Poser, Sigrid

[["dc.bibliographiccitation.firstpage","690"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","694"],["dc.bibliographiccitation.volume","248"],["dc.contributor.author","Ratzka, Peter"],["dc.contributor.author","Schröter, Andreas"],["dc.contributor.author","Cepek, Lukas"],["dc.contributor.author","Henkel, Karsten"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Poser, S."],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2017-09-07T11:44:31Z"],["dc.date.available","2017-09-07T11:44:31Z"],["dc.date.issued","2006"],["dc.description.abstract","Creutzfeldt-Jakob disease (CJD) belongs to the group of transmissible spongiform encephalopathies. It is suspected that a pathologically altered form of the prion protein (PrPSc) is the decisive trigger of the disease. Data from animal experiments suggest an involvement of the lymphatic system in the intracorporal transport of PrPSc. However, it has not so far been possible to detect PrPSc on mononuclear cells (MNCs) either in the sporadic form of CJD or in the new variant of CJD (vCJD). In order to determine a possible alteration of MNCs in CJD, we investigated the natural and induced apoptotic behaviour of these cells.MNCs from 19 patients with sporadic CJD and from 20 patients with other neurological disorders were used. The cells were analysed by fluorescence cytometry with and without apoptosis induction by xanthine oxidase and hypoxanthine. The apoptosis rate was quantified using the stain 7-amino-actinomycin D (7-AAD). In the morphological investigation of the cells before apoptosis induction, there were no significant differences between the groups with regard to cell size and granularity of the MNCs. After apoptosis induction, the typical significant decrease in cell size and increase in granularity of the cells occurred in both groups. Significant differences between the patient populations were not found.For the first time, our investigation has demonstrated that a functional impairment of MNCs with regard to their apoptotic behaviour does not occur in sporadic CJD. It remains open to question whether this mechanism plays an important role in forms of transmissible encephalopathy other than sporadic CJD, especially after oral transmission."],["dc.identifier.doi","10.1007/pl00007834"],["dc.identifier.gro","3151691"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8510"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","chake"],["dc.relation.issn","0340-5354"],["dc.title","Unaltered apoptotic behaviour of mononuclear cells from patients with sporadic Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2485"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","2490"],["dc.bibliographiccitation.volume","73"],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Otto, M."],["dc.contributor.author","Baxter, H. C."],["dc.contributor.author","Bodemer, M."],["dc.contributor.author","Steinacker, P."],["dc.contributor.author","Bahn, E."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Kornhuber, J."],["dc.contributor.author","Kretzschmar, H. A."],["dc.contributor.author","Poser, S."],["dc.contributor.author","Rüther, E."],["dc.contributor.author","Aitken, A."],["dc.date.accessioned","2017-09-07T11:44:33Z"],["dc.date.available","2017-09-07T11:44:33Z"],["dc.date.issued","1999"],["dc.description.abstract","Two-dimensional polyacrylamide gel electrophoresis of CSF has been used in the diagnosis of Creutzfeldt-Jakob disease (CJD). One of the two diagnostic protein spots was identified as isoform(s) of the 14-3-3 family of abundant brain proteins. This has led to the development of one-dimensional 14-3-3 sodium dodecyl sulfate polyacrylamide gel electrophoresis immunoblot, which is currently used to support the diagnosis of CJD. In the present study employing western blot analysis, we have identified the panel of 14-3-3 isoforms that appear in the CSF of 10 patients with CJD compared with 10 patients with other dementias. The results clearly show that the 14-3-3 isoforms β, γ, ε, and η are present in the CSF of patients with CJD and can be used to differentiate other dementias. 14-3-3η also gave a baseline signal in all patients with other dementias, including six patients with Alzheimer's disease. The presence of 14-3-3η in the CSF of a patient with herpes simplex encephalitis was particularly noteworthy. This study has determined that isoform-specific 14-3-3 antibodies against β, γ, and ε should be considered for the neurochemical differentiation of CJD from other neurodegenerative diseases."],["dc.identifier.doi","10.1046/j.1471-4159.1999.0732485.x"],["dc.identifier.gro","3151688"],["dc.identifier.pmid","10582609"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8506"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0022-3042"],["dc.title","Isoform Pattern of 14-3-3 Proteins in the Cerebrospinal Fluid of Patients with