Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2004-10-7
pubmed:abstractText
Late-onset Alzheimer's disease (LOAD) is the most common cause of dementia in the elderly. It is a complex and genetically heterogeneous disorder. Epidemiological studies demonstrated that nonsteroidal anti-inflammatory drugs could prevent or delay the onset of LOAD suggesting inflammation may be involved in AD. Tumor necrosis factor (TNF) is a potent immunomodulator and it might increase the production of amyloid beta(Abeta), which makes it an appropriate AD candidate gene. Alpha2 macroglobulin (A2M) is a serum protease inhibitor and a major low-density lipoprotein receptor-related protein (LRP) ligand. It can bind Abeta and mediate its clearance and degradation, suggesting it might be another AD candidate gene. In the present study, we analyzed the a 5 bp Ins/Del polymorphism of A2M gene (A2M-2), TNF alpha-308 A/G polymorphism and apolipoprotein E (APOE) polymorphisms of 67 sporadic late-onset AD patients and 142 normal elderly controls in the Chinese population. Our data showed that the APOE epsilon4 allele frequency in AD was significantly higher than that in the normal controls (chi2 = 11.66, P < 0.01) neither the frequencies of genotypes nor alleles of the TNF alpha-308 A/G and A2M polymorphisms were significantly different between AD and controls,suggesting the two polymorphisms were not risk factors to LOAD in Chinese.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0379-4172
pubmed:author
pubmed:issnType
Print
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Neither the tumor necrosis factor alpha-308 A/G polymorphism nor the alpha2-macroglobulin polymorphism was associated with late-onset Alzheimer's disease in the Chinese population.
pubmed:affiliation
Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't