Post-mortem Alzheimer’s diseased brain specimens reveals significant levels of Aβ (11-40/42) within insoluble amyloid pools. The β-secretaseEnzyme or β-amyloid precursor protein-cleavingEnzyme (BACE) generates the N terminus of Aβ, ultimately leading to the production of full-length Aβ (1-40/42) or truncated Aβ (11-40/42). The abundance of Aβ (11-40/42) produced by BACE suggests that their roles in AD pathogenesis may be important.
Proteins & Peptides
Peak Area by HPLC ≥95%
Ref: Huse, JT. et al. J. Biol. Chem. 277, 16278 (2002); Qahwash, I. et al. J. Biol. Chem. 279, 39010 (2004); Liu, K. et al. Biochem. 41, 3128 (2002).