In preclinical models of AD, mGluR5 has been hypothesized to mediate amyloid-β oligomer (Aβo) toxicity via several mechanisms, including promoting the clustering of Aβo as an extracellular scaffold for mGluR5 [9] and serving as a co-receptor for Aβo bound to cellular prion protein (PrPc) for postsynaptic activation of the tyrosine kinase Fyn [10, 11]. Here, ABO is linked to Alzheimer disease.