LRRK2 and Parkinson disease: Interestingly, while “normal” astrocytes express low levels of α-synuclein, cultured iPSC-derived astrocytes carrying the PD LRRK2 G2019S mutation exhibit progressive endogenous α-synuclein accumulation, dysfunctional chaperone-mediated autophagy, and impaired macroautophagy, resulting in the decreased astrocytic ability to clear neuronal-derived extracellular α-synuclein aggregates when co-cultured with WT dopaminergic neurons [71].