|Budget Amount *help
¥2,400,000 (Direct Cost : ¥2,400,000)
Fiscal Year 1997 : ¥1,000,000 (Direct Cost : ¥1,000,000)
Fiscal Year 1996 : ¥1,400,000 (Direct Cost : ¥1,400,000)
Immune dysfunction in aging animals has long been thought to be some cause of nonimmune diseases in the aged and be related to shortened life span, though how the immune system is involved in the aging process is not well understood. A series of related strains of SAM mice, a murine model for accelerated senescence, shows strain-unique age-related diseases, such as amyloidosis, and deficit in learning and memory, while many of these disease-prone mouse (SAMP) strains have impaired immune activity as young adults, and have a short life span. Using SAM mice, we investigated a possible causal relationships among the following three parameters, i.e., age-related decline of immune activity, generation of senile amyloidosis on the genetical basis of Apoa2c gene, which is a pathogenic key factor of senile amyloidosis, and shortened life span, all of which could be epigenetically modulated, or ameliorated such by immunologically clean environment and dietary conditions. Hybrids between original parental strain of SAMPI and BIO.BR,as a normal ordinary strain of mice, were analyzed. High autoantibody titer to DNA,which is accompanied with lower activity of the delayd-type hyper-sensitivity but not with the degree of the antibody response to conventional antigens, may be prospective for short life span caused by senile amyloidosis, especially in the Apoa2c homozygous, immune dysfunction being closely related to the senile amyloidogenesis in SAM mice.