| First Author | Takeda T | Year | 1997 |
| Journal | Exp Gerontol | Volume | 32 |
| Issue | 1-2 | Pages | 105-9 |
| PubMed ID | 9088907 | Mgi Jnum | J:38963 |
| Mgi Id | MGI:86349 | Doi | 10.1016/s0531-5565(96)00036-8 |
| Citation | Takeda T, et al. (1997) Senescence-accelerated mouse (SAM): a novel murine model of senescence. Exp Gerontol 32(1-2):105-9 |
| abstractText | The Senescence-Accelerated Mouse (SAM) has been under development by our research team at Kyoto University since 1970 through the selective inbreeding of the AKR/J strain of mice donated by the Jackson Laboratory in 1968, based on a graded score for senescence, life span, and pathologic phenotype. At present, there are 12 lines of SAM: nine senescence-prone inbred strains (SAMP) including SAMP1, SAMP2, SAMP3, SAMP6, SAMP7, SAMP8, SAMP9, SAMP10, and SAMP11; and three senescence-resistant inbred strains (SAMR) including SAMR1, SAMR4, and SAMR5. Data from survival curves, Gompertzian function, and grading score of senescence, together with growth patterns of body weight of these SAMP and SAMR, revealed that the characteristic feature of aging common to all SAMP mice is accelerated senescence; early onset and irreversible advance of senescence manifested by several signs and gross lesions such as the loss of normal behavior, various skin lesions, increased lordokyphosis, etc., after a period of normal development. In the course of SAM development, it became evident that SAMP strains manifest various pathologic phenotypes that are characteristic enough to differentiate the SAM strains. The genetic background and significance of SAM development are discussed. |
