| First Author | Qian Z | Year | 2024 |
| Journal | Mol Psychiatry | Volume | 29 |
| Issue | 10 | Pages | 3040-3055 |
| PubMed ID | 38658772 | Mgi Jnum | J:368207 |
| Mgi Id | MGI:7748941 | Doi | 10.1038/s41380-024-02565-x |
| Citation | Qian Z, et al. (2024) Thy1-ApoE4/C/EBPbeta double transgenic mice act as a sporadic model with Alzheimer's disease. Mol Psychiatry 29(10):3040-3055 |
| abstractText | Early onset familial Alzheimer's disease (FAD) with APP, PS1/2 (presenilins) mutation accounts for only a small portion of AD cases, and most are late-onset sporadic. However, majority of AD mouse models are developed to mimic the genetic cause of human AD by overexpressing mutated forms of human APP, PS1/2, and/or Tau protein, though there is no Tau mutation in AD, and no single mouse model recapitulates all aspects of AD pathology. Here, we report Thy1-ApoE4/C/EBPbeta double transgenic mouse model that demonstrates key AD pathologies in an age-dependent manner in absence of any human APP or PS1/2 mutation. Using the clinical diagnosis criteria, we show that this mouse model exhibits tempo-spatial features in AD patient brains, including progressive cognitive decline associated with brain atrophy, which is accompanied with extensive neuronal degeneration. Remarkably, the mice display gradual Abeta aggregation and neurofibrillary tangles formation in the brain validated by Abeta PET and Tau PET. Moreover, the mice reveal widespread neuroinflammation as shown in AD brains. Hence, Thy1-ApoE4/C/EBPbeta mouse model acts as a sporadic AD mouse model, reconstituting the major AD pathologies. |
