BACE1 and Alzheimer disease: It increases BACE1 mRNA stability in vitro in human cell lines and in vivo in murine brains, thus upregulating BACE1 protein that causes proteolysis of APP and formation of hydrophobic β-amyloid peptide aggregates, Aβ1-42, which are the hallmarks of AD pathology (Faghihi et al., 2008).