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.