Bodemer, Monika

[["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.issue","2"],["dc.bibliographiccitation.journal","Prion"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Kiesel, Petra"],["dc.contributor.author","Gibson, Toby J."],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Bodemer, Monika"],["dc.contributor.author","Kaup, Franz-Josef"],["dc.contributor.author","Bodemer, Walter"],["dc.contributor.author","Zischler, Hans"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T08:44:50Z"],["dc.date.available","2018-11-07T08:44:50Z"],["dc.date.issued","2010"],["dc.description.abstract","Alu DNA elements were long considered to be of no biological significance and thus have been only poorly defined. However, in the past Alu DNA elements with well-defined nucleotide sequences have been suspected to contribute to disease, but the role of Alu DNA element transcripts has rarely been investigated. For the first time, we determined in a real-time approach Alu DNA element transcription in buffy coat cells isolated from the blood of humans suffering from sporadic Creutzfeldt-Jakob disease (sCJD) and other neurodegenerative disorders. The reverse transcribed Alu transcripts were amplified and their cDNA sequences were aligned to genomic regions best fitted to database genomic Alu DNA element sequences deposited in the UCSC and NCBI data bases. Our cloned Alu RNA/cDNA sequences were widely distributed in the human genome and preferably belonged to the \"young\" Alu Y family. We also observed that some RNA/cDNA clones could be aligned to several chromosomes because of the same degree of identity and score to resident genomic Alu DNA elements. These elements, called paralogues, have purportedly been recently generated by retrotransposition. Along with cases of sCJD we also included cases of dementia and Alzheimer disease (AD). Each group revealed a divergent pattern of transcribed Alu elements. Chromosome 2 was the most preferred site in sCJD cases, besides chromosome 17; in AD cases chromosome 11 was overrepresented whereas chromosomes 2, 3 and 17 were preferred active Alu loci in controls. Chromosomes 2, 12 and 17 gave rise to Alu transcripts in dementia cases. The detection of putative Alu paralogues widely differed depending on the disease. A detailed data search revealed that some cloned Alu transcripts originated from RNA polymerase III transcription since the genomic sites of their Alu elements were found between genes. Other Alu DNA elements could be located close to or within coding regions of genes. In general, our observations suggest that identification and genomic localization of active Alu DNA elements could be further developed as a surrogate marker for differential gene expression in disease. A sufficient number of cases are necessary for statistical significance before Alu DNA elements can be considered useful to differentiate neurodegenerative diseases from controls."],["dc.identifier.isi","000280388200006"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20288"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.relation.issn","1933-6896"],["dc.title","Transcription of Alu DNA elements in blood cells of sporadic Creutzfeldt-Jakob disease (sCJD)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","811"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","815"],["dc.bibliographiccitation.volume","55"],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Pocchiari, Mauricio"],["dc.contributor.author","Collins, S."],["dc.contributor.author","Brandel, Jean-Philippe"],["dc.contributor.author","Cuesta, J. D."],["dc.contributor.author","Knight, Richard S. G."],["dc.contributor.author","Bernheimer, H."],["dc.contributor.author","Cardone, F."],["dc.contributor.author","Delasnerie-Laupretre, N."],["dc.contributor.author","Corrales, N. C."],["dc.contributor.author","Ladogana, Anna"],["dc.contributor.author","Bodemer, Monika"],["dc.contributor.author","Fletcher, A."],["dc.contributor.author","Awan, T."],["dc.contributor.author","Bremon, A. R."],["dc.contributor.author","Budka, H."],["dc.contributor.author","Laplanche, J. L."],["dc.contributor.author","Will, Robert G."],["dc.contributor.author","Poser, Sigrid"],["dc.date.accessioned","2018-11-07T10:04:54Z"],["dc.date.available","2018-11-07T10:04:54Z"],["dc.date.issued","2000"],["dc.description.abstract","Objective: To improve diagnostic criteria for sporadic Creutzfeldt-Jakob disease (CJD). Methods: Pooled data on initial and final diagnostic classification of suspected CJD patients were accumulated, including results of investigations derived from a coordinated multinational study of CJD. Prospective analysis for a comparison of clinical and neuropathologic diagnoses and evaluation of the sensitivity and specificity of EEG and 14-3-3 CSF immunoassay were conducted. Results: Data on 1,003 patients with suspected CJD were collected using a standard questionnaire. After follow-up was carried out, complete clinical data and neuropathologic diagnoses were available in 805 cases. In these patients, the sensitivity of the detection of periodic sharp wave complexes in the EEG was 66%, with a specificity of 74%. The detection of 14-3-3 proteins in the CSF correlated with the clinical diagnosis in 94% (sensitivity). The specificity (84%) was higher than that of EEG. A combination of both investigations further increased the sensitivity but decreased the specificity. Conclusions: Incorporation of CSF 14-3-3 analysis in the diagnostic criteria for CJD significantly increases the sensitivity of case definition. Amended diagnostic criteria for CJD are proposed."],["dc.identifier.isi","000089484800013"],["dc.identifier.pmid","10994001"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38795"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0028-3878"],["dc.title","Analysis