A recent study published in Engineering has provided novel insights into the involvement of α2,6-sialylation in Alzheimer’s disease (AD), revealing that the ablation of α2,6-sialyltransferase-I (ST6Gal-I), an enzyme responsible for α2,6-sialylation, can downregulate BACE1 expression and suppress the production of amyloid-β42 (Aβ42) plaques, which are hallmarks of AD.