WFRF:(Guo ZY)
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| Fältnamn | Indikatorer | Metadata |
|---|---|---|
| 000 | 03066naa a2200517 4500 | |
| 001 | oai:prod.swepub.kib.ki.se:148087125 | |
| 003 | SwePub | |
| 008 | 240701s2022 | |||||||||||000 ||eng| | |
| 024 | 7 | a http://kipublications.ki.se/Default.aspx?queryparsed=id:1480871252 URI |
| 024 | 7 | a https://doi.org/10.1038/s41422-021-00582-x2 DOI |
| 040 | a (SwePub)ki | |
| 041 | a engb eng | |
| 042 | 9 SwePub | |
| 072 | 7 | a ref2 swepub-contenttype |
| 072 | 7 | a art2 swepub-publicationtype |
| 100 | 1 | a Pang, KL4 aut |
| 245 | 1 0 | a An App knock-in rat model for Alzheimer's disease exhibiting Aβ and tau pathologies, neuronal death and cognitive impairments |
| 264 | c 2021-11-17 | |
| 264 | 1 | b Springer Science and Business Media LLC,c 2022 |
| 520 | a A major obstacle in Alzheimer’s disease (AD) research is the lack of predictive and translatable animal models that reflect disease progression and drug efficacy. Transgenic mice overexpressing amyloid precursor protein (App) gene manifest non-physiological and ectopic expression of APP and its fragments in the brain, which is not observed in AD patients. The App knock-in mice circumvented some of these problems, but they do not exhibit tau pathology and neuronal death. We have generated a rat model, with three familiar App mutations and humanized Aβ sequence knocked into the rat App gene. Without altering the levels of full-length APP and other APP fragments, this model exhibits pathologies and disease progression resembling those in human patients: deposit of Aβ plaques in relevant brain regions, microglia activation and gliosis, progressive synaptic degeneration and AD-relevant cognitive deficits. Interestingly, we have observed tau pathology, neuronal apoptosis and necroptosis and brain atrophy, phenotypes rarely seen in other APP models. This App knock-in rat model may serve as a useful tool for AD research, identifying new drug targets and biomarkers, and testing therapeutics. | |
| 700 | 1 | a Jiang, RC4 aut |
| 700 | 1 | a Zhang, W4 aut |
| 700 | 1 | a Yang, ZY4 aut |
| 700 | 1 | a Li, LL4 aut |
| 700 | 1 | a Shimozawa, Mu Karolinska Institutet4 aut |
| 700 | 1 | a Tambaro, Su Karolinska Institutet4 aut |
| 700 | 1 | a Mayer, Ju Karolinska Institutet4 aut |
| 700 | 1 | a Zhang, BG4 aut |
| 700 | 1 | a Li, M4 aut |
| 700 | 1 | a Wang, JS4 aut |
| 700 | 1 | a Liu, H4 aut |
| 700 | 1 | a Yang, AL4 aut |
| 700 | 1 | a Chen, X4 aut |
| 700 | 1 | a Liu, JZ4 aut |
| 700 | 1 | a Winblad, Bu Karolinska Institutet4 aut |
| 700 | 1 | a Han, H4 aut |
| 700 | 1 | a Jiang, TZ4 aut |
| 700 | 1 | a Wang, WW4 aut |
| 700 | 1 | a Nilsson, Pu Karolinska Institutet4 aut |
| 700 | 1 | a Guo, W4 aut |
| 700 | 1 | a Lu, B4 aut |
| 710 | 2 | a Karolinska Institutet4 org |
| 773 | 0 | t Cell researchd : Springer Science and Business Media LLCg 32:2, s. 157-175q 32:2<157-175x 1748-7838x 1001-0602 |
| 856 | 4 | u https://www.nature.com/articles/s41422-021-00582-x.pdf |
| 856 | 4 8 | u http://kipublications.ki.se/Default.aspx?queryparsed=id:148087125 |
| 856 | 4 8 | u https://doi.org/10.1038/s41422-021-00582-x |
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- Tambaro, S
- Mayer, J
- Zhang, BG
- Li, M
- Wang, JS
- Liu, H
- Yang, AL
- Chen, X
- Liu, JZ
- Winblad, B
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