Understanding the mechanisms of how we age could lead to interventions that can alter them, which could lead to “compression” of the period of disability relative to age — essentially delaying its onset so people stay healthy until end of life. Benefits of insights gleaned from this study won’t accrue only to old people. Finding ways to mitigate these processes is important across age cohorts. Ageing processes get under way the moment we are born and their fingerprints are being found in surprising places, from pregnancy complications to childhood cancer treatment to the long-term effects of prophylactic HIV drugs.
Research is currently illuminating the workings of some of these ageing mechanisms, including age-related build-up of defective proteins, accumulation of mutations in the DNA and change in the genome organisation, age-related dwindling of adult stem cell reserves, transcriptional slowdown,3 and an age-related increase in the number of senescent cells — which, among other events, drives an increase in chronic inflammation. In all, twelve interrelated hallmarks of ageing have now been identified.4 Additionally, there are genetic factors: recent research has identified a gene in naked mole rats that extends both lifespan and healthspan in transgenic mice, for example.5 There are also suggestions that gut microbe composition matters, as it changes differently in healthy versus unhealthy ageing.6 The main goal is to understand how all of these factors are connected to chronic disease and functional decline, and how these in turn are connected into the central system that regulates the ageing process.
