ADAM10-derived tau fragments in CSF have been shown to inversely correlate with cognitive function in humans (Henriksen et al. 2013), and blocking ADAM10 in a nontransgenic AD mouse model leads to AD-like pathology, including hyperphosphorylation of tau and accumulation of Aβ aggregates (Epis et al. 2010). This evidence concerns the gene MAPT and Alzheimer disease.