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.
Place of employment — Department of Neurosciences, Medical University of South Carolina, USA.
Contacts — 171 Ashley Avenue, Charleston, SC, 29403(843) 792–0808 kindyms@musc.edu .
Publications — Neprilysin: an enzyme candidate to slow the progression of Alzheimer’s disease. El-Amouri SS, Zhu H, Yu J, Marr R, Verma IM, Kindy MS. Am J Pathol. 2008 May;172(5):1342–54.Cysteine protease inhibitors reduce brain beta-amyloid and beta-secretase activity in vivo and are potential Alzheimer’s disease therapeutics. Hook G, Hook VY, Kindy M. Biol Chem. 2007 Sep;388(9):979–83.Inhibitors of cathepsin B improve memory and reduce beta-amyloid in transgenic Alzheimer disease mice expressing the wild-type, but not the Swedish mutant, beta-secretase site of the amyloid precursor protein.
