GRIN2B and Alzheimer disease: Because reductions in LTP resulting from applications of Aβ oligomers isolated from postmortem AD patients or of culture medium of an AD cell line can be rescued by a selective GluN2 inhibitor or eNMDAR antagonist memantine, the activation of eNMDARs containing GluN2B subunit may be a cause of the inhibition of LTP by Aβ oligomers10,42.