of EEG and CSF 14-3-3 protein as aids to the diagnosis of 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","637"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","643"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Sanchez-Juan, Pascual"],["dc.contributor.author","Green, A."],["dc.contributor.author","Ladogana, Anna"],["dc.contributor.author","Cuadrado-Corrales, Natividad"],["dc.contributor.author","Sanchez-Valle, Raquel"],["dc.contributor.author","Mitrova, Eva"],["dc.contributor.author","Stoeck, Katharina"],["dc.contributor.author","Sklaviadis, Theodoros"],["dc.contributor.author","Kulczycki, Jerzy"],["dc.contributor.author","Hess, Katharina"],["dc.contributor.author","Bodemer, Monika"],["dc.contributor.author","Slivarichova, Dana"],["dc.contributor.author","Saiz, Albert"],["dc.contributor.author","Calero, Miguel"],["dc.contributor.author","Ingrosso, L."],["dc.contributor.author","Knight, R."],["dc.contributor.author","Janssens, A. C. J. W."],["dc.contributor.author","van Duijn, C. M."],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T09:25:03Z"],["dc.date.available","2018-11-07T09:25:03Z"],["dc.date.issued","2006"],["dc.description.abstract","Objectives: To analyze the diagnostic sensitivity and specificity of various brain-derived proteins (14-3-3, Tau, neuron specific enolase [NSE], and S100b) in the CSF of patients with Creutzfeldt-Jakob disease (CJD) and to analyze biologic factors that modify these parameters. Methods: CSF was tested for 14-3-3, Tau, NSE, and S100b in 1,859 patients with sporadic, genetic, iatrogenic, and variant CJD, and in 1,117 controls. Results: The highest sensitivity was achieved for 14-3-3 and Tau in sporadic CJD (85% and 86%), and a combined determination of 14-3-3 and Tau, S100b, or NSE increased the sensitivity to over 93%. A multivariate analysis showed that the sensitivity of all tests was highest in patients with the shortest disease duration, age at onset > 40 years, and homozygosity at codon 129 of the prion protein gene. In a group of patients with repeated lumbar punctures, a second test also increased the diagnostic sensitivity. Conclusions: The detection of elevated levels of brain-derived proteins in the CSF in patients with suspected CreutzfeldtJakob disease is a valuable diagnostic test. A second lumbar puncture may be of value in patients with atypical clinical course in whom the first test was negative."],["dc.identifier.doi","10.1212/01.wnl.0000230159.67128.00"],["dc.identifier.isi","000239920100020"],["dc.identifier.pmid","16924018"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29980"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0028-3878"],["dc.title","CSF tests in the differential diagnosis of 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","163"],["dc.bibliographiccitation.issue","2-3"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","166"],["dc.bibliographiccitation.volume","371"],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Bodemer, Monika"],["dc.contributor.author","Kaboth, U."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Oellerich, M."],["dc.contributor.author","Armstrong, Victor William"],["dc.date.accessioned","2018-11-07T10:43:45Z"],["dc.date.available","2018-11-07T10:43:45Z"],["dc.date.issued","2004"],["dc.description.abstract","Human plasminogen has been shown to interact with the abnormal disease-specific prion protein. Till now, no data are available for patients with Creutzfeldt-Jakob disease (CJD). Therefore, we compared plasminogen concentrations and plasminogen activities in patients with sporadic CJD and controls with other dementia, which were collected in the framework of the German CJD Surveillance study. Patients with CJD had significantly higher plasminogen concentrations than patients with other forms of dementia and plasminogen specific activities were lower in CJD patients. The reasons for these abnormalities are Dot clear at the moment. The results may reflect a disease-specific prion protein and plasminogen interaction in patients with CJD. Other possible explanations are plasminogen polymorphisms and genotypes with distinct plasminogen activity levels in CJD than in controls, which should be a subject for further studies. (C) 2004 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.neulet.2004.08.063"],["dc.identifier.isi","000225203800016"],["dc.identifier.pmid","15519749"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47129"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","Plasminogen activities and concentrations in 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","441"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Transfusion"],["dc.bibliographiccitation.lastpage","448"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Volkel, D."],["dc.contributor.author","Zimmermann, K."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Bodemer, Monika"],["dc.contributor.author","Lindner, T."],["dc.contributor.author","Turecek, P. L."],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Schwarz, H. P."],["dc.date.accessioned","2018-11-07T09:15:32Z"],["dc.date.available","2018-11-07T09:15:32Z"],["dc.date.issued","2001"],["dc.description.abstract","BACKGROUND: Creutzfeldt-Jakob disease is thought to be caused by conversion of cellular prion protein (PrP) from its soluble form (PrPsen) to a pathologic form (PrPres). The occurrence of a new variant of CJD has increased the demand for a rapid assay capable of detecting a theoretical risk of transmission of the disease by blood or plasma. STUDY DESIGN AND METHODS: A quantitative sandwich ELISA for routine screening was developed for analysis of PrP levels in plasma. The time-resolved dissociation-enhanced fluorescence technology allowed a detection limit in plasma