Hidden amyloidoses.
The pathogenesis as well as the genetic disposition to develop clinical symptoms in transmissible spongiform encephalopathies (e.g. Creutzfeldt-Jakob disease, scrapie, bovine spongiform encephalopathy) relate these diseases to classical noninfectious amyloidoses (familial amyloidotic polyneuropathy as an example) and to Alzheimer's disease. This is not obvious to the nonexpert at first glance. This communication tries to elucidate this association, to reveal which immunochemical techniques have contributed their share.
Diringer
H
H
Robert-Koch-Institut des Bundesgesundheitsamtes, Berlin, FRG.
D000544:Alzheimer Disease / Q000235:genetics / Q000378:metabolism; D016564:Amyloid beta-Protein Precursor / Q000235:genetics; D000686:Amyloidosis / Q000209:etiology / Q000235:genetics / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D000818:Animals; D001921:Brain / Q000473:pathology; D006224:Cricetinae; D006801:Humans; D051379:Mice; D008810:Mice, Inbred C57BL / Q000235:genetics; D008954:Models, Biological; D009154:Mutation; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism; D018622:PrP 27-30 Protein; D011228:Prealbumin / Q000235:genetics / Q000378:metabolism; D017096:Prion Diseases / Q000235:genetics / Q000382:microbiology / Q000473:pathology / Q000635:transmission; D012756:Sheep
D016564:Amyloid beta-Protein Precursor; D009419:Nerve Tissue Proteins; D011228:Prealbumin; D018622:PrP 27-30 Protein