Although these results collectively imply AD in humans is a glycan-specific disorder that is characterized by the selective loss of WFA+ CS-GAGs over aggrecan+ and brevican+ CSPGs, other studies have been unsuccessful in recapitulating these initial observations (Morawski et al., 2012; Crapser et al., 2020) (Table 1). The gene discussed is ACAN; the disease is Alzheimer disease.