MME and early-onset autosomal dominant Alzheimer disease: The enzymehas displayed the ability to degrade Aβ but not its precursorAPP.4 The protein levels of neprilysinare downregulated during aging and Alzheimer’s disease, bothin transgenic mouse models of Alzheimer’s disease and in post-mortemhuman brains.5,6 Accordingly, molecules that enhancethe activity or levels of neprilysin are considered as potential therapeuticoptions for the treatment of Alzheimer’s disease.