FEBS Letters
Volume 583, Issue 16 , Pages 2685-2690, 20 August 2009

Serum amyloid A and protein AA: Molecular mechanisms of a transmissible amyloidosis

Edited by Peter Brzezinski

To the memory of D. Carleton Gajdusek (1923–2008).

  • Gunilla T. Westermark

      Affiliations

    • Division of Cell Biology, Diabetes Research Centre, Department of Clinical and Experimental Medicine, Linköping University, 58185 Linköping, Sweden
    • Department of Medical Cell Biology, Uppsala University, 75123 Uppsala, Sweden
  • ,
  • Per Westermark

      Affiliations

    • Department of Genetics and Pathology, Rudbeck Laboratory, Uppsala University, SE-75185 Uppsala, Sweden
    • Corresponding Author InformationCorresponding author. Fax: +46 18 552739.

Received 19 March 2009; received in revised form 15 April 2009; accepted 16 April 2009. published online 23 April 2009.

Abstract 

Systemic AA-amyloidosis is a complication of chronic inflammatory diseases and the fibril protein AA derives from the acute phase reactant serum AA. AA-amyloidosis can be induced in mice by an inflammatory challenge. The lag phase before amyloid develops can be dramatically shortened by administration of a small amount of amyloid fibrils. Systemic AA-amyloidosis is transmissible in mice and may be so in humans. Since transmission can cross species barriers it is possible that AA-amyloidosis can be induced by amyloid in food, e.g. foie gras. In mice, development of AA-amyloidosis can also be accelerated by other components with amyloid-like properties. A new possible risk factor may appear with synthetically made fibrils from short peptides, constructed for tissue repair.

Keywords: Amyloid, Fibril, Prion, Transmission, Seeding

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PII: S0014-5793(09)00310-X

doi:10.1016/j.febslet.2009.04.026

FEBS Letters
Volume 583, Issue 16 , Pages 2685-2690, 20 August 2009