Senescence-accelerated mouse (SAM): a biogerontological resource in aging research.
The senescence-accelerated mouse (SAM), consisting of 14 senescence-prone inbred strains (SAMP) and 4 senescence-resistant inbred strains (SAMR) has been under development since 1970 through the selective inbreeding of AKR/J strain mice donated by the Jackson laboratory in 1968, based on the data of the grading score of senescence, life span, and pathologic phenotypes. The characteristic feature of aging common to all SAMP and SAMR mice is accelerated senescence and normal aging, respectively. Furthermore, SAMP and SAMR strains manifest various pathobiological phenotypes which include such neurobiological phenotypes as deficits in learning and memory, emotional disorders, abnormal circadian rhythms, brain atrophy, hearing impairment, etc., and are often characteristic enough to differentiate the strains. Various efforts are currently being made using the SAM model to clarify the underlying mechanisms in accelerated senescence as well as the etiopathogenic mechanisms in age-associated pathobiologies. Genetic background and significance of SAM development are discussed.
Takeda
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Council for SAM Research, c/o Institute for Frontier Medical Sciences, Kyoto University, Japan.
D000375:Aging / Q000235:genetics* / Q000502:physiology*; D000686:Amyloidosis / Q000235:genetics; D000818:Animals; D004195:Disease Models, Animal; D005853:Geriatrics / Q000379:methods*; D007592:Joint Diseases / Q000235:genetics; D051379:Mice; D008815:Mice, Inbred Strains / Q000235:genetics*; D010024:Osteoporosis / Q000235:genetics; D010641:Phenotype