On APP, ADAM10 activity causes the generation of a C-terminal membrane-anchored fragment and a neuroprotective soluble ectodomain (sAPPα), precluding amyloid-β (Aβ) formation and their aggregation leading to amyloid plaque load [13,14,15] that is a hallmark of Alzheimer’s disease (AD). Here, ADAM10 is linked to early-onset autosomal dominant Alzheimer disease.