The notion that trafficking may be altered in amyloid disorders is also supported by genetic studies of Parkinson disease, in which disease-associated mutations in VPS35, Rab7L1, and LRRK2 result in Golgi and endolysosomal trafficking defects (72, 73), whereas phosphatidylinositol-binding clathrin assembly protein, a protein with a role in endocytosis, is a modulatory factor in Alzheimer disease (74, –, 76). This evidence concerns the gene RAB29 and Alzheimer disease.