The presence of complements in amyloid plaques of Creutzfeldt-Jakob disease and Gerstmann-Straussler-Scheinker disease.
The presence of complements Clq, C4, C3, C3b, C3c and C3d, as well as amyloid P component, in the amyloid plaques of Creutzfeldt-Jakob disease (CJD) and Gerstmann-Straussler-Scheinker disease (GSS) brains was demonstrated by means of immunofluorescent and immunoperoxidase techniques. Positive reaction was not observed in other tissue elements, including the blood vessels. These findings may not be due to an adsorption, but to the immunological binding of complements to the amyloid. Proteins such as scrapie associated fibrils or prion in the brain of patients with "unconventional' slow virus diseases are related to the amyloid plaques. It is conceivable that the complements in amyloid are related to these proteins.
D000686:Amyloidosis / Q000150:complications / Q000276:immunology* / Q000378:metabolism; D003165:Complement System Proteins / Q000378:metabolism*; D007562:Creutzfeldt-Jakob Syndrome / Q000150:complications / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D007120:Immunochemistry; D007729:Kuru / Q000276:immunology / Q000378:metabolism; D000683:Serum Amyloid P-Component / Q000378:metabolism; D012897:Slow Virus Diseases / Q000150:complications / Q000276:immunology* / Q000378:metabolism
D000683:Serum Amyloid P-Component; D003165:Complement System Proteins