| First Author | Zhang Y | Year | 2018 |
| Journal | Aging Cell | Volume | 17 |
| Issue | 3 | Pages | e12754 |
| PubMed ID | 29577585 | Mgi Jnum | J:261918 |
| Mgi Id | MGI:6158050 | Doi | 10.1111/acel.12754 |
| Citation | Zhang Y, et al. (2018) nNOS-CAPON interaction mediates amyloid-beta-induced neurotoxicity, especially in the early stages. Aging Cell 17(3):e12754 |
| abstractText | 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. |
