SNCA and Parkinson disease: Alternatively, and as proposed here, the mechanisms leading to LB formation in a subset of LRRK2-PD patients may be independent of the LRRK2-mediated lysosomal deficits, and involve α-synuclein oligomer formation triggered by altered lipid composition due to the existence of additional genetic LSD variants in those patients, or due to additional environmental and/or age-related changes (Figure 6).