TO ENCOURAGE people to take his ideas seriously, Aubrey de Grey, the originator of the strategies for engineered negligible senescence, has organised a competition. He is offering a prize for the development of what he calls a Methuselah mouse.
There are actually two prizes to be had. One is for longevity, the other for rejuvenation. The prize for longevity can be won by a new strain of mouse—one bred or genetically engineered to live a long time. That for rejuvenation requires treatment to begin when the mice are already in middle age.
Unlike other engineering prizes (for example, the X Prize for lunar exploration), an award of the Methuselah mouse prize is not the end of the matter. The winner establishes a record that others have to break. At the moment the records for longevity and rejuvenation are five years and almost four in an animal that normally lives for three.
How translatable the lesson of a Methuselah mouse will be to people is a matter of debate. The logic of disposable-soma theory (see article) applies to both species. But that theory also explains their different lifespans. The reason mice age rapidly is that they have lots of predators and would get killed quickly anyway. Humans have few predators and tend not to get killed—at least not as easily as mice. It is therefore worthwhile for people to evolve better repair mechanisms than mice, and thus to age more slowly.
The rate at which an animal aged was once believed to be related to its size. Small animals have faster metabolisms, so it was thought they would wear out more quickly. That relationship, however, is just a coincidence caused by the fact that small beasts usually have more predators than large ones do. If they do not, as for some species of bat, then even a small creature can live for decades in just the way that a large animal would. For this reason, it is difficult to draw firm conclusions about human ageing from mice, even Methuselah mice. The repair mechanisms in the two species may be different.
In the Methuselah mice that exist today, the rejuvenation prize is held by a mouse on a calorie-restricted diet (see article). The longevity prize is held by an animal that could not make the receptor molecule for growth hormone and was thus a fraction of the size of normal mice. One explanation for this mouse's abnormally long lifespan is that slower growth allows for “higher fidelity” growth, with better error-correction during development. The result would be a mouse that is born with less congenital damage and which thus takes longer to accumulate enough further damage to kill it.