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Several lines of evidence indicate that amyloid   β   (A  β  ), particularly A  β   oligomers (A  β  Os), plays a causative role in Alzheimer's disease. However, the mechanisms underlying the action of an anti-A  β  O antibody to clarify the toxic action of A  β  Os remain elusive. Here, we showed that the anti-A  β  O antibody (monoclonal 72D9) can modify the A  β   aggregation pathway. We also found that 72D9 directly sequesters both extracellular and intraneuronal A  β  Os in a nontoxic state. Thus, therapeutic intervention targeting A  β  Os is a promising strategy for neuronal protection in Alzheimer's disease.

Disease Modifying Therapies for Alzheimer's Disease Targeting AβOligomers: Implications for Therapeutic Mechanisms