RESUMO
Amyloid-ß peptide (Aß) is recognized by many as the leading cause of Alzheimer's disease (AD), and Aß oligomers play a major role in the early-onset form of AD. Recently, the application of passive immunization targeting Aß has been investigated as a potential method of AD immunotherapy. We used a strain of monoclonal antibody against Aß42 oligomers, designated A8, as an Aß inhibitor to suppress Aß aggregation and Aß-derived cell toxicity in vitro, and as a passive immunotherapy approach to treat SAMP8 (senescence accelerated mouse sub-line P8) mice, an animal model of AD, in vivo. First, our results showed that pre-incubation of A8 with Aß oligomers inhibited both the maturation of Aß fiber and Aß oligomer toxicity on SH-SY5Y cells. Second, learning and memory was improved through intraperitoneal administration of A8 in SAMP8 mice. Third, Aß pathology was ameliorated with decreased Aß oligomers and phospho-tau levels in SAMP8 mice. Our data suggest that our monoclonal antibody A8 may be a candidate as a potential immunotherapeutic agent in AD.