Creutzfeldt-Jakob Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","200"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","208"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Brechlin, Peter"],["dc.contributor.author","Schindehuette, Jan"],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T10:33:04Z"],["dc.date.available","2018-11-07T10:33:04Z"],["dc.date.issued","2006"],["dc.description.abstract","Measurement of tau-protein and beta-amyloid(1-42) (A beta 42) in cerebrospinal fluid (CSF) has gained increasing acceptance in the differential diagnosis of Alzheimer's disease. We investigated CSF tau-protein and A beta 42 concentrations in 73 patients with advanced idiopathic Parkinson's disease with dementia (PDD) and 23 patients with idiopathic Parkinson's disease without dementia (PD) and in a comparison group of 41 non-demented neurological patients (CG) using commercially available enzyme-linked-immunoabsorbant- assay ( ELISA). tau-Protein levels were statistically significantly higher and A beta 42 lower in the PDD patients compared to PD patients and the CG. This observation was most marked ( p < 0.05) in a subgroup of patients with PDD carrying the apolipoprotein genotype epsilon 3/epsilon 3. The distribution of the apolipoprotein genotypes in PDD and PD patients was similar to that of the CG. Although a significant difference in tau-protein values was observed between PDD and CG, no diagnostic cut-off value was established. These findings suggest that such protein CSF changes may help to support the clinical diagnosis of cognitive decline in PD and that there may be apolipoprotein-E-isoform- specific differences in CSF protein regulation in advanced PDD. Copyright (C) 2006 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000094871"],["dc.identifier.isi","000242167100003"],["dc.identifier.pmid","16899997"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44513"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1420-8008"],["dc.title","Beta-amlyoid 1-42 and tau-protein in cerebrospinal fluid of patients with Parkinson's disease dementia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","263"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","267"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Esselmann, Herrmann"],["dc.contributor.author","Smirnov, Alexey"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Buerger, Katharina"],["dc.contributor.author","Hampel, Harald"],["dc.contributor.author","Paul, S."],["dc.contributor.author","Neumann, M."],["dc.contributor.author","Maler, M."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T10:37:04Z"],["dc.date.available","2018-11-07T10:37:04Z"],["dc.date.issued","2003"],["dc.description.abstract","Decreased levels of beta-amyloid peptide 1-42 (Abeta1-42) in cerebrospinal fluid (CSF) are a characteristic feature of Alzheimer's disease (AD) but recently were also observed in Creutzfeldt-Jakob disease (CJD). We analyzed the CSF of patients with CJD, and AD and nondemented controls using a quantitative urea-based Abeta sodium dodecyl sulfate polyacrylamide gel electrophoresis immunoblot. Like in AD and nondemented controls, we found a highly conserved pattern of carboxyterminally truncated Abeta1-37/38/39 in addition to Abeta1-40/42 also in CJD patients. By the introduction of the ratio Abeta1-39 to Abeta1-42, CJD and AD can effectively be differentiated. We conclude that the immunoblot shows disease-specific CSF Abeta peptide patterns in CJD and AD and suppose that measurement of the Abeta peptide pattern seems to be a promising diagnostic tool in the differential diagnosis of dementias."],["dc.identifier.doi","10.1002/ana.10661"],["dc.identifier.isi","000184352700021"],["dc.identifier.pmid","12891683"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45476"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0364-5134"],["dc.title","beta-Amyloid peptides 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","668"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Der Nervenarzt"],["dc.bibliographiccitation.lastpage","670"],["dc.bibliographiccitation.volume","70"],["dc.contributor.author","Otto, M."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Poser, S."],["dc.contributor.author","Kornhuber, J."],["dc.date.accessioned","2017-09-07T11:44:46Z"],["dc.date.available","2017-09-07T11:44:46Z"],["dc.date.issued","1999"],["dc.identifier.doi","10.1007/s001150050494"],["dc.identifier.gro","3151732"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8553"],["dc.language.iso","de"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0028-2804"],["dc.title","Tau Protein: Ein potentieller biologischer Indikator zur Früherkennung der Alzheimer-Krankheit"],["dc.title.subtitle","Anmerkung zur Arbeit von K. Buch et al. Nervenarzt (1998) 69: 