The Senescence-accelerated Mouse (SAM): A Higher Oxidative Stress and Age-dependent Degenerative Diseases Model

Author： Chiba Yoichi Shimada Atsuyoshi Kumagai Naoko Yoshikawa Keisuke Ishii Sanae Furukawa Ayako Takei Shiro Sakura Masaaki Kawamura Noriko Hosokawa Masanori

Publisher： Springer Publishing Company

ISSN： 0364-3190

Source： Neurochemical Research, Vol.34, Iss.4, 2009-04, pp. : 679-687

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Abstract

The SAM strain of mice is actually a group of related inbred strains consisting of a series of SAMP (accelerated senescence-prone) and SAMR (accelerated senescence-resistant) strains. Compared with the SAMR strains, the SAMP strains show a more accelerated senescence process, a shorter lifespan, and an earlier onset and more rapid progress of age-associated pathological phenotypes similar to human geriatric disorders. The higher oxidative stress status observed in SAMP mice is partly caused by mitochondrial dysfunction, and may be a cause of this senescence acceleration and age-dependent alterations in cell structure and function. Based on our recent observations, we discuss a possible mechanism for mitochondrial dysfunction resulting in the excessive production of reactive oxygen species, and a role for the hyperoxidative stress status in neurodegeneration in SAMP mice. These SAM strains can serve as a useful tool to understand the cellular mechanisms of age-dependent degeneration, and to develop clinical interventions.