Ciesielczyk, Barbara

[["dc.bibliographiccitation.firstpage","45"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","European Neurology"],["dc.bibliographiccitation.lastpage","51"],["dc.bibliographiccitation.volume","47"],["dc.contributor.author","Bitsch, Annette"],["dc.contributor.author","Horn, C."],["dc.contributor.author","Kemmling, Y."],["dc.contributor.author","Seipelt, M."],["dc.contributor.author","Hellenbrand, U."],["dc.contributor.author","Stiefel, M."],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Bahn, Erik"],["dc.contributor.author","Ratzka, P."],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T10:33:03Z"],["dc.date.available","2018-11-07T10:33:03Z"],["dc.date.issued","2002"],["dc.description.abstract","Biochemical markers of brain damage, e.g. ischemic stroke, should reflect the volume of irreversibly damaged brain parenchyma and the clinical outcome in a single patient in order to allow estimation of prognosis at an early stage. Tau protein, which derives predominantly from neurons and axons, is elevated in the cerebrospinal fluid of patients with neurodegenerative disease. This makes tau protein a potential marker of neuronal/axonal injury. In order to test this hypothesis, the current study aimed at showing that tau protein is measurable in the blood after acute ischemic stroke and that it correlates with clinical disability and stroke volume. In a longitudinal prospective study we measured tau protein serum levels with an ELISA in 30 patients longitudinally after ischemic stroke. Tau protein was detectable within 5 days after ischemia in the sera of 7/20 patients with MRI-proven infarction and in 2/10 patients with transitory ischemic attack; both of them had a small infarction visible on the MRI scan. Tau protein was measurable within 6 h after symptom onset, peaked after 3-5 days and correlated with infarct volume and disability after 3 months. In conclusion, serum tau protein is a candidate marker of axonal injury. In stroke, its clinical use is limited, because it is detectable only in a proportion of patients. Copyright (C) 2002 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000047946"],["dc.identifier.isi","000173547300008"],["dc.identifier.pmid","11803192"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44511"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","0014-3022"],["dc.title","Serum tau protein level as a marker of axonal damage in acute ischemic stroke"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","164"],["dc.bibliographiccitation.issue","2-3"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","170"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Mollenhauer, B."],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Bibl, M."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Schulz-Schaeffer, W. J."],["dc.contributor.author","Ciesielczyk, B."],["dc.contributor.author","Neumann, M."],["dc.contributor.author","Steinacker, P."],["dc.contributor.author","Kretzschmar, H. A."],["dc.contributor.author","Poser, S."],["dc.contributor.author","Trenkwalder, C."],["dc.contributor.author","Otto, M."],["dc.date.accessioned","2018-11-07T08:37:27Z"],["dc.date.available","2018-11-07T08:37:27Z"],["dc.date.issued","2005"],["dc.description.abstract","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."],["dc.identifier.doi","10.1159/000083178"],["dc.identifier.isi","000226979100018"],["dc.identifier.pmid","15637452"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18536"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation.issn","1420-8008"],["dc.title","Tau protein, A beta 42 and S-100B protein in cerebrospinal fluid of patients with dementia with Lewy bodies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","933"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","948"],["dc.bibliographiccitation.volume","112"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Stiens, G."],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Neubert, K."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T09:19:19Z"],["dc.date.available","2018-11-07T09:19:19Z"],["dc.date.issued","2005"],["dc.description.abstract","Measuring proteins in cerebrospinal fluid (CSF) has gained wide acceptance for the differential diagnosis of dementia. Some groups have already extended these investigations in Alzheimer's disease (AD) by asking how stable these markers are in follow-up analysis, if they depend on the stage of disease and whether they can be used to monitor the progression and biological effects of treatment. We evaluated 21 patients with dementia with Lewy bodies (DLB) and 19 patients with AD, on two occasions, with regard to levels of tau protein, tau protein phosphorylated at threonine 181 (p-tau), A beta 42, A beta 40 and S-100B protein, using a set of commercially available assays. Tau protein levels were lower in DLB in first and second LP compared to AD and decreased during course of both groups. P-tau levels were increased in AD and DLB and decreased during follow-up. A beta 42 and A beta 40 remained relatively stable during follow-up but we found a slight increase of the median A beta 42 level in DLB, whereas in AD, A beta 42 tends to decrease during follow-up. S-100B protein increased during follow-up in both diseases. The protein dynamics in DLB and AD are relatively similar. S-100B protein may be a useful marker for follow-up in neurodegenerative diseases but has to be analysed in longer follow-up periods. Tau protein may be used to