Other
11 Authors
- Sun H,
- Fukui Y,
- Yamashita T,
- Ishiura H,
- Yu H,
- Ota-Elliott R,
- Bian Y,
- Abe K,
- Morihara R,
- Hu X,
- Bian Z
| First Author | Yu H | Year | 2023 |
| Journal | Brain Res | Volume | 1821 |
| Pages | 148565 | PubMed ID | 37683777 |
| Mgi Jnum | J:341234 | Mgi Id | MGI:7532370 |
| Doi | 10.1016/j.brainres.2023.148565 | Citation | Yu H, et al. (2023) Injection of exogenous amyloid-beta oligomers aggravated cognitive deficits, and activated necroptosis, in APP23 transgenic mice. Brain Res 1821:148565 |
| abstractText | Alzheimer's disease (AD) is a neurodegenerative disease that is characterized by the loss of synapses and neurons in the brain, and the accumulation of amyloid plaques. Abeta oligomers (AbetaO) play a critical role in the pathogenesis of AD. Although there is increasing evidence to support the involvement of necroptosis in the pathogenesis of AD, the exact mechanism remains elusive. In the present study, we explored the effect of exogenous AbetaO injection on cell necroptosis and cognitive deficits in APP23 transgenic mice. We found that intrahippocampal injection of AbetaO accelerated the development of AD pathology and caused cognitive impairment in APP23 mice. Specifically, AbetaO injection significantly accelerated the accumulation of AbetaO and increased the expression level of phosphorylated-tau, and also induced necroptosis. Behavioral tests showed that AbetaO injection was associated with cognitive impairment. Furthermore, necroptosis induced by AbetaO injection occurred predominantly in microglia of the AD brain. We speculate that AbetaO increased necroptosis by activating microglia, resulting in cognitive deficits. Our results may aid in an understanding of the role played by AbetaO in AD from an alternative perspective and provide new ideas and evidence for necroptosis as a potential intervention and therapeutic target for AD. |
