BACE-1 and ADAM-10 as Potential Peripheral Biomarkers for Alzheimer’s Disease

Amyloid beta (Aβ) dyshomeostasis is considered the main biological aberration in Alzheimer’s Disease (AD) pathology. The interplay between Aβ formation and clearance is predominantly modulated by a disintegrin and a metalloproteinase 10 (ADAM10, α-secretase) and β-site APP Cleaving Enzyme 1 (BACE1), the two pivotal enzymes in both non-amyloidogenic/amyloidogenic and amyloidolytic pathways. Emerging evidence suggests that aberrations in ADAM10 and BACE1 expression, activity, and function in the brain of AD patients also manifest in peripheral fluids, suggesting their potential as blood-based biomarkers for AD diagnosis. This review provides a comprehensive overview of the literature by exploring the roles of ADAM10 and BACE1 in AD, spanning from their involvement as pathological AD drivers to their potential utility as promising biomarkers.