[Mechanism of accumulation of prion amyloid in the CNS in experimental amyotrophic leukospongiosis].
The mechanism of accumulation of prion amyloid in guinea pig CNS in experimental slow virus disease--amyotrophic leuco-spongiosis (AL) was studied. The complex histochemical, immuno-cytochemical and ultrastructural studies revealed specific amyloid deposits in a few brain capillaries and in most of pia matter vessels. Taking into account the high AL agent titer in spleen throughout the disease period, conclusion was drawn of entering AL agent in CNS through blood-liquor barrier and blood-brain barrier. It was supposed that primary immune system damaging took place in AL pathogenesis.
Poleshchuk
N N
NN
Votiakov
V I
VI
Il'kevich
Iu G
IuG
Dubovskaia
G P
GP
Kolomiets
N D
ND
D000682:Amyloid / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000382:microbiology / Q000648:ultrastructure; D001927:Brain Diseases / Q000378:metabolism* / Q000382:microbiology; D006168:Guinea Pigs; D006651:Histocytochemistry; D007150:Immunohistochemistry; D010841:Pia Mater / Q000378:metabolism* / Q000382:microbiology / Q000648:ultrastructure; D011328:Prions; D012897:Slow Virus Diseases / Q000378:metabolism* / Q000382:microbiology
D000682:Amyloid; D011328:Prions
K mekhanizmu nakopleniia prionovogo amiloida v TsNS pri éksperimental'nom amiotroficheskom leĭkospongioze.