Affiliations: [a] Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, TX, USA
| [b] Cell Biology & Biochemistry Department, Texas Tech University Health Sciences Center, Lubbock, TX, USA
| [c] Neuroscience & Pharmacology Department, Texas Tech University Health Sciences Center, Lubbock, TX, USA
| [d] Neurology Department, Texas Tech University Health Sciences Center, Lubbock, TX, USA
| [e] Speech, Language and Hearing Sciences Departments, Texas Tech University Health Sciences Center, Lubbock, TX, USA
| [f] Garrison Institute on Aging, South West Campus, Texas Tech University Health Sciences Center, Lubbock, TX, USA
Correspondence:
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Correspondence to: Rui Wang, Garrison Institute on Aging, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, USA. Tel.: +1 8067432385; Fax.: +1 8067432698; E-mail: rui.wang@ttuhsc.edu.
Abstract: Excitatory glutamatergic neurotransmission via N-methyl-d-aspartate receptor (NMDAR) is critical for synaptic plasticity and survival of neurons. However, excessive NMDAR activity causes excitotoxicity and promotes cell death, underlying a potential mechanism of neurodegeneration occurred in Alzheimer’s disease (AD). Studies indicate that the distinct outcomes of NMDAR-mediated responses are induced by regionalized receptor activities, followed by different downstream signaling pathways. The activation of synaptic NMDARs initiates plasticity and stimulates cell survival. In contrast, the activation of extrasynaptic NMDARs promotes cell death and thus contributes to the etiology of AD, which can be blocked by an AD drug, memantine, an NMDAR antagonist that selectively blocks the function of extrasynaptic NMDARs.
