One hallmark of Alzheimer's disease (AD) pathology is the presence of extracellular plaques composed of β-amyloid peptides (Aβ), a 38-42 amino acid fragment from amyloid precursor protein (APP) by the sequential action of β-site APP cleaving enzyme (BACE) and γ-secretase. The accumulation of Aβ42, the longer form Aβ, is believed to lead to aggregation, plaque deposition and neurotoxicity. Therefore, a BACE or γ-secretase inhibitor may serve as a treatment for AD. ...