ATP-promoted amyloidosis of an amyloid β peptide

Abstract

AMYLOIDOSIS is implicated in the aetiology of a number of disorders of human health. The factors that influence its instigation and subsequent rate of progress are the subject of a considerable research effort. The peptide fragment Aβ(25–35) is amyloidogenic and has proven to be a useful model of the processes involved in amyloidosis. It is demonstrated herein that the assembly of Aβ(25–35) into thioflavin T-reactive fibrils and their subsequent rearrangement into advanced glycation end-products is accelerated by ATP. Aluminium potentiated these effects of ATP, suggesting a possible link with the aetiology of amyloidoses in vivo.