Amyloid resistance in A/J mice is not determined by genetic variants at, or close to, the serum amyloid P component locus.

An experimental model to assess the utility of variants of the serum amyloid P component (SAP) gene in predicting resistance to amyloidosis resulting from chronic inflammation was developed. F2 mice were generated from amyloid resistant (A/J) and amyloid susceptible (C57BL/6J) progenitor strains. Mice were injected daily with azocasein for 30 days, a treatment protocol determined to produce little amyloid deposition in the A/J progenitor strain and substantial amyloid deposition in the C57BL/6J progenitor strain. In a blind study the F2 spleens were subjectively scored for amyloid deposition and DNA was isolated from F2 livers and subjected to Southern blot analysis to determine the inheritance of progenitor strain specific SAP restriction fragment length polymorphisms (RFLPs). No correlation between relative amyloid resistance and SAP genotype was observed, indicating that SAP RFLPs have no value in predicting predisposition to amyloid disease in the mouse model studied.