NeurochemistryATP-promoted amyloidosis of an amyloid β peptideExley, Christopher1 Author Information 1Birchall Centre for Inorganic Chemistry and Materials Science, Department of Chemistry, Keele University, Staffordshire ST5 5BG, UK ACKNOWLEDGEMENTS: C.E. is a Royal Society University Research Fellow. Website publication 3 October 1997 Received 15 July 1997; accepted 8 August 1997 NeuroReport: October 20, 1997 - Volume 8 - Issue 15 - p 3411-3414 Buy 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. © Lippincott-Raven Publishers.