ABSTRACT
Secondary (AA) amyloidosis is a not uncommon complication of chronic inflammatory diseases. AA amyloidosis can be induced in mice provoked by inflammatory challenge. This chapter presents nucleating features of some different naturally occurring amyloid-like protein fibrils in murine model of AA amyloidosis. It suggests that exposure to naturally occurring amyloid-like fibrillary proteins may introduce seeds that can start the nucleation in predisposed individuals, i.e. those with persistent high serum amyloid A production. AA amyloid fibrils and synthetic amyloid-like fibrils were shown to serve as nucleus for fibril formation in experimental AA amyloidosis. The chapter shows that all fibril preparations were sufficient to induce amyloidosis in experimental animals, and thus possessed amyloid enhancing activity. Hypothetically, environmental factors may be important risk factors not only for prion diseases, but also for AA amyloidosis and perhaps even other human amyloid diseases.
