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

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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.

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Acknowledgments

Our studies were supported in part by Grants-in-Aid for Scientific Research C (No. 14570186) and Grants-in-Aid for Exploratory Research (No. 17659118) from the Ministry of Education, Culture, Sports, Science and Technology of Japan, and the Sasakawa Scientific Research Grant from The Japan Science Society (No. 18-130).

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Authors and Affiliations

  1. Department of Pathology, Institute for Developmental Research, Aichi Human Service Center, 713-8 Kamiya-cho, Kasugai, Aichi, 480-0392, Japan

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

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  1. Yoichi Chiba
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  2. Atsuyoshi Shimada
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  3. Naoko Kumagai
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  10. Masanori Hosokawa
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Correspondence to Masanori Hosokawa.

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Special issue article in honor of Dr. Akitane Mori.

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Chiba, Y., Shimada, A., Kumagai, N. et al. The Senescence-accelerated Mouse (SAM): A Higher Oxidative Stress and Age-dependent Degenerative Diseases Model. Neurochem Res 34, 679–687 (2009). https://doi.org/10.1007/s11064-008-9812-8

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