Neurochemical Research

, Volume 34, Issue 4, pp 679–687

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
MINI-REVIEW

DOI: 10.1007/s11064-008-9812-8

Cite this article as:
Chiba, Y., Shimada, A., Kumagai, N. et al. Neurochem Res (2009) 34: 679. doi:10.1007/s11064-008-9812-8

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.

Keywords

Senescence-accelerated mouseHigher oxidative stress statusMitochondrial dysfunctionNeurodegenerationNeuroinflammation

Copyright information

© Springer Science+Business Media, LLC 2008

Authors and Affiliations

  • Yoichi Chiba
    • 1
  • Atsuyoshi Shimada
    • 1
  • Naoko Kumagai
    • 1
  • Keisuke Yoshikawa
    • 1
  • Sanae Ishii
    • 1
  • Ayako Furukawa
    • 1
  • Shiro Takei
    • 1
  • Masaaki Sakura
    • 1
  • Noriko Kawamura
    • 1
  • Masanori Hosokawa
    • 1
  1. 1.Department of Pathology, Institute for Developmental ResearchAichi Human Service CenterKasugai, AichiJapan