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Amyloid deposition is delayed in mice with targeted deletion of the serum amyloid P component gene

Nature Medicine volume 3, pages 855–859 (1997)Cite this article

Abstract

The tissue amyloid deposits that characterize systemic amyloidosis, Alzheimer's disease and the transmissible spongiform encephalopathies always contain serum amyloid P component (SAP) bound to the amyloid fibrils. We have previously proposed that this normal plasma protein may contribute to amyloidogenesis by stabilizing the deposits. Here we show that the induction of reactive amyloidosis is retarded in mice with targeted deletion of the SAP gene. This first demonstration of the participation of SAP in pathogenesis of amyloidosis in vivo confirms that inhibition of SAP binding to amyloid fibrils is an attractive therapeutic target in a range of serious human diseases.

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Authors and Affiliations

  1. Immunological Medicine Unit, Royal Postgraduate Medical School Hammersmith Hospital, Du Cane Road, London, W12 ONN, UK

    Philip N. Hawkins, Jeff Herbert, Winston L. Hutchinson, Glenys A. Tennent & Mark B. Pepys

  2. Rheumatology Unit, Royal Postgraduate Medical School Hammersmith Hospital, Du Cane Road, London, W12 ONN, UK

    Marina Botto, Maria C.M. Bickerstaff, Anne E. Bygrave & Mark J. Walportz

  3. Radiological Sciences Unit, Royal Postgraduate Medical School Hammersmith Hospital, Du Cane Road, London, W12 ONN, UK

    Alan Mcbride

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Botto, M., Hawkins, P., Bickerstaff, M. et al. Amyloid deposition is delayed in mice with targeted deletion of the serum amyloid P component gene. Nat Med 3, 855–859 (1997). https://doi.org/10.1038/nm0897-855

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