Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2009-4-16
pubmed:abstractText
Amyloid beta peptide (Abeta) accumulation is the major event in the brain of cases with Alzheimer's disease (AD). The serine protease plasmin, which is generated from the inactive zymogen plasminogen, could accelerate Abeta degradation, and thus may play a role in AD pathogenesis. It has been reported that the increasing of plasminogen activator inhibitor-1 (PAI-1) inhibits the activity of plasminogen activator and thus reduces the generation of plasmin in vivo. For seeking the correlation of the PAI-1 promoter with sporadic AD (SAD), we performed a case-control study in a group of Chinese Han population. In the study, we detected two polymorphisms, a G/A single base substitution polymorphism at -844bp (rs2227631) and a single guanosine deletion/insertion 4G/5G polymorphism at -675bp (rs1799889) upstream from the start of transcription. Direct sequencing was used for genotyping in 324 SAD patients and 278 controls. We failed to find any associations between these two polymorphisms and SAD even after stratified by age of onset, gender and apolipoprotein E (APOE) epsilon4 status. Our data do not support that there is an association between the PAI-1 promoter polymorphisms and SAD in the Chinese Han population.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1872-7972
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
455
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
97-100
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
No association between the promoter polymorphisms of PAI-1 gene and sporadic Alzheimer's disease in Chinese Han population.
pubmed:affiliation
Department of Neurology, Xuan Wu Hospital of the Capital Medical University, Beijing 100053, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't