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- W4229004748 abstract "The Ca2+ hypothesis for Alzheimer's disease (AD) conceives Ca2+ dyshomeostasis as a common mechanism of AD; the cause of Ca2+ dysregulation, however, is obscure. Meanwhile, hyperactivities of N-Methyl-D-aspartate receptors (NMDARs), the primary mediator of Ca2+ influx, are reported in AD. GluN3A (NR3A) is an NMDAR inhibitory subunit. We hypothesize that GluN3A is critical for sustained Ca2+ homeostasis and its deficiency is pathogenic for AD. Cellular, molecular, and functional changes were examined in adult/aging GluN3A knockout (KO) mice. The GluN3A KO mouse brain displayed age-dependent moderate but persistent neuronal hyperactivity, elevated intracellular Ca2+ , neuroinflammation, impaired synaptic integrity/plasticity, and neuronal loss. GluN3A KO mice developed olfactory dysfunction followed by psychological/cognitive deficits prior to amyloid-β/tau pathology. Memantine at preclinical stage prevented/attenuated AD syndromes. AD patients' brains show reduced GluN3A expression. We propose that chronic degenerative excitotoxicity leads to sporadic AD, while GluN3A represents a primary pathogenic factor, an early biomarker, and an amyloid-independent therapeutic target." @default.
- W4229004748 created "2022-05-08" @default.
- W4229004748 creator A5001588859 @default.
- W4229004748 creator A5007149679 @default.
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- W4229004748 creator A5047143313 @default.
- W4229004748 creator A5057676063 @default.
- W4229004748 creator A5060458448 @default.
- W4229004748 date "2021-06-20" @default.
- W4229004748 modified "2023-10-13" @default.
- W4229004748 title "Pathogenesis of sporadic Alzheimer's disease by deficiency of NMDA receptor subunit GluN3A" @default.
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