Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
328796 | Neurobiology of Aging | 2007 | 10 Pages |
The senescence-accelerated mouse (SAM) is an animal model for studying senescence and age-associated disorders due to its inherited aging phenotype. The SAM/prone8 (SAMP8) is a useful animal model to investigate the fundamental mechanisms involved in age-related learning and memory deficits that may have relevance to age-associated AD, while SAM/resistant1 (SAMR1) shows normal. To identify genes rendering the cognitive deterioration with aging, the subtractive cDNA libraries containing 1924 clones with the positive ratio of 96.18% were generated and the microarray containing 3136 cDNA was prepared. The results of screening libraries by the microarray showed that of all 91 differentially expressed genes, 50 were over-expressed and 41 were low-expressed in SAMP8. Some of the identified genes were confirmed by the real time quantitative RT-PCR. These results indicated the profiles of gene expression in the hippocampus of SAMP8 and SAMR1 were significantly different, which may play important roles in the age-related cognitive deficit in SAMP8, suggesting those genes related to the cognitive deficient or pathology change in the brain of SAMP8 may be potential gene targets for Alzheimer's disease therapy.