For example, cleavage of APP by meprin-β can generate a N-terminally truncated Aβ (Aβ2–X), which is more prone to aggregation than Aβ40; while the inhibitor of meprin-β, fetuin-A, was reduced in CSF of AD patients (Puchades et al., 2003), indicating a potentially pathogenic role of enhanced meprin-β activity in AD. This evidence concerns the gene APP and Alzheimer disease.