[Senescence-accelerated mouse (SAM): with special reference to age-associated pathologies and their modulation]

Area of Science:

• Gerontology and aging research
• Animal models in biomedical research
• Pathology and disease mechanisms

Background:

• The senescence-accelerated mouse (SAM) model was established at Kyoto University in 1970.
• Development involved selective inbreeding of AKR/J mice, focusing on senescence grading, lifespan, and pathological phenotypes.
• The model comprises 12 lines: 9 senescence-prone (SAMP) and 3 senescence-resistant (SAMR) strains.

Purpose of the Study:

• To characterize the senescence-accelerated mouse (SAM) model, including its senescence-prone (SAMP) and senescence-resistant (SAMR) strains.
• To detail the specific age-associated pathologies observed in different SAM substrains.
• To highlight the utility of the SAM model for investigating aging mechanisms and developing therapeutic interventions.

Main Methods:

• Selective inbreeding of mice based on senescence grading, lifespan, and pathological phenotypes.
• Analysis of survival curves and Gompertzian function to assess aging rates.
• Routine postmortem examinations and systematic studies to identify and characterize pathobiological features.

Main Results:

• All SAMP mice exhibit 'accelerated senescence' characterized by early onset and irreversible aging signs.
• Distinct pathological phenotypes differentiate SAM strains, including senile amyloidosis, contracted kidney, lymphomas, and neurological deficits.
• Age-associated pathologies like impaired immune response, osteoporosis, cataracts, and brain atrophy increase with age in SAM strains.

Conclusions:

• The SAM model provides a valuable tool for understanding the pathogenic mechanisms of age-associated diseases.
• Specific SAMP and SAMR strains exhibit unique aging phenotypes, enabling targeted research.
• The SAM model is crucial for research aimed at modulating or ameliorating age-related pathologies.