differentiate between DLB and AD. Follow-up CSF analyses are of limited value for the differentiation of AD and DLB. We conclude that more specific markers have to be established for the differentiation and follow-up of these diseases."],["dc.identifier.doi","10.1007/s00702-004-0235-7"],["dc.identifier.isi","000229624600008"],["dc.identifier.pmid","15937638"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28602"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","0300-9564"],["dc.title","Follow-up investigations in cerebrospinal fluid of patients with dementia with Lewy bodies and Alzheimer's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","376"],["dc.bibliographiccitation.issue","5-6"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","382"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Wiese, B."],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T08:37:30Z"],["dc.date.available","2018-11-07T08:37:30Z"],["dc.date.issued","2005"],["dc.description.abstract","Background: S-100B and tau protein have a high differential diagnostic potential for the diagnosis of Creutzfeldt-Jakob disease (CJD). So far there has been only limited information available about the dynamics of these parameters in the cerebrospinal fluid (CSF). However, there is a special interest in finding biochemical markers to monitor disease progression for differential diagnosis and treatment. Patients and Methods: We analyzed CSF of 45 patients with CJD and of 45 patients with other neurological diseases for tau protein and S-100B in a follow-up setting. All diagnoses of CJD were later neuropathologically verified. A ratio between tau protein differences and the time between lumbar puncture was calculated. The same was done for S-100B. Results: Tau protein levels of 34 cases were above the cut-off level for CJD (>1,300 pg/ml) in the first CSF sample. In 7 of 11 patients with lower tau levels in the first CSF sample, tau levels rose. The above-mentioned ratio was significantly higher in the CJD group than in the group with other neurological diseases. Similar results were obtained for S-100B. Conclusion: We conclude that follow-up investigations and calculation of ratios is a useful tool in the differential diagnosis of CJD. Variations in this pattern were observed in single cases. Copyright (C) 2005 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000084708"],["dc.identifier.isi","000228848200019"],["dc.identifier.pmid","15802913"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18547"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1420-8008"],["dc.title","Follow-up investigations of tau protein and S-100B levels in cerebrospinal fluid of patients with Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","192"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","197"],["dc.bibliographiccitation.volume","58"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Neumann, Manuela"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Ciesielczyk, B."],["dc.contributor.author","Schulz-Schaeffer, W."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Poser, Sigrid"],["dc.date.accessioned","2017-09-07T11:44:31Z"],["dc.date.available","2017-09-07T11:44:31Z"],["dc.date.issued","2012"],["dc.description.abstract","Background: Diagnosis of Creutzfeldt–Jakob disease (CJD) is made according to the typical clinical picture and can be supported by a positive 14-3-3 CSF immunoblot. Promising results for the diagnostic sensitivity and specificity of tau-protein measurement in CSF already have been described in a smaller group of patients. Both tests in a larger group of patients with the differential diagnosis of CJD were evaluated.Methods: CSF of 297 patients under the differential diagnosis of CJD (109 definite, 55 probable, 39 possible; 85 others, 1 iatrogenic, 8 genetic), 23 nondemented control subjects, and 15 non-CJD patients with positive 14-3-3 immunoblots were analyzed. The 14-3-3 immunoblot bands were semiquantitatively rated as strong, medium, and weak. Tau-protein was analyzed using a commercially available ELISA. In addition, patients were neuropathologically classified according to prion protein type and polymorphism at codon 129.Results: A diagnostic sensitivity of 94%, a diagnostic specificity of 90%, and a positive predictive value of 92% were achieved for tau-protein at a cut-off of 1,300 pg/mL. These results are comparable with those of the 14-3-3 immunoblot. For patients with type II prion protein and methionine/valine or valine/valine polymorphism at codon 129, tau-protein has a higher diagnostic sensitivity than 14-3-3 protein. Tau-protein levels were significantly higher in patients with higher-rated 14-3-3 immunoblot bands.Conclusion: The differential diagnostic significance of the 14-3-3 immunoblot is similar to that of the tau-protein ELISA. The advantage of the tau-protein ELISA is that it is easy to use in routine laboratories. Patients with a negative 14-3-3 immunoblot already have measurable tau-protein levels. This increases information on 14-3-3—negative patients with CJD and especially on patients with other diseases."],["dc.identifier.doi","10.1212/wnl.58.2.192"],["dc.identifier.gro","3151690"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8509"],["dc.language.iso","en"],["dc.notes.status","public"],["dc.notes.submitter","chake"],["dc.relation.issn","0028-3878"],["dc.title","Tau protein and 14-3-3 protein in the differential diagnosis of Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]