The RMg largely exhibited pathology that suggested impaired LC3-OPTN interaction and autophagosome-lysosome fusion across all stages (based on consistently decreased percent of colocalized puncta seen in Figures 6C,D), and likely exhaustion of the autophagosome pool at end-stage PD (especially when considering the decreasing number of LC3 puncta coinciding with increasing OPTN puncta in Figures 3D,E). This evidence concerns the gene MAP1LC3A and Parkinson disease.