ABSTRACT
In mouse strains with the amyloidogenic apolipoprotein A-II (apoA-II) gene, which codes the type C apoA-II protein, apoA-II polymerize to form amyloid fibrils; AApoAII. Sonicated amyloid samples were injected immediately into tail vain to induce AApoAII amyloidosis. The intensity of AApoAII amyloid deposition was determined semiquantatively using amyloid index (AI). AI was determined to represent the mean value of the scores of amyloid deposition graded 0 to 4 in the seven major tissues stained with Congo red. Significant differences in the values of AI among the various groups of mice were examined with Mann-Whitney’s U-test. Amyloid deposition was significantly accelerated in offspring of amyloidosis-induced mothers. Initial amyloid deposition was found in the intestine of offspring. Acceleration of amyloidosis can be seen only in the offspring that were nursed by amyloidosis-induced mice. The chapter argues that mouse AApoAII amyloidosis may propose a general mechanism which explains the onset, progress and prevention of various amyloidosis.
