The evolution of senescence is thought to follow from the progressive decline in the force of natural selection after the onset of reproduction. Cellular senescence caused by telomere shortening has been suggested as one potential causal agent of aging. In some tissues, telomeres are maintained by telomerase. The presence of telomerase promotes tumor formation however, suggesting a trade-off between aging and cancer. Weinstein and Ciszek's reserve-capacity hypothesis (2002) suggests that the strategies organisms have evolved to cope with this trade-off may vary with lifespan. I am testing the hypothesis that species with short lifespans down-regulate telomerase throughout most of life, until the end of life when critically short telomeres are rescued by forced telomerase expression, possibly leading to an increased incidence of cancer. Species with longer lifespans have a slower rate of telomere shortening, possibly due regulated expression of telomerase, and thus some risk of tumor formation throughout life. I investigated telomerase activity in different tissues from hatchling, young adult and old zebra finches (Taeniopygia guttata) to determine at what age and in which tissues telomerase was expressed. In muscle, liver and gonadal tissue telomerase activity was greater in old individuals than in young adults, although generally activity was not as high as in the hatchlings. This suggests a possible "rescue effect" in old age, although we cannot rule out that this activity may indicate neoplastic tissue. These results are in agreement with the short-lifespan strategy. In the short-lived zebra finch, telomerase expression maybe up-regulated in old age to rescue tissues with short telomeres at the risk of tumor formation. We are now investigating the telomerase profiles of avian species with long lifespans to determine whether differential regulation of telomerase activity through life coevolves with lifespan.