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BioMed Research International
Volume 2013, Article ID 984041, 6 pages
Research Article

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

1Department of Neurology, Institute of Brain Science, Hirosaki University Graduate School of Medicine, Aomori 036-8562, Japan
2Shin-Yurigaoka General Hospital, Kanagawa 215-0026, Japan
3Immunas Pharma Incorporation, Kanagawa 213-0012, Japan

Received 30 April 2013; Revised 22 July 2013; Accepted 22 July 2013

Academic Editor: Patrick Kehoe

Copyright © 2013 Etsuro Matsubara et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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