Linked Life Data

9180223

Source:http://linkedlifedata.com/resource/pubmed/id/9180223

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1997-7-21
pubmed:abstractText
In Creutzfeldt-Jakob disease (CJD), a transmissible spongiform encephalopathy, the deposition of the pathological prion protein (PrP-res) in the brain of affected individuals is the key event that triggers the appearance of the disease. Since a polymorphism in the signal peptide of the serine-protease inhibitor alpha1 antichymotrypsin (ACT) is one of the factors that may enhance amyloid formation, we studied this polymorphism in 63 CJD patients and 103 control subjects. No difference in allele frequencies and genotype distribution was found between CJD cases and controls, nor any difference was found between the ACT genotype and the age at onset and disease duration. Interestingly, there was a significantly different (P = 0.04) ACT distribution between CJD patients and controls in apolipoprotein E (ApoE) E4, and the interaction between ACT and ApoE was almost significant (P = 0.053). Further studies on a larger number of patients will clarify whether this association can identify a possible risk factor for CJD.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0304-3940
pubmed:author
pubmed:issnType
Print
pubmed:day
16
pubmed:volume
227
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
140-2
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Alpha1 antichymotrypsin signal peptide polymorphism in sporadic Creutzfeldt-Jakob disease.
pubmed:affiliation
Laboratory of Virology, Istituto Superiore di Sanita, Rome, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't