A molecular correlate of clinicopathology in transthyretin amyloidosis

The mechanisms responsible for amyloid deposition at different times and in different organs, even in individuals with the same amyloidogenic mutation, are not known. The demonstration, in hereditary systemic transthyretin Val30Met amyloidosis, that such differences are consistently associated with amyloid fibrils composed of different length transthyretin fragments sheds new light on this question and will open the way to further informative studies. Copyright (C) 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.