Aging is a complex phenotype associated with a decline in health and an increased probability of death. There are multiple visible aging effects at the organismal level in terms of health and disease, and the diversity is overwhelming. Importantly, the molecular changes that drive aging are less diverse, irrespective of the tissue or organ that is affected. Hence, improving the negative effects of aging may be more feasible at the molecular, rather than the organismal, level.

The aim of our research is to better understand the primary molecular changes, or hallmarks, that occur during the processes of cellular senescence and aging. We are particularly interested in the regulation of telomeres, DNA mutation rates and the preservation of proteostasis during aging and senescence. We hope that a complete mechanistic understanding of these processes will lead to increased overall healthspan.