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ATP-promoted amyloidosis of an amyloid β peptide

Exley, Christopher1

Neurochemistry

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.

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

© Lippincott-Raven Publishers.