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The senescence-accelerated mouse (SAM) models were developed through phenotypic selection from a genetic pool of AKR/J mice in early 1980. The SAM strains have been used as models for studying age-related disorders and consist of nine major senescence accelerated mouse-prone (SAMP) sub-strains that undergo accelerated aging and three senescence accelerated mouse-resistant (SAMR) sub-strains that undergo normal aging process. Among them, SAMP8 mice mimic several features of Alzheimer's disease, such as cognitive impairment and Aβ deposition. In addition, there are alterations of genes and proteins relating to neuroprotection, signal transduction, immune response, energy metabolism, mitochondrial function in the brain of SAMP8 mice.
Creative Bioarray focuses on drug research and development services and helps customers evaluate the drug efficacy and study the associated pathological mechanisms of AD by SAMP8 mouse model.
Figure. 1. SAMP8 mice
With extensive experience in the field of AD, we are confident to help you to overcome any upcoming challenges. Our experts are fully capable of customizing our protocols and assays to meet your specific needs. With our help, we wish to facilitate your research with high efficiency.
Figure. 2. Western blots of hippocampal tissue from SAMP8 mice chronically treated with pramlintide demonstrated. (A) decreased hippocampal expression of the cellular stress marker heme-oxygenase-1 (HO-1) (p = 0.035), (B) decreased synapsin I expression (p = 0.004), and (C) increased expression of cyclin-dependent kinase-5 (CDK5) (p = 0.002). Pramlintide treatment did not have a significant effect on the expression of p35, p25, or the p25/35 ratio (p > 0.05). Results are depicted as mean±standard error of mean (SEM). (Student t test, * p < 0.05, ** p < 0.01; n = 7-10 per group). Abbreviations: HO-1, heme-oxygenase-1; SEM, standard error of mean.
Figure. 3. (A) Chronic pramlintide treatment decreased expression of the inflammatory marker cyclooxygenase 2 (COX-2) in the hippocampus as detected by immunohistochemistry (p = 0.042). (B) There is a trend toward decreased expression of the oxidative stress marker 4-hydroxynonenal (HNE) in the hippocampus of pramlintide-treated mice (p = 0.090). The results are depicted as mean±standard error of mean (SEM). (Student t test, * p < 0.05; n = 5-6 per group). Abbreviations: COX-2, cyclooxygenase 2; HNE, 4-hydroxynonenal; SEM, standard error of mean.
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Adler BL et al. Neuroprotective effects of the amylin analogue pramlintide on Alzheimer's disease pathogenesis and cognition. Neurobiology of Aging. 2014; 35: 793-801.