Anti-Human Beta-Site APP Cleaving Enzyme 2 (NT) (BACE2)

Accumulation of the amyloid-β (αβ) plaque in the cerebral cortex is a critical event in the pathogenesis of Alzheimer’s disease. αβ peptide is generated by proteolytic cleavage of the β-amyloid protein precursor (APP) at β- and γ-sites by proteases. The long-sought β-secretase was recently identified by several groups independently and designated β-site APP cleaving enzyme (BACE) and aspartyl protease 2 (Asp2).1-4 A BACE homolog was recently cloned and designated BACE2, Asp1, DRAP (for Down region aspartic protease), and memapsin 1.4-9 BACE2 also cleaves APP at β-site and at a different site within αβ.8 BACE2 locates on chromosome 21q22.3, the so-called ‘Down critical region’, suggesting that BACE2 and αβ may also contribute to the pathogenesis of Down syndrome.6,7