SAMP8/TaHsd mice are an inbred senescence accelerated mouse (SAM) strain that occurred spontaneously. Mice overproduce the amyloid precursor protein (APP) and are a model of early senescence, aging, Alzheimer’s disease, and oxidative stress.
As key marker of aging, the senescence-associated β-galactosidase (β-Gal) activity and the autophagy-related marker p62 (also known as SQSTM1), are significantly increased in the cortex of 5 and 9 months old SAMP8 mice compared to senescence resistant SAMR1 mice (Figure 1).
Figure 1: Senescence and autophagy marker in the cortex of SAMP8 and SAMR1 mice at the age of 5 and 9 months. β-galactosidase (β-Gal) activity (A) as well as p62 protein levels (B) were assessed in cortical samples of 5 and 9 months old SAMP8 and SAMR1 control animals (n=4-8 per group). Two-way ANOVA followed by Bonferroni’s post hoc test. Mean ± SEM. **p <0.01; ***p <0.001.
SAMP8 mice further show aging-related deterioration by learning and motor deficits in the contextual fear conditioning test and wire hanging test, respectively, as early as 4 months old (Figure 2).
Figure 2: Cognitive and motor impairments of SAMP8 mice. SAMP8 mice were evaluated for learning deficits in the contextual fear conditioning test (A) and motor deficits in the wire hanging test (B) at the age of 4 months compared to SAMR1 mice of the same age as senescence resistant control mice. A: Mean freezing duration for 5 minutes after receiving the foot shock. B: Wire hanging time in seconds. 300 seconds cut-off time. Mean + SEM, n = 12 per group, unpaired t-test, *p <0.05, ***p <0.001.
Scantox offers a custom-tailored study design for your study in SAMP8 mice, and we are flexible to accommodate to your special interests. We are also happy to advice you and propose study designs.
We would be happy to test your compounds in the SAMP8 mouse model of aging! The most common readouts of SAMP8 research are:
We are happy to receive your inquiry.
