Xth International Symposium on Amyloid and Amyloidosis April 18-22, 2004 (Selected Highlights) Tours, Loire Valley, France

Abstract

T he Xth International Amyloid Symposium, organized by Gilles Grateau together with local and international committees, was held at the Vinci Conference Center in Tours, France, April 18–22, 2004. The Symposium considered advances in knowledge of amyloid protein structure, disease pathogenesis, new fibril-forming proteins and a number of approaches to therapy, some at the bench and some that are showing efficacy in ongoing clinical trials. A hotly debated topic was whether the deposited amyloid fibrils themselves cause organ and tissue damage, or are inert byproducts of toxic transient intermediates in the protein refolding and self assembly pathway that leads to amyloid fibril formation. This led to the question as to whether treatments that block fibrillogenesis or dissolve fibrils might increase the levels of toxic oligomeric intermediates. Particularly well received were the Monday and Tuesday afternoon workshops. On each of the afternoons there were two concurrent workshops on diagnosis and typing of amyloidosis and clinical management of patients. The need for better standardized reagents and methodology was voiced throughout these workshops, and there was the feeling that publication of workshop summaries could be a valuable feature of future Symposia. The Symposium was launched with a Sunday evening dinner buffet following the satellite meeting sponsored by Neurochem Inc. ‘Emerging clinical practices in AA amyloidosis’ – chaired by H Filit, B Hazenberg, J Kelly, G Merlini, P Hawkins, and M Skinner reported that, in developed countries, inflammatory conditions most often underlie amyloid A (AA) amyloidosis. The incidence of AA amyloidosis in these countries appears to be declining, perhaps due to the development of new antiinflammatory treatments such as tumor necrosis factor (TNF) receptor antagonists. Nonetheless, in as many as 10% of patients, the etiology of AA amyloidosis cannot be identified. In developing countries, infectious diseases remain the major predisposing condition. There was the opinion that AA amyloidosis may be underdiagnosed, and the importance of ruling out AL and ATTR was stressed. Strategies for treatment include inhibition of serum