Ratzka, Peter

[["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","S131"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neurobiology of Aging"],["dc.bibliographiccitation.lastpage","S132"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Ratzka, P."],["dc.contributor.author","Doehlinger, S."],["dc.contributor.author","Boekhoff, I."],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Irle, W."],["dc.contributor.author","Pergande, G."],["dc.contributor.author","Eller-Lenz, B."],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.date.accessioned","2018-11-07T10:23:11Z"],["dc.date.available","2018-11-07T10:23:11Z"],["dc.date.issued","2002"],["dc.identifier.isi","000177465300486"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42407"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.publisher.place","New york"],["dc.relation.issn","0197-4580"],["dc.title","Efficacy of flupirtine on cognitive function in patients with Creutzfeldt-Jakob-disease"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","29"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","32"],["dc.bibliographiccitation.volume","343"],["dc.contributor.author","Ratzka, Peter"],["dc.contributor.author","Döhlinger, Susanne"],["dc.contributor.author","Cepek, Lukas"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Arlt, Sönke"],["dc.contributor.author","Jacobi, Christian"],["dc.contributor.author","Schröter, Andreas"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Poser, Sigrid"],["dc.date.accessioned","2021-06-01T10:50:14Z"],["dc.date.available","2021-06-01T10:50:14Z"],["dc.date.issued","2003"],["dc.description.abstract","In Creutzfeldt-Jakob disease (CJD), progressive neuronal cell death probably occurs as a result of a change in conformation of the physiological prion protein (PrPC). There is evidence of participation of the lymphatic system and in particular of lymphocytes in the intracorporeal transportation of the pathological prion protein (PrPSc) in new variant CJD and scrapie. Using fluorescence cytometry, we investigated a possible alteration of PrPC on lymphocytes of patients with sporadic CJD. We demonstrated a significantly lower binding pattern of antibodies (3F4) against physiological prion protein to lymphocytes of patients with sporadic CJD (n = 16) compared with control patients. In contrast this difference was not found on platelets (n = 23). For the first time we were able to present a measurable difference of antibody binding on lymphocytes of patients with CID. One interpretation of this finding is that lymphocytes patrolling the brain bind and transport PrPSc which has a lower binding affinity for the antibodies directed against physiological PrP. (C) 2003 Elsevier Science Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/S0304-3940(03)00315-X"],["dc.identifier.isi","000183128900008"],["dc.identifier.pmid","12749990"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86584"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","Different binding pattern of antibodies to prion protein on lymphocytes from patients with sporadic 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","1099"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","1102"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Esselmann, Herrmann"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Neumann, M."],["dc.contributor.author","Schroter, A."],["dc.contributor.author","Ratzka, P."],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Wiltfang, J."],["dc.date.accessioned","2018-11-07T08:45:04Z"],["dc.date.available","2018-11-07T08:45:04Z"],["dc.date.issued","2000"],["dc.description.abstract","Objectives: Decreased levels of A beta(1-42) are found in CSF of patients with AD. Because early stages of Creutzfeldt-Jakob disease (CJD) and AD share several clinical features, we investigated A beta(1-42) levels in CSF of these groups, inferring that this might give additional help in differentiating patients with CJD from AD patients. Methods: We investigated 27 patients with CJD, 14 patients with AD, 19 patients with other dementias, and 20 nondemented controls (NDC) for A beta(1-42) in CSF. Twenty-four of the 27 CJD patients were neuropathologically verified. All the neuropathologically verified patients presented with a type 1 prion protein pattern. CJD patients were all homozygous for methionine at codon 129. Except in five CJD patients, no beta-amyloid plaques were seen. Additionally, APOE status was determined in patients with CJD. Results: Levels of A beta(1-42) in CSF were decreased in patients with AD as well as in CJD. Levels of A beta(1-42) in CSF of patients with CJD and AD were significantly different from the other dementia and NDC groups. There was no substantial difference between the CJD and AD groups (p = 0.66). Decreased levels of A beta(1-42) did not correlate with the APOE epsilon 4 load in patients with CJD. Conclusion: Low levels of A beta(1-42) in CSF do not exclude a diagnosis of CJD. Decreased levels of A beta(1-42) in CSF can occur without p-amyloid plaque formation in the brain. However, the underlying mechanism of this phenomenon must be elucidated."],["dc.identifier.isi","000085785700017"],["dc.identifier.pmid","10720281"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20346"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0028-3878"],["dc.title","Decreased beta-amyloid(1-42) 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","1099"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","1102"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Schulz-Schaeffer, W."],["dc.contributor.author","Neumann, Manuela"],["dc.contributor.author","Schröter, A."],["dc.contributor.author","Ratzka, P."],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Windl, O."],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2017-09-07T11:44:28Z"],["dc.date.available","2017-09-07T11:44:28Z"],["dc.date.issued","2012"],["dc.description.abstract","bjectives: Decreased levels of Aβ1-42 are found in CSF of patients with AD. Because early stages of Creutzfeldt-Jakob disease (CJD) and AD share several clinical features, we investigated Aβ1-42 levels in CSF of these groups, inferring that this might give additional help in differentiating patients with CJD from AD patients.Methods: We investigated 27 patients with CJD, 14 patients with AD, 19 patients with other dementias, and 20 nondemented controls (NDC) for Aβ1-42 in CSF. Twenty-four of the 27 CJD patients were neuropathologically verified. All the neuropathologically verified patients presented with a type 1 prion protein pattern. CJD patients were all homozygous for methionine at codon 129. Except in five CJD patients, no β-amyloid plaques were seen. Additionally, APOE status was determined in patients with CJD.Results: Levels of Aβ1-42 in CSF were decreased in patients with AD as well as in CJD. Levels of Aβ1-42 in CSF of patients with CJD and AD were significantly different from the other dementia and NDC groups. There was no substantial difference between the CJD and AD groups (p = 0.66). Decreased levels of Aβ1-42 did not correlate with the APOE ε4 load in patients with CJD.Conclusion: Low levels of Aβ1-42 in CSF do not exclude a diagnosis of CJD. Decreased levels of Aβ1-42 in CSF can occur without β-amyloid plaque formation in the brain. However, the underlying mechanism of this phenomenon must be elucidated."],["dc.identifier.doi","10.1212/wnl.54.5.1099"],["dc.identifier.gro","3151662"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8479"],["dc.language.iso","en"],["dc.notes.status","public"],["dc.notes.submitter","chake"],["dc.relation.issn","0028-3878"],["dc.title","Decreased  β-amyloid1-42 in cerebrospinal fluid of patients with Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]