PMID: 9422374Jan 9, 1998Paper

Congo red inhibits proteoglycan and serum amyloid P binding to amyloid beta fibrils

Journal of Neurochemistry
R Gupta-Bansal, K R Brunden

Abstract

Various data suggest that Alzheimer's disease results from the accumulation of amyloid beta (A beta) peptide fibrils and the consequent formation of senile plaques in the cognitive regions of the brain. One approach to lowering senile plaque burden in Alzheimer's disease brain is to identify compounds that will increase the degradation of existing amyloid fibrils. Previous studies have shown that proteoglycans and serum amyloid P (SAP), molecules that localize to senile plaques, bind to A beta fibrils and protect the amyloid peptide from proteolytic breakdown. Therefore, molecules that prevent the binding of SAP and/or proteoglycans to fibrillar A beta might increase plaque degradation and prove useful in the treatment of Alzheimer's disease. The nature of SAP and proteoglycan binding to A beta is defined further in the present study. SAP binds to both fibrillar and nonfibrillar forms of A beta. However, only the former is rendered resistant to proteolysis after SAP association. It is interesting that both SAP and proteoglycan binding to A beta fibrils can be inhibited by glycosaminoglycans and Congo red. Unexpectedly, Congo red protects fibrillar A beta from breakdown, suggesting that this compound and other structurally relat...Continue Reading

Citations

Jul 6, 2002·Anais Da Academia Brasileira De Ciências·Fernanda G Defelice, Sergio T Ferreira
Mar 4, 2005·American Journal of Physiology. Cell Physiology·Ranjit K GiriVijay K Kalra
Aug 27, 2015·PloS One·Sanjai Kumar PachaharaRamakrishnan Nagaraj
May 13, 2003·Chembiochem : a European Journal of Chemical Biology·Boris Schmidt
Dec 3, 2013·European Journal of Microbiology & Immunology·Szilvia VeszelkaZoltán Urbányi
Mar 17, 2005·Neurochemistry International·Zoltán UrbányiTamás Pázmány
Sep 9, 2006·Brain Research Reviews·Petrea FridNatalija Popovic

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