期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 57, 期 4, 页码 1041-1048出版社
IOS PRESS
DOI: 10.3233/JAD-160763
关键词
Alzheimer's disease; excitotoxicity; extrasynaptic NMDA receptors; glutamate; memantine; NMDA receptors
资金
- NATIONAL INSTITUTE ON AGING [R01AG042178, R01AG047812] Funding Source: NIH RePORTER
- NIA NIH HHS [R01 AG042178, R01 AG047812] Funding Source: Medline
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.
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