71 research outputs found

    Tau protein, A beta 42 and S-100B protein in cerebrospinal fluid of patients with dementia with Lewy bodies

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    The intra vitam diagnosis of dementia with Lewy bodies (DLB) is still based on clinical grounds. So far no technical investigations have been available to support this diagnosis. As for tau protein and beta-amyloid((1-42)) (Abeta42), promising results for the diagnosis of Alzheimer's disease ( AD) have been reported; we evaluated these markers and S-100B protein in cerebrospinal fluid (CSF), using a set of commercially available assays, of 71 patients with DLB, 67 patients with AD and 41 nondemented controls (NDC) for their differential diagnostic relevance. Patients with DLB showed significantly lower tau protein values compared to AD but with a high overlap of values. More prominent differences were observed in the comparison of DLB patients with all three clinical core features and AD patients. Abeta42 levels were decreased in the DLB and AD groups versus NDC, without significant subgroup differences. S-100B levels were not significantly different between the groups. 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 due to mixed pathology. We conclude that more specific markers have to be established for the differentiation of these diseases. Copyright (C) 2005 S. Karger AG, Basel

    Insight of brain degenerative protein modifications in the pathology of neurodegeneration and dementia by proteomic profiling

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    Vom Kinderspielnamen zum Adverb

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    Quantification of amyloid-beta 40 in cerebrospinal fluid

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    Background: Truncated forms and full-length forms of the amyloid-beta 40 (Aβ40) are key molecules in the pathogenesis of dementia, and are detectable in CSF. Reliable methods to detect these biomarkers in CSF are of great importance for understanding the disease mechanisms and for diagnostic purposes. Methods: VU-α-Aβ40, a monoclonal antibody (mAb) specifically detecting Aβ40, was generated and characterized by solid and fluid phase ELISA, surface plasmon resonance spectroscopy (SPRS), immunoprecipitation (IP), immunohistochemical and Western blot (WB) analysis. In addition, an ELISA with VU-α-Aβ40 as catching and 6E10 as detecting mAbs was set up and validated. This ELISA was used to measure Aβ40 in CSF of controls (N = 27), patients with Alzheimer's disease (AD; N = 20), frontotemporal lobe dementia (FTLD; N = 14), noninflammatory (N = 15) and inflammatory (N = 15) neurological conditions. Results: VU-α-Aβ40 specifically recognizes Aβ40 with high affinity (
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