NR ADLA
AU Diringer,H.
TI Hidden amyloidoses
QU Experimental and Clinical Immunogenetics 1992; 9(4): 212-29
PT journal article; review; review, academic
AB 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.
ZR 111
MH Alzheimer Disease/genetics/metabolism; Amyloid beta-Protein Precursor/genetics; *Amyloidosis/etiology/genetics/immunology/metabolism/pathology; Animal; Brain/pathology; Hamsters; Human; Mice; Mice, Inbred C57BL/genetics; Models, Biological; Mutation; Nerve Tissue Proteins/genetics/metabolism; PrP 27-30 Protein; Prealbumin/genetics/metabolism; Prion Diseases/genetics/microbiology/pathology/transmission; Sheep; Support, Non-U.S. Gov't
AD H. Diringer, Robert Koch-Institut des Bundesgesundheitsamtes, Nordufer 20, D-13353 Berlin, Germany.
SP englisch
PO Schweiz
OR Prion-Krankheiten D