Deposition of the β-amyloid peptide (Aβ) play key role in Alzheimer’s disease (AD) pathogenesis. So, the Alzheimer’s disease may be delayed if we lessen accumulation of the amyloid in the brain or hasten its excretion. Activity of neprilysin decreases at the early stages of Alzheimer’s disease and during age-related changes in the organism. M. Kindy investigated how introduction of neprilysin affected mice having Alzheimer’s disease at the early stages (before amyloid placque were formed). Then he evaluated how that impact affected deposition of the β-amyloid and how it affected allied pathogenetic changes. It was found, that after mice had been exposed to that impact, they showed improvement of spatial memory in Morris labyrinth. Those data show that replenishment of neprilysin in brain at early stages of Alzheimer’s disease is an effective method to prevent or ease Alzheimer’s disease pathogenesis. Neprilysin is the main brain enzyme responsible for destruction of the β-amyloid. Data obtained give evidence that neprilysin overexpression leads to the decrease of β-amyloid and related pathological processes.