ABO and Alzheimer disease: Mounting evidence suggests that the selective neuronal vulnerability manifest in AD derives from specific AβO binding to high affinity receptors3,6,49 expressed by particular subtypes of neurons1,50, leading to disruption of synaptic signaling pathways51–54, blockade of long-term potentiation1,55,56, and alterations in spine morphology and density27,37,47,48,51.