Linked Life Data

16171999

Source:http://linkedlifedata.com/resource/pubmed/id/16171999

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-2-28
pubmed:abstractText
The epsilon4 allele of apolipoprotein (apo)E associates with an increased risk of developing Alzheimer's disease (AD) as well as an earlier age of onset. However, the exact mechanisms by which apoE4 confers such susceptibility is currently unknown. We used a human apoE targeted replacement (hE-TR) mouse model to investigate the allele-specific response to entorhinal cortex lesion (ECL). We observed a marked impairment in reactive sprouting in hE4 mice compared to hE3 mice. ApoE expression was similar between genotypes at days post-lesion (DPL) 2 and 14. Thirty days post-lesion, hE4 mice had more reactive astrocytes as well as a defective outward migration pattern of the astrocytes in the dentate gyrus. The expression of the anti-inflammatory cytokine IL-1ra was delayed in hE4 mice compared to hE3 mice. ApoE and beta-amyloid (Abeta) 1-40 accumulated at 30 DPL in hE4 mice. These results suggest that the presence of apoE4 delays the astroglial repair process and indirectly compromises synaptic remodeling.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0969-9961
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
505-14
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
A deficit in astroglial organization causes the impaired reactive sprouting in human apolipoprotein E4 targeted replacement mice.
pubmed:affiliation
Department of Neurology and Neurosurgery, McGill University, Montreal, Quebec, Canada H4A 2B4.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural