Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2-3
pubmed:dateCreated
1995-1-25
pubmed:abstractText
PrP accumulation in the brains of mice infected with scrapie takes several different forms: amyloid plaques, widespread accumulation in neuropile, and perineuronal deposits. PrP is also sometimes detected within microglia and in or around astrocytes. There are dramatic and reproducible differences between scrapie strains in the relative prominence of these changes and their distribution in the brain. Depending on the scrapie strain, PrP pathology is targeted precisely to particular brain areas, often showing a clear association with identifiable groups of neurons. These results suggest that PrP changes are primarily associated with neurons, and that different scrapie strains recognize and selectively replicate in different populations of neurons. Immunostaining at the ultrastructural level demonstrates an association of PrP with neurite plasmalemma, around amyloid plaques, and in areas of widespread neuropile and perineuronal accumulation. It is probable that PrP is encoded by the Sinc gene, which controls the incubation period of scrapie in mice. Studies using the intraocular infection route show that the Sinc gene controls the onset rather than the rate of replication, suggesting that PrP may be involved in cell-to-cell spread of infection. The accumulation of PrP at the surface of neurons is consistent with such a role.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0893-7648
pubmed:author
pubmed:issnType
Print
pubmed:volume
8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
105-12
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:articleTitle
PrP in pathology and pathogenesis in scrapie-infected mice.
pubmed:affiliation
IAH AFRC & MRC Neuropathogenesis Unit, Edinburgh, UK.
pubmed:publicationType
Journal Article