| pubmed-article:17132972 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17132972 | lifeskim:mentions | umls-concept:C0085220 | lld:lifeskim |
| pubmed-article:17132972 | lifeskim:mentions | umls-concept:C0282460 | lld:lifeskim |
| pubmed-article:17132972 | lifeskim:mentions | umls-concept:C0062961 | lld:lifeskim |
| pubmed-article:17132972 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:17132972 | pubmed:dateCreated | 2006-11-29 | lld:pubmed |
| pubmed-article:17132972 | pubmed:abstractText | No treatments have been identified to lower the risk of intracerebral hemorrhage due to cerebral amyloid angiopathy (CAA). A potential approach to prevention is the use of agents that interfere with the pathogenic cascade initiated by the beta-amyloid peptide (Abeta). Tramiprosate (3-amino-1-propanesulfonic acid) is a candidate molecule shown in preclinical studies to reduce CAA in a transgenic mouse model. | lld:pubmed |
| pubmed-article:17132972 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17132972 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17132972 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17132972 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17132972 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17132972 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17132972 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17132972 | pubmed:issn | 0893-0341 | lld:pubmed |
| pubmed-article:17132972 | pubmed:author | pubmed-author:FitzsimmonsBr... | lld:pubmed |
| pubmed-article:17132972 | pubmed:author | pubmed-author:GreenbergStev... | lld:pubmed |
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| pubmed-article:17132972 | pubmed:author | pubmed-author:SmithEric EEE | lld:pubmed |
| pubmed-article:17132972 | pubmed:author | pubmed-author:RovnerBarryB | lld:pubmed |
| pubmed-article:17132972 | pubmed:author | pubmed-author:LaurinJulieJ | lld:pubmed |
| pubmed-article:17132972 | pubmed:author | pubmed-author:Creed... | lld:pubmed |
| pubmed-article:17132972 | pubmed:author | pubmed-author:Edip GurolMM | lld:pubmed |
| pubmed-article:17132972 | pubmed:author | pubmed-author:SchwabKristin... | lld:pubmed |
| pubmed-article:17132972 | pubmed:author | pubmed-author:GarceauDenisD | lld:pubmed |
| pubmed-article:17132972 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17132972 | pubmed:volume | 20 | lld:pubmed |
| pubmed-article:17132972 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17132972 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17132972 | pubmed:pagination | 269-74 | lld:pubmed |
| pubmed-article:17132972 | pubmed:dateRevised | 2011-9-22 | lld:pubmed |
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| pubmed-article:17132972 | pubmed:articleTitle | A phase 2 study of tramiprosate for cerebral amyloid angiopathy. | lld:pubmed |
| pubmed-article:17132972 | pubmed:affiliation | Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. sgreenberg@partners.org | lld:pubmed |
| pubmed-article:17132972 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17132972 | pubmed:publicationType | Randomized Controlled Trial | lld:pubmed |
| pubmed-article:17132972 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:17132972 | pubmed:publicationType | Multicenter Study | lld:pubmed |
| pubmed-article:17132972 | pubmed:publicationType | Clinical Trial, Phase II | lld:pubmed |
| pubmed-article:17132972 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:17132972 | lld:pubmed |
