The in vitro modeling of human disease via iPSC-technology has proven successful for numerous developmental and early-onset disorders. However, recreating the pathogenesis of age-dependent conditions such as Parkinson’s Disease (PD) is limited by a rejuvenating effect of the reprogramming process. In fact, our group has recently shown that iPSC-derived cells are reset to a “younger” state, preventing the appearance of age-related phenotypes.

My work focuses on understanding how the transition through pluripotency rewinds the biological clock and exploring possibilities to accelerate cellular aging in vitro for the development of more accurate iPSC models of late-onset disorders.