Dr. Ivana Bjedov, UCL Cancer Institute, London
Tuesday 7th November, 1.00 p.m., Stacey Lecture Theatre 1
A remarkable recent discovery is that ageing is a malleable process and that surprisingly single mutations are sufficient to delay ageing in model organisms such as yeast, worms, flies and mice. These mutations extend lifespan by down-regulating the main cellular nutrient-sensing pathways: insulin and target-of-rapamycin signalling. Importantly, these long-lived mutant animals are healthier and more youthful for longer, and protected from a variety of age-related diseases. However, despite the well-established role of nutrient signalling pathways in ageing, the down-stream effectors are still largely unknown. There is evidence that improved protein turnover, by increased major cellular degradation pathways, such as autophagy and proteasome, could be beneficial. Down-regulation of protein translation has positive effect on lifespan in model organisms, but the underlying mechanism is unclear. With life expectancy continuously increasing in modern societies, the number of people suffering from age-related diseases is rising steeply. Therefore investigation into the basic mechanisms of ageing is expected to provide important new findings that could improve health in elderly population.
In our laboratory, we use the fruit fly Drosophila melanogaster, which has already greatly contributed to the recent findings in the biology of ageing. By combining in vitro and in vivo models, as well as transcriptome and metabolome wide approaches, we hope to improve our understanding of the basic mechanisms of the ageing process. We are interested in understanding how anti-ageing drugs, rapamycin and lithium, extend lifespan and if this approach is applicable to mammalian systems. I will present how up-regulation of autophagy, which is a major cellular degradation pathway, can be used to improve ageing. In addition, we are investigating how lowering protein synthesis can increase lifespan and what the underlying mechanisms are.