Deletion of the Mitochondrial Superoxide Dismutase sod-2 Extends Lifespan in C. Elegans

This paper examines one of the most widely studied theories of why people age. This is called the free radical theory of aging, and proposes that aging results from the accumulation of damage caused by toxic oxygen containing molecules (oxidative damage). While it is generally agreed that oxidative damage increases over time as we age, it is not certain to what extent this damage determines our lifespan. 

In order to do this work, Jeremy used a genetic model organism - the worm (Caenorhabditis elegans). By removing individual genes which encode antioxidants, it was possible to examine the effect of increasing oxidative damage on lifespan.

In this work, Jeremy found that increasing oxidative damage did not result in decreased lifespan. This result is at odds with the prediction of the free radical theory of aging which indicates that by decreasing antioxidants, oxidative damage should increase. This, in turn, should decrease lifespan. These findings suggest that, although the levels of oxidative damage increase as we age, this doesn't necessarily contribute to functional decline and eventual death.

For Jeremy's doctoral studies, he had been working with mouse models of Huntington disease. This work provided him with the opportunity to learn to work with worms and also to learn about research in aging.

He is currently completing his postdoctoral research at McGill University examining the genetics of aging. In the future, Jeremy would like to be an independent investigator using both worm and mouse models to answer questions about aging and neurodegenerative disease.