Morten Scheibye-Knudsen did his medical training at the University of Copenhagen including a short scholarship investigating mitochondrial physiology. During medical school he founded his first company, Forsoegsperson.dk, which has grown to be the largest provider of volunteers for clinical trials in Denmark. After medical school he worked as a medical doctor in Denmark and Greenland before moving to basic science as a post doctoral fellow at the National Institute on Aging, NIH, in Baltimore. Here, he utilized computational and wet lab science to investigate how DNA damage contributes to the complex phenotypes seen in premature and normal aging. In 2016 he returned to Copenhagen as an assistant professor to start his own research program focusing on aging. In 2018, he received tenure and was promoted to associate professor. His team (~20 people) utilizes computational science, animal models, gene editing, and high-throughput approaches such as high-content microscopy and omics investigations to understand the molecular basis of aging and age-associated phenotypes. Lab generated data is routinely analyzed through AI-assisted pipelines such as novel cellular senescence classifiers and fully automated animal tracking (www.tracked.bio). He has published his work in some of the best journals in the world including Cell, Cell Metabolism, Nature Aging, New England Journal of Medicine and many others. In addition to his core research, he has been lecturing at Johns Hopkins School of Public Health for 8 years; He is a chief editor at Frontiers in Aging running the Aging Interventions section; He organizes the largest annual conference on Aging Research and Drug discovery (www.agingpharma.org); He is an advisor to Deep Longevity, the Longevity Vision Fund and Ars Salus; He has given invited presentations at top institutions (NIH, MIT, Harvard, NUS, Karolinska and others); and received several awards for his research.

Ageing and major chronic diseases are associated with an accumulation of damage to our DNA. Accordingly, hereditary diseases displaying premature/accelerated aging are most often caused by defects in various DNA repair processes. In this lecture, I will elucidate our work utilising computational approaches, wet lab analysis, animal models and clinical trials to understanding how DNA damage leads to diseases and what we can do to attenuate the consequence of damage to our genome allowing everyone longer and healthier lives.