Given that Aβ and C99 peptides are amyloidogenic and can induce synaptic failure, neurodegeneration and memory loss [34,55-59], behavioral stress-dependent elevations in both β-cleavage products through BACE1 and APP upregulation have important implications for the pathogenesis of sporadic AD and the progression of neuronal dysfunction. Here, BACE1 is linked to Alzheimer disease.