Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2008-10-7
pubmed:abstractText
Inflammation has been shown to play an important role in the progression of Alzheimer's disease (AD). Recent epidemical study indicates that the incidence of AD in some populations is substantially influenced by the gene polymorphisms of the inflammation mediators. Meanwhile, an ensured risk factor, the ApoE epsilon4 allele is also reported to directly promote inflammation. Accordingly, it appears that an individual genetic background has partly determined his predisposition for AD by the extent of the inflammation response to the chronic stimulus by beta-amyloid peptide (Abeta) deposits and other antigen stressor in the elderly. Hence we present a hypothesis that the inflammation genotypes may contribute to AD susceptibility. This may provide a new orientation both for future identification of individuals at risk and for personalized medication.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1673-7067
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
314-22
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Genetic predisposition to inflammation: a new risk factor of Alzheimer's disease.
pubmed:affiliation
Department of Neurology/Neuroscience Institute, Ruijin Hospital affiliated to Shanghai Jiaotong University School of Medicine, Shanghai 200025, China.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't