The senescence-accelerated mouse (SAM): A higher oxidative stress and age-dependent degenerative diseases model

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

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36 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)679-687
Number of pages9
JournalNeurochemical Research
Volume34
Issue number4
DOIs
StatePublished - Apr 1 2009

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Cellular and Molecular Neuroscience

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    Chiba, Y., Shimada, A., Kumagai, N., Yoshikawa, K., Ishii, S., Furukawa, A., Takei, S., Sakura, M., Kawamura, N., & Hosokawa, M. (2009). The senescence-accelerated mouse (SAM): A higher oxidative stress and age-dependent degenerative diseases model. Neurochemical Research, 34(4), 679-687. https://doi.org/10.1007/s11064-008-9812-8