Twelve drivers
Aging is not a single process but a convergence of interlocking hallmarks — genomic instability, telomere attrition, mitochondrial dysfunction, cellular senescence, chronic inflammation and disrupted intercellular signalling. Rather than treating one disease at a time, the lab asks whether targeting these shared drivers can slow aging itself.
Our central ambition is translational: to turn mechanistic insight into interventions that extend healthy human lifespan. We test targeted strategies at multiple points along the damage cascade — inhibiting PARP1 to spare NAD⁺, boosting NAD⁺ directly with precursors such as nicotinamide riboside, raising acetyl-CoA through ketogenic substrates, and exploring compounds that enhance DNA repair and clear senescent cells.
Each strategy is tested in cellular and animal models of both normal and accelerated aging, and increasingly in human studies. The guiding hypothesis is simple: if normal aging and age-associated disease share the same underlying mechanisms, they may yield to the same interventions — and the goal is not merely longer life, but more years lived in good health.
See the full list of the lab's publications on Google Scholar.