Given a longevity mutation, the logical thing to ask is "how does it work?" This is especially true in the case where the mutants suffer undesirable characteristics, as in the case of dwarf mice - we'd like to see if there's something to be salvaged. The rapid advance in biotechnology takes us ever close to answers; more can be done in a year by a single small group now than by the entire research establishment of 1980. "Long-lived strains of dwarf mice carry mutations that suppress growth hormone (GH) and insulin-like growth factor I (IGF-I) signaling. The downstream effects of these endocrine abnormalities, however, are not well understood and it is unclear how these processes interact with aging mechanisms. ... Comparative analysis of microarray datasets can identify patterns and consistencies not discernable from any one dataset individually. ... In this context, 43 longevity-associated genes are identified and individual genes with the highest level of support among all microarray experiments are highlighted. These results provide promising targets for future experimental investigation as well as potential clues for understanding the functional basis of lifespan extension in mammalian systems." This would be life extension through manipulating the system rather than by repairing it however; I see building a better metabolism as the less promising way forward.

Link: http://dx.doi.org/10.1186/1471-2164-8-353