Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) resets 
their identity back to an embryonic age and, thus, presents a significant hurdle 
for modeling late-onset disorders. In this study, we describe a strategy for 
inducing aging-related features in human iPSC-derived lineages and apply it to 
the modeling of Parkinson's disease (PD). Our approach involves expression of 
progerin, a truncated form of lamin A associated with premature aging. We found 
that expression of progerin in iPSC-derived fibroblasts and neurons induces 
multiple aging-related markers and characteristics, including dopamine-specific 
phenotypes such as neuromelanin accumulation. Induced aging in PD iPSC-derived 
dopamine neurons revealed disease phenotypes that require both aging and genetic 
susceptibility, such as pronounced dendrite degeneration, progressive loss of 
tyrosine hydroxylase (TH) expression, and enlarged mitochondria or 
Lewy-body-precursor inclusions. Thus, our study suggests that progerin-induced 
aging can be used to reveal late-onset age-related disease features in 
hiPSC-based disease models.