Diet, amyloid enhancing factor (AEF) and amyloidogenesis: an hypothesis.

At least two forms of amyloidosis, amyloid A (AA) and prion protein (PrP), can be transmitted by dietary ingestion of an agent(s) present in crude mammalian tissues. Although the incubation time for PrP or scrapie-induced diseases to develop in experimental animals extends over months or years, AA or secondary amyloidosis in mice is inducible within a week. In response to inflammatory stimuli we hypothesize that dietary factor(s) modulate the rate at which beta-pleated sheet fibrils accumulate in most forms of amyloidosis. The critical importance of precursor protein polymorphism, cell surface proteoglycans (PG), lipids and apolipoprotein metabolism has also been addressed in this hypothesis.