LRRK2 and Parkinson disease: Taken together, the data from PD iPSC models relating to autophagy and LRRK2 mutations point to a model where defective autophagosome-lysosome fusion and delayed turnover of damaged mitochondria might conspire with impaired CMA, thus favoring α-synuclein accumulation, increased sensitivity to oxidative stress, and eventually demise of DA neurons.