Invited Symposium: Molecular Mechanisms of Ageing
The SAM (Senescence-Accelerated Mouse) strain was established in the Department of Senescence Biology, Chest Disease Research Institute, Kyoto University, Japan as a novel murine model of senescence acceleration and age-associated disorders. This strain is actually a group of related inbred strains (recombinant inbred strain-like) including nine strains of accelerated senescence-prone, short lived mice (SAMP) and three strains of accelerated senescence-resistant, long lived mice (SAMR). Each SAMP strain shows relatively strain specific age-associated pathologies. These characteristic pathological phenotypes are similar to age-associated disorders often observed in elder humans. They include senile osteoporosis, osteoarthrosis, age-related deficits in learning and memory with/without forebrain atrophy, presbycusis, senile amyloidosis, age-related impairment of the immune response and so on. The common aging characteristic of SAMP strains is senescence acceleration after normal development and maturation. One possible mechanism that can accelerate the senescence process, and cause and/or exacerbate these age-associated pathologies in SAMP mice at early calendric time is hyperoxidative status. Recent studies also revealed some genetic and molecular aspects of these age-associated pathologies and senescence acceleration.
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|Hosokawa, M; (1998). The SAM Strain Of Mice; An Animal Model Of Senescence Acceleration And Age-associated Disorders. Presented at INABIS '98 - 5th Internet World Congress on Biomedical Sciences at McMaster University, Canada, Dec 7-16th. Invited Symposium. Available at URL http://www.mcmaster.ca/inabis98/higuchi/hosokawa0508/index.html|
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