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","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","888"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Der Nervenarzt"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","74"],["dc.contributor.author","Schmidt, H."],["dc.contributor.author","Kaboth, U."],["dc.contributor.author","Brinck, Ulrich"],["dc.contributor.author","Ratzka, P."],["dc.contributor.author","Rustenbeck, Hans Heino"],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T10:35:55Z"],["dc.date.available","2018-11-07T10:35:55Z"],["dc.date.issued","2003"],["dc.description.abstract","Up to 40% of patients with malignant thymoma suffer from paraneoplastic symptoms (90% myasthenia, 10% other symptoms). A 55-year-old patient developed ascending symmetrical, sensorimotor tetraparesis. A malignant thymoma without metastases was diagnosed 6 months, later. Despite thymectomy followed by radiation and high-dose corticosteroid therapy, the, polyneuropathy progressed. Six months after onset, the patient was bound to a wheelchair. Immunosuppressive therapy with cyclophosphamide was initiated, leading to marked remission. After ten cycles, the patient was able to walk independently with walking aids. After the sixth and tenth cycle, respectively, attempts to discontinue immunosuppression led to relapse. In several diagnostic workups, however, there was no tumour relapse. After 13 cycles, cyclophosphamide was replaced by immunoglobulins (0.4 g/kg per day i.v. for 5 days/month) due to progressive renal failure. The patient died just before the secondcourse of this treatment. In conclusion, in the differential diagnosis of rapidly progressive polyneuropathy a malignant thymoma should be considered, even in the absence of myasthenia. Immunosuppression with cyclophosphamide resulted in amelioration of symptoms in this patient."],["dc.identifier.doi","10.1007/s00115-003-1552-z"],["dc.identifier.isi","000186443000009"],["dc.identifier.pmid","14551694"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45203"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0028-2804"],["dc.title","Polyneuropathy as a sole syndrome in mialignant thymoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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.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.issue","9505"],["dc.bibliographiccitation.journal","The Lancet"],["dc.bibliographiccitation.volume","367"],["dc.contributor.author","Ratzka, Peter"],["dc.contributor.author","Schlachetzki, Johannes C. M."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2017-09-07T11:53:35Z"],["dc.date.available","2017-09-07T11:53:35Z"],["dc.date.issued","2006"],["dc.format.extent","182"],["dc.identifier.doi","10.1016/S0140-6736(06)67967-1"],["dc.identifier.gro","3143749"],["dc.identifier.isi","000234655500033"],["dc.identifier.pmid","16413882"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1297"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Lancet Ltd"],["dc.relation.issn","0140-6736"],["dc.title","Varicella zoster virus cerebellitis in a 66-year-old patient without herpes zoster"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","letter_note"],["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","714"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","718"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Otto, M."],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Ratzka, P."],["dc.contributor.author","Doehlinger, S."],["dc.contributor.author","Boekhoff, I."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Irle, E."],["dc.contributor.author","Pergande, G."],["dc.contributor.author","Ellers-Lenz, B."],["dc.contributor.author","Prange, H."],["dc.date.accessioned","2021-06-01T10:48:09Z"],["dc.date.available","2021-06-01T10:48:09Z"],["dc.date.issued","2004"],["dc.description.abstract","Background: In cell culture experiments, flupirtine maleate ( FLU), a triaminopyridine compound, was able to protect neuronal cells from apoptotic cell death induced by prion protein fragments and beta-amyloid peptides. As FLU is a clinically safe drug, the authors started a double-blind placebo-controlled study in patients with Creutzfeldt - Jakob disease (CJD). Methods: Twenty-eight patients with CJD were randomized to an oral treatment with either FLU ( n = 13) or matching placebo (PLA; n = 15). For inclusion and continuing the study, the patients had to achieve at least 50% in two of the subscales of the dementia tests employed. A battery of standardized questionnaires was employed to monitor the progression of the disease. The main outcome variable was the cognitive part of the Alzheimer's Disease Assessment Scale (ADAS-Cog); the difference between baseline and the best score under treatment was defined as the primary efficacy variable for hypothesis testing. Results: CJD types were homogeneously distributed among the treatment groups. Patients treated with FLU showed significantly less deterioration in the dementia tests than patients treated with PLA. The mean change in ADAS-Cog ( baseline to best) was + 8.4 ( +/- 15.3) in the FLU group and + 20.6 ( +/- 15.1) in the PLA group ( p = 0.02, one-sided t-test). Conclusions: FLU has beneficial effects on cognitive function in patients with CJD. These positive results also may suggest a treatment potential of FLU in other neurodegenerative disorders. However, further studies are necessary."],["dc.identifier.doi","10.1212/01.WNL.0000113764.35026.EF"],["dc.identifier.isi","000220083000008"],["dc.identifier.pmid","15007119"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85845"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.eissn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","Efficacy of flupirtine on cognitive function in patients with CJD: A double-blind study"],["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"]]