This special binding could be explained by the colocalization of mGluR1 and Aβ and the presence of Aβ and GluN2B immunoreactivities in neurites [35, 36] In AD, AβO prevents physiological activation of the cellular prion protein-mGluR5 (PrPC-mGluR5) complex by glutamate. Here, GRM1 is linked to Alzheimer disease.