The endosomal structural anomalies of AD, defined as “endosomopathy of AD,” encompass functional and morphologic abnormalities of endosomes that derive mainly from the overactivation of the small GTPase Rab5 (Kim et al., 2016), as well as alterations of trafficking route to and from sorting endosomes (Small & Petsko, 2015). This evidence concerns the gene RAB5A and Alzheimer disease.