Source:http://linkedlifedata.com/resource/pubmed/id/15265595
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2004-7-21
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pubmed:abstractText |
Abeta peptides are naturally occurring peptides, which are thought to play a key role in the pathophysiology of Alzheimer's disease (AD). In AD cases, levels of soluble and insoluble Abeta peptides increase in the brain as well as in the cerebrovasculature, a phenomenon that does not occur in extra-cranial vessels. There are frequently anomalies in the cerebrovasculature in AD, and despite increases in several pro-angiogenic factors in AD brain, evidence for increased vascularity is lacking; in fact there is evidence to the contrary. It has also been recently shown that Abeta peptides may have profound anti-angiogenic effects in vitro and in vivo. We therefore investigated whether there is evidence for altered angiogenesis in the vasculature in a transgenic mouse model of Abeta amyloidosis (Tg APPsw line 2576). In vitro, the formation of capillary-like structures on a reconstituted extracellular matrix by endothelial cells isolated from Tg APPsw is impaired. Ex vivo, the sprouting of new capillaries from arterial explants (over expressing Abeta) isolated from 9-month-old Tg APPsw is reduced compared to arterial explants isolated from control littermates. In addition, Tg APPsw mice show a reduction in vascular density in the cortex and hippocampus compared to control littermates. Altogether, our data suggest that the over expression of APPsw in the vasculature may oppose angiogenesis.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Amyloid beta-Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/Collagen,
http://linkedlifedata.com/resource/pubmed/chemical/Drug Combinations,
http://linkedlifedata.com/resource/pubmed/chemical/Laminin,
http://linkedlifedata.com/resource/pubmed/chemical/Proteoglycans,
http://linkedlifedata.com/resource/pubmed/chemical/matrigel
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0304-3940
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
5
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pubmed:volume |
366
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
80-5
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:15265595-Aging,
pubmed-meshheading:15265595-Amyloid beta-Peptides,
pubmed-meshheading:15265595-Amyloidosis,
pubmed-meshheading:15265595-Animals,
pubmed-meshheading:15265595-Aorta,
pubmed-meshheading:15265595-Brain,
pubmed-meshheading:15265595-Cerebral Cortex,
pubmed-meshheading:15265595-Collagen,
pubmed-meshheading:15265595-Drug Combinations,
pubmed-meshheading:15265595-Endothelial Cells,
pubmed-meshheading:15265595-Hippocampus,
pubmed-meshheading:15265595-Laminin,
pubmed-meshheading:15265595-Mice,
pubmed-meshheading:15265595-Mice, Transgenic,
pubmed-meshheading:15265595-Microcirculation,
pubmed-meshheading:15265595-Neovascularization, Pathologic,
pubmed-meshheading:15265595-Proteoglycans,
pubmed-meshheading:15265595-Venae Cavae
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pubmed:year |
2004
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pubmed:articleTitle |
Impaired angiogenesis in a transgenic mouse model of cerebral amyloidosis.
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pubmed:affiliation |
The Roskamp Institute, 2040 Whitfield Avenue, Sarasota, FL 34243, USA. dparis@rdfn.org
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pubmed:publicationType |
Journal Article,
In Vitro
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