Akasaka-Manya et al. demonstrated that the level of GnT-III mRNA had significantly increased in AD brains compared to controls54, and Kizuka et al. indicated that GnT-III-deficient AD model mice showed reduced amyloid-β (Aβ) accumulation in the brain by suppressing the function of a key Aβ-generating enzyme, β-site APP-cleaving enzyme-1 (BACE1), and greatly improved AD pathology55. This evidence concerns the gene MGAT3 and Alzheimer disease.