Understanding the clinical phenotype and underlying biology in such individuals is critical for molecularly-targeted therapeutic development.6 Other pathologies present in some individuals with LRRK2-associated parkinsonism who do not demonstrate evidence of asyn aggregates include tauopathy, with Alzheimer’s disease type tau (3R and 4R) predominating, but some demonstrate hyper-phosphorylated tau resembling progressive supranuclear palsy (PSP) and less commonly Transactive response DNA binding protein 43 kDa (TDP-43).3,7,8. This evidence concerns the gene MAPT and Parkinsonism.