Linked Life Data

11124423

Source:http://linkedlifedata.com/resource/pubmed/id/11124423

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2001-2-9
pubmed:abstractText
Immunocytochemical studies of postmortem human tissue have shown that the neurons at risk for degeneration in Alzheimer's are marked by the ectopic expression of several cell cycle components. The current work investigates the roles that beta-amyloid activated microglia might play in leading neurons to re-express cell cycle components. Stable cultures of E16.5 mouse cortical neurons were exposed to beta-amyloid alone, microglial cells alone, or microglial cells activated by beta-amyloid. Increased cell death was found in response to each of these treatments, however, only the amyloid activated microglial treatment increased the number of neurons that were positive for cell cycle markers such as PCNA or cyclin D and incorporation of BrdU. Double labeling with BrdU and TUNEL techniques verified that the 'dividing' neurons were dying, most likely through an apoptotic mechanism. The identity of the soluble factor(s) elaborated by the microglia remains unknown, but FGF2, a suspected neuronal mitogen, was ruled out. These results further support a model in which microglial activation by beta-amyloid is a key event in the progression in Alzheimer's disease.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0197-4580
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
797-806
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:articleTitle
Beta-amyloid activated microglia induce cell cycling and cell death in cultured cortical neurons.
pubmed:affiliation
Alzheimer Research Laboratory, University Hospitals of Cleveland, Case Western Reserve University, School of Medicine, 10900 Euclid Avenue, Cleveland, OH 44106, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't