pubmed-article:18436874 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18436874 | lifeskim:mentions | umls-concept:C0040300 | lld:lifeskim |
pubmed-article:18436874 | lifeskim:mentions | umls-concept:C0085220 | lld:lifeskim |
pubmed-article:18436874 | lifeskim:mentions | umls-concept:C0338656 | lld:lifeskim |
pubmed-article:18436874 | lifeskim:mentions | umls-concept:C0332281 | lld:lifeskim |
pubmed-article:18436874 | lifeskim:mentions | umls-concept:C0392747 | lld:lifeskim |
pubmed-article:18436874 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:18436874 | pubmed:dateCreated | 2008-6-24 | lld:pubmed |
pubmed-article:18436874 | pubmed:abstractText | Cerebral amyloid angiopathy (CAA) is a major cause of lobar intracerebral hemorrhage and cognitive impairment and is associated with white matter hyperintensities and cerebral microbleeds. MRI diffusion tensor imaging detects microstructural tissue damage in advanced CAA even in areas that appear normal on conventional MRI. We hypothesized that higher global mean apparent diffusion coefficient (mean ADC), reflecting a higher amount of chronic tissue disruption caused by CAA, would be independently associated with CAA-related cognitive impairment. | lld:pubmed |
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pubmed-article:18436874 | pubmed:language | eng | lld:pubmed |
pubmed-article:18436874 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18436874 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:18436874 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18436874 | pubmed:month | Jul | lld:pubmed |
pubmed-article:18436874 | pubmed:issn | 1524-4628 | lld:pubmed |
pubmed-article:18436874 | pubmed:author | pubmed-author:GreenbergStev... | lld:pubmed |
pubmed-article:18436874 | pubmed:author | pubmed-author:PatelPratikP | lld:pubmed |
pubmed-article:18436874 | pubmed:author | pubmed-author:RosandJonatha... | lld:pubmed |
pubmed-article:18436874 | pubmed:author | pubmed-author:ChabriatHugue... | lld:pubmed |
pubmed-article:18436874 | pubmed:author | pubmed-author:SmithEric EEE | lld:pubmed |
pubmed-article:18436874 | pubmed:author | pubmed-author:RahmanRosanna... | lld:pubmed |
pubmed-article:18436874 | pubmed:author | pubmed-author:ViswanathanAn... | lld:pubmed |
pubmed-article:18436874 | pubmed:author | pubmed-author:NandigamR N... | lld:pubmed |
pubmed-article:18436874 | pubmed:author | pubmed-author:KinnecomCathe... | lld:pubmed |
pubmed-article:18436874 | pubmed:author | pubmed-author:BracoudLucL | lld:pubmed |
pubmed-article:18436874 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:18436874 | pubmed:volume | 39 | lld:pubmed |
pubmed-article:18436874 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18436874 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18436874 | pubmed:pagination | 1988-92 | lld:pubmed |
pubmed-article:18436874 | pubmed:dateRevised | 2011-5-9 | lld:pubmed |
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pubmed-article:18436874 | pubmed:meshHeading | pubmed-meshheading:18436874... | lld:pubmed |
pubmed-article:18436874 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:18436874 | pubmed:articleTitle | Tissue microstructural changes are independently associated with cognitive impairment in cerebral amyloid angiopathy. | lld:pubmed |
pubmed-article:18436874 | pubmed:affiliation | Hemorrhagic Stroke Research Program, Massachusetts General Hospital, Stroke Research Center, 175 Cambridge Street, Suite 300, Boston, MA 02114, USA. aviswanathan1@partners.org | lld:pubmed |
pubmed-article:18436874 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:18436874 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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