Figure 8.

A schematic model for bi-phasic dysregulation of autophagic activity by loss of LRRK2. Loss of LRRK2 initially causes induction of autophagy, but later leads to autolysosome accumulation and depletion of the autophagy machinery due to trapping of autophagic components in the form of autolysosomes and the eventual formation of lipofuscin granules, which would in turn result in accumulation and aggregation of a large number of autophagy substrate proteins during aging.