Biological determinants of ageing and late life health, and their pharmacological manipulation.

Getting older is the single biggest risk factor for diseases like cancer, heart disease and dementia, but a handful of gene mutations can make laboratory animals live longer and stay healthier. This research aims to understand why. The problem is that we treat each age-related disease separately, rather than targeting the ageing process itself. Decades of work in yeast, worms, flies and mice have shown that dialling down a specific nutrient-sensing network—the insulin/IGF/TOR signalling pathway—extends healthy lifespan. So does cutting calories. Both changes protect against multiple diseases at once, not just one. But we do not yet know exactly how this protection works at the molecular level, or whether we can mimic it safely with drugs. If this programme succeeds, it could shift medicine from treating individual late-life diseases to slowing the underlying ageing process. That would mean more years of good health for older people, reducing the burden on healthcare systems and families. The researchers will first map the signalling mechanisms in model organisms, then test existing and new drugs that target key molecules, and finally use human genetic and drug-response data to translate those findings into real treatments. This is fundamental biology with a clear translational path—if the mechanisms are conserved in humans, the payoff could be a single intervention that delays multiple diseases at once.