Indeed, extra-synaptic NMDA-NR2B receptors have emerged as a key factor in mediating the effects of amyloid on synaptic depression and toxicity (Kessels et al., 2013, Wang et al., 2013); for example, low nanomolar levels of soluble Aβ oligomers enhance NR2B-mediated NMDA receptor currents and extra-synaptic responses (Li et al., 2011). Here, GRIN2B is linked to amyloidosis.