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- W2810261013 abstract "Introduction Alzheimer's disease (AD) symptoms reflect synaptic dysfunction and neuron death. Amyloid-β oligomers (AβOs) induce excess calcium entry into neurons via N-methyl-D-aspartate receptors (NMDARs), contributing to synaptic dysfunction. The study described here tested the hypothesis that AβO-stimulated calcium entry also drives neuronal cell cycle reentry (CCR), a prelude to neuron death in AD. Methods Pharmacologic modulators of calcium entry and gene expression knockdown were used in cultured neurons and AD model mice. Results In cultured neurons, AβO-stimulated CCR was blocked by NMDAR antagonists, total calcium chelation with 1,2-Bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid tetrakis(acetoxymethyl ester) (BAPTA-AM), or knockdown of the NMDAR subunit, NR1. NMDAR antagonists also blocked the activation of calcium-calmodulin-dependent protein kinase II and treatment of Tg2576 AD model mice with the NMDAR antagonist, memantine, prevented CCR. Discussion This study demonstrates a role for AβO-stimulated calcium influx via NMDAR and CCR in AD and suggests the use of memantine as a disease-modifying therapy for presymptomatic AD." @default.
- W2810261013 created "2018-07-10" @default.
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- W2810261013 date "2018-07-04" @default.
- W2810261013 modified "2023-10-05" @default.
- W2810261013 title "N‐methyl‐D‐aspartate receptor–mediated calcium influx connects amyloid‐β oligomers to ectopic neuronal cell cycle reentry in Alzheimer's disease" @default.
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- W2810261013 doi "https://doi.org/10.1016/j.jalz.2018.05.017" @default.
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