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GluN2B-NMDA receptors in Alzheimer's disease: beyond synapse loss and cell death

Alzheimer's disease (AD) is one of the most devastating diseases affecting the life and health of aging population. Two hallmarks of AD are senile plaques and neurofibrillary tangles, and AD is well known for the massive loss of neurons and impaired cognitive functions especially memory loss. Despite extensive search for effective treatment, available drugs have limited efficacy without affecting the course of AD. Significant efforts have been devoted to curb the production of amyloid β (Aβ; the major component of plaques) or enhance the clearance of it, with the aim to reduce the accumulation of plaque in the brain. Antibodies that can bind Aβ to increase their removal have received a lot of attention although recent clinical trial results have been largely negative and disappointing (Panza et al., 2014). Targets that are not directly related to Aβ have also been pursued. One such target is N-methyl-D-aspartate (NMDA) receptors (NMDARs), a subclass of glutamate receptors. The antagonist of NMDAR memantine has been approved for treating moderate to severe AD, although the exact mechanism underlying its action is still in debate (Kotermanski and Johnson, 2009).