| First Author | Lok K | Year | 2013 |
| Journal | Neurosci Lett | Volume | 557 Pt B |
| Pages | 84-9 | PubMed ID | 24176881 |
| Mgi Jnum | J:207860 | Mgi Id | MGI:5559824 |
| Doi | 10.1016/j.neulet.2013.10.051 | Citation | Lok K, et al. (2013) Characterization of the APP/PS1 mouse model of Alzheimer's disease in senescence accelerated background. Neurosci Lett 557 Pt B:84-9 |
| abstractText | The APP/PS1 mouse model of Alzheimer's disease (AD) exhibits remarkable elevation of beta-amyloid production associated with certain behavioral abnormalities, while the senescence accelerated mouse prone 8 (SAMP8) is characterized by early and age-related deterioration of learning and memory. In order to obtain an AD model that develops earlier pathological changes and cognitive impairment, we generated SAMP8-APP/PS1, a novel senescence accelerated APP/PS1 transgenic mouse model of AD. Standard histological staining and immunohistochemistry using an amyloid beta (Abeta) antibody showed an age, genotype and strain-dependent progression of amyloid deposition and neuron loss in the cerebral cortex and hippocampus of SAMP8-APP/PS1 mice. Results from the cognitive behavioral tests revealed early deficits in learning and memory in SAMP8-APP/PS1 mice in the two way active avoidance and Morris water maze tests compared with C57-APP/PS1, SAMP8 wild-type and control mice. These results suggest that accelerated senescence exacerbates amyloid deposition and cognitive dysfunction in APP/PS1 mice and the senescence accelerated-APP/PS1 (SAMP8-APP/PS1) mouse model might be a valuable tool to study AD progression and to evaluate the effect of drugs on AD. |
