Journal
AGING CELL
Volume 17, Issue 3, Pages -Publisher
WILEY
DOI: 10.1111/acel.12754
Keywords
amyloid-beta; Dexras1; ERK-CREB-BDNF; neurotoxicity; nNOS-CAPON interaction; S-nitrosylation
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Funding
- National Natural Science Foundation of China [31530091]
- Natural Science Foundation of Jiangsu Province [BK20140905]
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In neurons, increased protein-protein interactions between neuronal nitric oxide synthase (nNOS) and its carboxy-terminal PDZ ligand (CAPON) contribute to excitotoxicity and abnormal dendritic spine development, both of which are involved in the development of Alzheimer's disease. In models of Alzheimer's disease, increased nNOS-CAPON interaction was detected after treatment with amyloid-beta in vitro, and a similar change was found in the hippocampus of APP/PS1 mice (a transgenic mouse model of Alzheimer's disease), compared with age-matched background mice in vivo. After blocking the nNOS-CAPON interaction, memory was rescued in 4-month-old APP/PS1 mice, and dendritic impairments were ameliorated both in vivo and in vitro. Furthermore, we demonstrated that S-nitrosylation of Dexras1 and inhibition of the ERK-CREB-BDNF pathway might be downstream of the nNOS-CAPON interaction.
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