379–385"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","577"],["dc.bibliographiccitation.issue","7131"],["dc.bibliographiccitation.journal","BMJ"],["dc.bibliographiccitation.lastpage","582"],["dc.bibliographiccitation.volume","316"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Schütz, Ekkehard"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Otto, A."],["dc.contributor.author","Pfahlberg, A."],["dc.contributor.author","Gefeller, Olaf"],["dc.contributor.author","Uhr, Manfred"],["dc.contributor.author","Giese, A."],["dc.contributor.author","Weber, Thomas"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Poser, Sigrid"],["dc.date.accessioned","2017-09-07T11:44:30Z"],["dc.date.available","2017-09-07T11:44:30Z"],["dc.date.issued","2011"],["dc.description.abstract","Objective: To analyse serum concentrations of brain specific S100 protein in patients with Creutzfeldt-Jakob disease and in controls.Design: Prospective case-control study.Setting: National Creutzfeldt-Jakob disease surveillance unit.Subjects: 224 patients referred to the surveillance unit with suspected Creutzfeldt-Jakob disease and 35 control patients without dementia.Main outcome measure: Serum concentration of S100 protein in patients with Creutzfeldt-Jakob disease, in patients with other diseases causing dementia, and in the control group.Results: Of the 224 patients with suspected Creutzfeldt-Jakob disease, 65 were classed as definitely having the disease after neuropathological verification, an additional 6 were classed as definitely having the disease as a result of a genetic mutation, 43 as probably having the disease, 36 as possibly having the disease, and 74 patients were classed as having other disease. In the 108 patients classed as definitely or probably having Creutzfeldt-Jakob disease the median serum concentration of S100 was 395 pg/ml (SD 387 pg/ml). This was significantly higher than concentrations found in the 74 patients classed as having other diseases (median 109 pg/ml; SD 177 pg/ml; P=0.0001). At a cut off point of 213 pg/ml sensitivity for the diagnosis of the disease was 77.8% (95% confidence interval 68.8% to 85.2%) and specificity was 81.1% (70.3% to 89.3%). There was a significant difference in survival at different concentrations of S100 in Kaplan-Meier curves (P=0.023).Conclusion: Measurement of serum concentrations of S100 is a valuable tool which can be used more easily than tests on cerebrospinal fluid in the differential diagnosis of Creutzfeldt-Jakob disease. More studies are needed to determine whether serial testing of serum S100 improves diagnostic accuracy.Key messages Creutzfeldt-Jakob disease is a rare, fatal neurodegenerative disease. Diagnosis is made clinically and neuropathologically There is no serum test which allows the diagnosis to be made while the patient is alive In this study raised serum concentrations of S100 protein were found in patients with Creutzfeldt-Jakob disease Serum concentrations of S100 could be used with a sensitivity of 77.8% and a specificity of 81.1% to confirm Creutzfeldt-Jakob disease in the differential diagnosis of diseases that cause dementia Serial measurement of S100 concentrations will enhance diagnostic accuracy"],["dc.identifier.doi","10.1136/bmj.316.7131.577"],["dc.identifier.gro","3151673"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8491"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","chake"],["dc.relation.issn","0959-8138"],["dc.title","Diagnosis of Creutzfeldt-Jakob disease by measurement of S100 protein in serum: prospective case-control study"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3283"],["dc.bibliographiccitation.issue","51-52"],["dc.bibliographiccitation.journal","Deutsches Ärzteblatt"],["dc.bibliographiccitation.lastpage","3286"],["dc.bibliographiccitation.volume","95"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Ratzka, P."],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Boekhoff, Immo"],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Prange, Hilmar Walter"],["dc.date.accessioned","2017-11-21T12:33:49Z"],["dc.date.available","2017-11-21T12:33:49Z"],["dc.date.issued","1998"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/10140"],["dc.language.iso","de"],["dc.notes.status","final"],["dc.title","Therapeutische Ansätze bei der Creutzfeldt-Jakob-Krankheit"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.volume","56"],["dc.contributor.author","Tschampa, H. J."],["dc.contributor.author","Schulz-Schaeffer, W."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Poser, S."],["dc.contributor.author","Otto, M."],["dc.contributor.author","Neumann, M."],["dc.contributor.author","Kretzschmar, H. A."],["dc.contributor.author","Kanemaru, K."],["dc.date.accessioned","2017-09-07T11:44:34Z"],["dc.date.available","2017-09-07T11:44:34Z"],["dc.date.issued","2012"],["dc.identifier.doi","10.1212/wnl.56.4.576"],["dc.identifier.gro","3151707"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8526"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0028-3878"],["dc.title","Decreased CSF amyloid  42 and normal tau levels in dementia with Lewy bodies"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["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"]]