TY - JOUR
T1 - The senescence-accelerated mouse (SAM)
T2 - A higher oxidative stress and age-dependent degenerative diseases model
AU - Chiba, Yoichi
AU - Shimada, Atsuyoshi
AU - Kumagai, Naoko
AU - Yoshikawa, Keisuke
AU - Ishii, Sanae
AU - Furukawa, Ayako
AU - Takei, Shiro
AU - Sakura, Masaaki
AU - Kawamura, Noriko
AU - Hosokawa, Masanori
N1 - Funding Information:
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).
PY - 2009/4
Y1 - 2009/4
N2 - 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.
AB - 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.
UR - https://www.scopus.com/pages/publications/62349108360
UR - https://www.scopus.com/inward/citedby.url?scp=62349108360&partnerID=8YFLogxK
U2 - 10.1007/s11064-008-9812-8
DO - 10.1007/s11064-008-9812-8
M3 - Review article
C2 - 18688709
AN - SCOPUS:62349108360
SN - 0364-3190
VL - 34
SP - 679
EP - 687
JO - Neurochemical Research
JF - Neurochemical Research
IS - 4
ER -