APP and Alzheimer disease: AOE1 attenuated the cognitive dysfunction of APP/PS1 transgenic mice by reducing Aβ burden, especially Aβ oligomers with the molecular size of 40–60 kDa, including a 56 kDa soluble Aβ oligomer (Aβ*56) that impaired long-lasting synaptic plasticity and disrupted cognition independently of neuron loss or plaque deposition in AD [47].