Linked Life Data

9273460

Source:http://linkedlifedata.com/resource/pubmed/id/9273460

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1997-8-28
pubmed:abstractText
Since its first description by H.G. Creutzfeldt and A. Jakob, six forms of human spongiform encephalopathies have been described. Besides Creutzfeldt-Jakob disease (CJD), a new variant CJD (nvCJD), Gerstmann-Sträussler-Scheinker syndrome (GSS), fatal familial insomnia (FFI) and potentially familial progressive subcortical gliosis have been reported. The most likely causative agent of these and at least six animal-transmissible spongiform encephalopathies (TSE) is a structurally altered form of a regular cellular protein, designated prion. The best known animal forms are bovine spongiform encephalopathy (BSE) and scrapie. The clinical spectrum of human spongiform encephalopathies has been expanded in recent years by the discovery of new, partially genetically determined forms. The currently available clinical, neurophysiological, neuroradiological, biochemical and molecular-biological methods permit only a probable diagnosis of CJD. A definite diagnosis can only be achieved by the neuropathological demonstration of the pathological prion protein (PrPSc). The transmission of BSE to humans has neither been shown nor definitely excluded.
pubmed:language
ger
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0028-2804
pubmed:author
pubmed:issnType
Print
pubmed:volume
68
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
309-23
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
[Expanded illness spectrum of human spongiform encephalopathies or prion diseases].
pubmed:affiliation
Neurologische Klinik, Marienkrankenhaus, Hamburg.
pubmed:publicationType
Journal Article, English Abstract, Review