A molecule which can stop the formation of long protein strands, known as amyloid fibrils, that cause joint pain in kidney dialysis patients has been identified by researchers at the University of Leeds. The discovery could lead to new methods to identify drugs to prevent, treat or halt the progression of other conditions in which amyloid fibrils play a part, including Alzheimer's, Parkinson's and type II diabetes. The research, funded by the Biotechnology and Biological Sciences Research Council and the Wellcome Trust, is published August 28 in Nature Chemical Biology. The team -- from Leeds' Astbury Centre for Structural Molecular Biology and Faculty of Biological Sciences -- found that an antibiotic known as Rifamycin SV was able to prevent the protein β2microglobulin (β2m) from forming into fibrils. β2m is known to accumulate in renal dialysis patients and forms fibrils within the joints, causing extreme pain and arthritis. By using a specialised analytical technique ...