Recent evidence from Reinders et al., demonstrated that AβOs cause synaptic failure only in neurons expressing GluA3 subunits [118], and mice with severe AD neuropathology but deficient in GluA3 were cognitively resilient [118], strongly indicating that synaptic vulnerability to AβOs may depend on the stoichiometry of synaptic receptors. Here, GRIA3 is linked to Alzheimer disease.