Linked Life Data

1472019

Source:http://linkedlifedata.com/resource/pubmed/id/1472019

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1993-1-28
pubmed:abstractText
The cellular pathology of Alzheimer's disease includes an accumulation of microglia surrounding the amyloid plaques. We report that human amyloid beta-protein is chemotactic for murine resident peritoneal macrophages and rat microglia, which may account for the increased density of microglia in plaques. A maximal chemotactic response was observed at 1-10nM, with a 2.5 fold increase in activity over controls for both classes of mononuclear phagocytes. The neurotoxic peptide fragment (25-35) of amyloid beta-protein is similarly chemotactic, while a control scrambled version and the precursor protein are not chemotactic. These results indicate that beta-protein may influence plaque formation via the recruitment of phagocytes, with consequent implications for the future development of treatments for Alzheimer's disease.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
189
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1096-100
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
The amyloid beta-protein of Alzheimer's disease is chemotactic for mononuclear phagocytes.
pubmed:affiliation
Salk Institute for Biological Studies, San Diego, CA 92186-5800.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't