Abstract
SAMP1 mice show impaired immune activity as young adults and suffer from senile amyloidosis due to Apoa2 gene expression at around a year of age, and this factor may be responsible for their short life. To examine the relationship between low immune activity, senile amyloidosis and a shortened life span, we investigated hybrid mice from original parental strains of SAMP1 ( Apoa2c) and B10.BR ( Apoa2a), an ordinary strain of mice. Our results show that more than 90% of Apoa2c-homozygous siblings had shortened life spans with either low or high immune activity in equal proportions. Thus, the development of senile amyloidosis may directly cause the shorter life span, while low immune activity does not seem to correlate with a shorter life span. Siblings with both the Apoa2 gene of a/c heterozygous type and high immune activity showed a wide distribution in length of life. Among those who died early there was a heavy deposit of inflammatory amyloyd A-protein (AA)- but not any deposits of AApoAII senile amyloid. It is interesting that 2 out of 24 mice homozygous for Apoa2c displayed relatively long life spans, even though they showed heavy deposition of AApoAII and that these two were found to have low autoimmune antibodies. This means that age-related pathogenesis and life span could be delayed and controlled by some factors other than senile amyloidogenesis.
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