Aging varies not just by species but also by the genetic background of each individual. This fact has greatly hindered all attempts to understand aging as a general phenomena. Despite this problem, oxidative stress and its effect on cellular signaling appears important in many studies of aging. Although I originally started working with ants that live a very long time, I have been shifting my model to Drosophila melanogaster where it is easier to study these genetic and environmental affects. Most of my laboratory research comes back to this central question.

The Superoxide Dismutase (SOD) family of antioxidants has long been thought involved in aging by protecting various cellular compartments from oxidative damage. I am currently characterizing the extra-cellular SOD in Drosophila melanogaster. Recently, the evidence suggests that the SODs not only have a general protective role (proposed by the free radical theory of aging), but also important involvement in reactive oxygen signaling that mediates aging. The next steps after understanding how the superoxide dismutases work together, or separately, will be to investigate how they might affect lifespan through cellular signaling.

The heterogeneity of aging and the effect of environment on aging are well known, but not understood. In addition, oxidative stress and its effect on cellular signaling appears to be a key variable in many studies of aging. Oxidative stress and signaling is also involved in immune responses to parasitism and infection. Could aging be a side effect of alterations in the redox balance caused by infection? We are currently using Drosophila melanogaster and the common insect endosymbiont Wolbachia to study these genetic and environmental affects in a controlled way.

While at Southampton, my lab and Andrew Bourke’s lab at UEA explored how social structure affects resource inheritance and aging in bumble bees at the molecular and behavioral levels. Ruan (2008) discovered that social environment can also have a major effect on aging in a non-social insect. He showed that the presence of young individuals) can rescue a shorter lived phenotype of a Drosophila cytoplasmic superoxide dismutase mutant. I am now extending these findings by testing the effect of young helpers on an under expressing extra-cellular superoxide dismutase mutant fly and two wild caught lines cleared of Wolbachia.

Dysfunctional cells normally remove themselves by programmed cell death. Occasionally this process is arrested increasing the risk of cancer and aging. Senolytic drugs cause these hyperfunctional or arrested cells to resume programmed cell death which should lead to as longer and healthier lifespan. We are exploring one such drug's ability to extend lifespan in Drosophila.