Curr Neurol Neurosci Rep (2012) 12:237–242 Conclusions iPSCs offer a new platform for studying human diseases in the most endogenous form possible when patient primary cell lines are unavailable [62 , 63 ]. Further, differentiation and maturation of the IPSCs enable the study of disease phenotypes during development and aging of the cell type of interest. Using this approach, we have demonstrated a caus- al role of SNCA-triplication and LRRK2-G2019S in devel- oping PD-related phenotypes. Broadly speaking, iPSC models may be readily extended to other neurodegenerative diseases with genomic mutations underpinnings, and is not just limited to PD [61 , 64, 65]. Disclosure Conflicts of interest: B. Byers: has received grant support from California Institute for Regenerative Medicine; H.-l. Lee: none; R. Reijo Pera: has received grant support from California Institute for Regenerative Medicine. 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