Linked Life Data

20940625

Source:http://linkedlifedata.com/resource/pubmed/id/20940625

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2010-10-27
pubmed:abstractText
Cerebral amyloid angiopathy (CAA) affects brain parenchymal and leptomeningeal arteries and arterioles but sometimes involves capillaries (capCAA) with spread of the amyloid into the surrounding neuropil, that is, dyshoric changes. We determined the relationship between capCAA and larger vessel CAA, ? amyloid (A?) plaques, neurofibrillary changes, inflammation, and apolipoprotein E (APOE) in 22 cases of dyshoric capCAA using immunohistochemistry. The dyshoric changes contained predominantly A?1-40, whereas dense bulblike deposits adjacent to the capillary wall contained mostly A?1-42. There was an inverse local correlation between A? plaque load and capCAA severity (p = 0.01), suggesting that A? transport between the neuropil and the circulation may be mechanistically involved. Deposits of hyperphosphorylated tau and ubiquitin and clusters of activated microglia, resembling the changes around A? plaques, were found around capCAA but were absent around larger vessel CAA. In 14 cases for which APOE genotype was available, there was a high APOE-?4 allele frequency (54%; 43% homozygous). The severity of CapCAA increased with the number of ?4-alleles; and APOE4 seemed to colocalize with capCAA by immunohistochemistry. These results suggest that capCAA is pathologically and possibly pathogenetically distinct from larger vessel CAA, and that it is associated with a high APOE-?4 allele frequency.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-3069
pubmed:author
pubmed:issnType
Print
pubmed:volume
69
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1158-67
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Characteristics of dyshoric capillary cerebral amyloid angiopathy.
pubmed:affiliation
Department of Neurology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. e.richard@amc.uva.nl
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't