title: Pathobiology of the senescence-accelerated mouse (SAM).
abstract: Routine postmortem examinations and the pathobiological features revealed by systematically designed studies have shown several pathologic phenotypes that are often characteristic enough to differentiate among the various SAM strains: senile amyloidosis in SAMP1, -P2, -P7, -P9, -P10, and -P11; secondary amyloidosis in SAMP2 and -P6; contracted kidney in SAMP1, -P2, -P10, and -P11; immunoblastic lymphoma in SAMR1 and -R4; histiocytic sarcoma in SAMR1 and -R4; ovarian cysts in SAMR1; impaired immune response in SAMP1, -P2, and -P8; hyperinflation of the lungs in SAMP1; hearing impairment in SAMP1; degenerative temporomandibular joint disease in SAMP3; senile osteoporosis in SAMP6; deficits in learning and memory in SAMP8 and -P10; emotional disorders in SAMP8 and -P10; cataracts in SAMP9; and brain atrophy in SAMP10. These are all age-associated pathologies, the incidence and severity of which increase with advancing age. The SAM model in which these pathobiological features have been carefully monitored will be a valuable tool in the clarification of the pathogenic mechanisms of age-associated pathologies and in the research for effective methods to modulate or ameliorate these pathologies.
authors.affiliation: Department of Senescence Biology, Kyoto University, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Takeda
authors.forename: T
authors.initials: T
authors.lastname: Matsushita
authors.forename: M
authors.initials: M
authors.lastname: Kurozumi
authors.forename: K
authors.initials: K
authors.lastname: Takemura
authors.forename: K
authors.initials: K
authors.lastname: Higuchi
authors.forename: M
authors.initials: M
authors.lastname: Hosokawa
mesh_terms: D000375:Aging / Q000473:pathology*; D000686:Amyloidosis / Q000473:pathology; D000818:Animals; D005260:Female; D030342:Genetic Diseases, Inborn / Q000473:pathology; D007668:Kidney / Q000002:abnormalities; D008223:Lymphoma / Q000473:pathology; D008297:Male; D051379:Mice; D008806:Mice, Inbred AKR; D010641:Phenotype; D013997:Time Factors