Congophilia in cerebral amyloidosis is modified by inactivation procedures on slow transmissible pathogens.
Cerebral tissues with amyloid deposits were treated by various chemicals which inactivated the agent of subacute spongiform encephalopathy (SSE). We discovered Congophilia in the amyloid plaques in cases of Creutzfeldt-Jakob disease (CJD) and Gerstmann-Sträussler syndrome (GSS) correlated to the chemical inactivation profiles of SSE. After incubation with trichloroacetate, guanidine-SCN, guanidine-HCl, formic acid, phenol and autoclaving, amyloid plaques in unfixed frozen sections of human brains with CJD or GSS, lost the affinity of Congo red and green birefringence under polarized light. In formalin-fixed, paraffin-embedded tissue sections, amyloid plaques of CJD and GSS lost the affinity of Congo red after most of these treatments. On the other hand, senile plaques in the aged, patients with Alzheimer's disease and with senile dementia of the Alzheimer type did not lose the affinity of Congo red after most of these treatments. Therefore, the amyloid deposits in the amyloid plaques differ from those in senile plaques. The methods we used facilitate differentiation of amyloid and senile plaques in formalin-fixed, paraffin-embedded tissues.
D000544:Alzheimer Disease / Q000382:microbiology; D000682:Amyloid / Q000378:metabolism*; D000686:Amyloidosis / Q000382:microbiology*; D001921:Brain / Q000382:microbiology*; D001927:Brain Diseases / Q000382:microbiology*; D003224:Congo Red; D007562:Creutzfeldt-Jakob Syndrome / Q000382:microbiology; D003704:Dementia / Q000382:microbiology; D006801:Humans; D011328:Prions / Q000502:physiology*; D013194:Staining and Labeling
D000682:Amyloid; D011328:Prions; D003224:Congo Red