Administration of amyloid-β42 oligomer-specific monoclonal antibody improved memory performance in SAMP8 mice.

Amyloid-β peptide (Aβ) is recognized by many as the leading cause of Alzheimer's disease (AD), and Aβ oligomers play a major role in the early-onset form of AD. Recently, the application of passive immunization targeting Aβ has been investigated as a potential method of AD immunotherapy. We used a strain of monoclonal antibody against Aβ42 oligomers, designated A8, as an Aβ inhibitor to suppress Aβ aggregation and Aβ-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.

Preparation and characterization of a monoclonal antibody with high affinity for soluble Abeta oligomers.

Amyloid beta-protein (Abeta) has been causally implicated in the neurodegenerative processes that accompany Alzheimer's disease. Soluble oligomers of the Abeta(1-42) fragment are thought to be significantly more neurotoxic than higher molecular weight aggregates. We report the isolation and characterization of a mouse monoclonal antibody (MAb) directed against soluble Abeta(1-42) oligomers.