Aging is a major risk factor for chronic diseases and neurocognitive disorders such as Parkinson’s disease, Alzheimer’s disease, depression, and dementia. In many of these diseases, the balance of dopamine is disrupted. Effective treatment often involves inhibiting monoamine oxidase-B (MAO-B), a protein that regulates dopamine concentration. The drug deprenyl (l-deprenyl, Selegiline) is one of these MAO-B inhibitors. Studies suggest that deprenyl could also be used to highlight important mechanisms of aging. Deprenyl treatment increases lifespan of rats (Knoll, 1988) and mice (Archer and Harrison, 1996), but the mechanism of lifespan extension is unknown. This study explores the mechanisms by which deprenyl extends the lifespan of C. elegans, a model organism with highly conserved signaling pathways including those that regulate aging. Wild-type animals were exposed to 1.0 x 10-5 mM, 1.0 x 10-3 mM, and 1.0 x 10-1 mM deprenyl. Median and maximum lifespan were scored along with deprenyl’s ability to prevent age-induced paralysis and delay death due to chronic heat stress. Our results demonstrate that 1.0 x 10-1 mM deprenyl increases median and maximum lifespan in wild-type animals, and that this increase in lifespan is not due to decreased caloric intake. Additionally, deprenyl reduces the onset of aging-induced paralysis and delays heat-induced death. Further research into the mechanisms by which deprenyl extends lifespan and protects against paralysis and heat stress will give insight into controlling the balance of signaling networks to delay progression of senescence and will suggest molecular targets for improved clinical treatments to increase human health span.

Effect of deprenyl on the lifespan of C. Elegans

251st National Meeting (2016)

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