Abstract
A critical feature of Alzheimer's disease (AD) is the deposition of Amyloid plaque, high levels of amyloid beta-peptide, Aβ. BACE 1 protease initiates the formation of Aβ from β-Amyloid precursor protein (APP). We recently showed that BALE 1 is also involved in the cleavage and secretion of ST6Gal I, sialyltransferase that modifies N-linked oligosaccharide. In this review, first of all, I describe how we previously found that BACE1 is involved in the cleavage and secretion of ST6Gal I. Next, I report our recent data showing that cleaved ST6Gal I by BALE1 is not simply secreted out of the cell, but the enzyme receives a subsequent processing event before its secretion.
