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. © 2013 Etsuro Matsubara et al.
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Matsubara, E., Takamura, A., Okamoto, Y., Oono, H., Nakata, T., Wakasaya, Y., … Shoji, M. (2013). Disease modifying therapies for alzheimer’s disease targeting a β oligomers: Implications for therapeutic mechanisms. BioMed Research International, 2013. https://doi.org/10.1155/2013/984041