alone can extend lifespan, and that together they act additively to extend the lifespan of mice even more. We found that CR and DF additively affected the expression of a group of genes. Individually and together, DF and CR independently affected the expression of other groups of genes. These results indicate that DF and CR affect overlapping sets of genes, and additively affect a subset of genes associated with enhanced longevity. These results provide a focused group of new genes which are important in regulating the lifespan of mammals, and which may be 'drugable targets' for anti-aging therapeutics.