%0 Journal Article
%T nNOS每CAPON interaction mediates amyloid坼汕坼induced neurotoxicity, especially in the early stages
%A Chun坼Xia Luo
%A Hai坼Ying Liang
%A Huan坼Yu Ni
%A Lei Zhang
%A Qi坼Gang Zhou
%A Yu Zhang
%A Zhu Zhu
%J Archive of "Aging Cell".
%D 2018
%R 10.1111/acel.12754
%X In neurons, increased protein每protein interactions between neuronal nitric oxide synthase (nNOS) and its carboxy坼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每CAPON interaction was detected after treatment with amyloid坼汕 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坼matched background mice in vivo. After blocking the nNOS每CAPON interaction, memory was rescued in 4坼month坼old APP/PS1 mice, and dendritic impairments were ameliorated both in vivo and in vitro. Furthermore, we demonstrated that S坼nitrosylation of Dexras1 and inhibition of the ERK每CREB每BDNF pathway might be downstream of the nNOS每CAPON interaction
%K amyloid坼汕
%K Dexras1
%K ERK每CREB每BDNF
%K neurotoxicity
%K nNOS每CAPON interaction
%K S坼nitrosylation
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5946066/