The hypothesis that oligomeric Aβ species are responsible for AD pathogenesis rather than the fibrillar amyloid plaques is supported by many studies including a mouse model engineered to express oligomeric Aβ but not plaques (amyloid precursor protein [APP]E693Q) (6, 9), where mice engineered to convert oligomers into plaques (APPE693Q/PS1ΔE9) were not impaired to a greater extent than the mice generating only oligomeric Aβ (10). Here, APP is linked to Alzheimer disease.