Currently, the pathways and potential disease modifier genes that explain this striking pleomorphic presentation of LRRK2 parkinsonism and variable clinical penetrance/AAO are unknown, although many cellular phenotypes and molecular pathways, including endolysosomal stress [60,61,62], neuroinflammation [63,64,65], mitochondrial dysfunction and damage [66,67], and alterations of exosomes [68,69] have been described due to altered LRRK2 signaling. Here, LRRK2 is linked to Parkinsonism.