Source:http://linkedlifedata.com/resource/pubmed/id/16475906
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2006-2-14
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pubmed:abstractText |
The intra vitam diagnosis of different dementias is still based on clinical grounds. So far, no technical investigations have been available to support these diagnoses. For tau protein and beta-amyloid(1-42) in cerebrospinal fluid (CSF), promising results for the diagnosis of Alzheimer's disease (AD) have been reported; however, their differential diagnostic spectrum is limited, as was recently shown for dementia with Lewy bodies (DLB) and for AD. Therefore, further marker proteins have to be established to ameliorate, support, and differentiate these clinical diagnoses. We evaluated beta-amyloid(1-40) and phosphorylated tau protein (181p), in addition to total tau protein and beta-amyloid(1-42), in 20 patients with DLB, 34 AD patients, and 20 non-demented neurological controls (NDCs). All markers could differentiate between the dementia groups (AD, DLB) and the controls. AD and DLB could be differentiated only by levels of total tau protein and by the ratio total tau protein/phosphorylated tau protein. However, values still overlapped markedly. In some cases, tau protein levels in CSF may contribute to the clinical distinction between DLB and AD, but the value of the markers is still limited, especially because of mixed pathology. We conclude that more specific markers have to be established to differentiate between these diseases.
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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/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/amyloid beta-protein (1-40),
http://linkedlifedata.com/resource/pubmed/chemical/amyloid beta-protein (1-42),
http://linkedlifedata.com/resource/pubmed/chemical/tau Proteins
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pubmed:status |
MEDLINE
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pubmed:issn |
1434-6621
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
44
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
192-5
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:16475906-Aged,
pubmed-meshheading:16475906-Aged, 80 and over,
pubmed-meshheading:16475906-Alzheimer Disease,
pubmed-meshheading:16475906-Amyloid beta-Peptides,
pubmed-meshheading:16475906-Dementia,
pubmed-meshheading:16475906-Diagnosis, Differential,
pubmed-meshheading:16475906-Female,
pubmed-meshheading:16475906-Humans,
pubmed-meshheading:16475906-Lewy Body Disease,
pubmed-meshheading:16475906-Male,
pubmed-meshheading:16475906-Middle Aged,
pubmed-meshheading:16475906-Peptide Fragments,
pubmed-meshheading:16475906-Phosphorylation,
pubmed-meshheading:16475906-tau Proteins
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pubmed:year |
2006
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pubmed:articleTitle |
Total tau protein, phosphorylated tau (181p) protein, beta-amyloid(1-42), and beta-amyloid(1-40) in cerebrospinal fluid of patients with dementia with Lewy bodies.
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pubmed:affiliation |
Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. bmollenhauer@rics.bwh.harvard.edu
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pubmed:publicationType |
Journal Article
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