Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1992-7-24
pubmed:abstractText
The effects of a synthetic homolog of beta-amyloid (beta 1-42) on the secretion of interleukin-1 (IL-1) and basic fibroblast growth factor (bFGF) from cultures of microglia and astrocytes, cells that surround beta-amyloid-containing plaques in Alzheimer's disease, were examined. Our results show that beta-amyloid not only enhances glial cell secretion of these factors, it stimulates the proliferation and morphological transformation of microglia. Since IL-1 and bFGF are known to elevate the synthesis of the beta-amyloid precursor protein and other plaque components, it is suggested that in this way, cascades may arise that contribute to the process of plaque development.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
8
pubmed:volume
569
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
141-5
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Beta-amyloid stimulates glial cells in vitro to produce growth factors that accumulate in senile plaques in Alzheimer's disease.
pubmed:affiliation
Department of Psychobiology, University of California, Irvine 92717.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't