samples of approximately 50 pg/mL. Levels of PrPsen were tested in plasma from 31 patients with CJD, from 11 patients with other neurodegenerative diseases, and from a control group of 200 healthy subjects. RESULTS: The assay recognized both PrPsen and pathologic PrPres, but did not differentiate between the two isoforms. PrPsen levels were higher in plasma from both patient groups than in plasma from the control group: 27 of the 31 (87%) CJD patients and all patients with other neurodegenerative diseases had higher levels than the highest concentration found in the control group. No correlation was found between age and PrP level. No signal could be detected in the CJD samples after protease K digestion, indicating that all detected PrP was protease-sensitive and therefore not pathologic. CONCLUSION: These data suggest that soluble PrPsen in plasma samples might be useful as a surrogate marker for a broad spectrum of neurologic diseases as well as for CJD."],["dc.identifier.doi","10.1046/j.1537-2995.2001.41040441.x"],["dc.identifier.isi","000168296800004"],["dc.identifier.pmid","11316892"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27717"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Blood Banks"],["dc.relation.issn","0041-1132"],["dc.title","Immunochemical determination of cellular prion protein in plasma from healthy subjects and patients with sporadic CJD or other neurologic diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1591"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","ARCHIVES OF NEUROLOGY"],["dc.bibliographiccitation.lastpage","1594"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Stoeck, Katharina"],["dc.contributor.author","Bodemer, Monika"],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Bartl, Mario"],["dc.contributor.author","Heinemann, U."],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T10:55:05Z"],["dc.date.available","2018-11-07T10:55:05Z"],["dc.date.issued","2005"],["dc.description.abstract","Background: In neurodegenerative diseases, increasing attention has been focused on inflammatory mediators such as pro-inflammatory and anti-inflammatory cytokines and their potential influence in the process of neurodegeneration. In prion diseases, much data has been gained on the cell culture and animal disease models level, but only limited information is available on humans affected by Creutzfeldt-Jakob disease (CJD). Objective: To obtain data on anti-inflammatory cytokines interleukin 4 and interleukin 10 in the cerebrospinal fluid of patients with CJD, patients with other dementia, and nondemented neurological patients and controls. Design: Cerebrospinal fluid samples were collected from CJD patients and control subjects, and concentrations of the anti-inflammatory cytokines interleukin 4 and interleukin 10 were determined using an enzyme-linked immunosorbent assay. Patients: Cerebrospinal fluid samples from 61 patients were analyzed. The group was composed of patients with CJD (n = 20), patients with other forms of dementia (n = 10), patients with motoneuron disease (n = 6), patients with normal pressure hydrocephalus (n = 5), and control subjects (n = 20). Conclusions: Elevated levels of the anti-inflammatory cytokines interleukin 4 and interleukin 10 in cerebrospinal fluid of patients with CJD are new findings. The data of the present study provide a clue toward the possible role of cytokines as immunological modifiers in the neurodegenerative process of CJD."],["dc.identifier.doi","10.1001/archneur.62.10.1591"],["dc.identifier.isi","000232502900014"],["dc.identifier.pmid","16216944"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49709"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Medical Assoc"],["dc.relation.issn","0003-9942"],["dc.title","Interleukin 4 and interleukin 10 levels are elevated in the 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","231"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Virological Methods"],["dc.bibliographiccitation.lastpage","237"],["dc.bibliographiccitation.volume","69"],["dc.contributor.author","Weber, T."],["dc.contributor.author","Klapper, P.E."],["dc.contributor.author","Cleator, G.M."],["dc.contributor.author","Bodemer, M."],["dc.contributor.author","Lüke, W."],["dc.contributor.author","Knowles, W."],["dc.contributor.author","Cinque, P."],["dc.contributor.author","Van Loon, A.M."],["dc.contributor.author","Grandien, M."],["dc.contributor.author","Hammarin, A.L."],["dc.contributor.author","Bogdanovic, G."],["dc.date.accessioned","2022-10-06T13:33:49Z"],["dc.date.available","2022-10-06T13:33:49Z"],["dc.date.issued","1997"],["dc.identifier.doi","10.1016/S0166-0934(97)00152-3"],["dc.identifier.pii","S0166093497001523"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/115737"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.issn","0166-0934"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.title","Polymerase chain reaction for detection of JC virus DNA in cerebrospinal fluid: a quality control study"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1842"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Neurobiology of Aging"],["dc.bibliographiccitation.lastpage","1850"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Gmitterova, Karin"],["dc.contributor.author","Heinemann, U."],["dc.contributor.author","Bodemer, Monika"],["dc.contributor.author","Krasnianski, Anna"],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T11:23:01Z"],["dc.date.available","2018-11-07T11:23:01Z"],["dc.date.issued","2009"],["dc.description.abstract","Background: The 14-3-3 protein is a physiological cellular protein expressed in various tissues, and its release to CSF reflects extensive neuronal damage as in Creutzfeldt-Jakob disease (CJD), but also in other neurological diseases. 14-3-3 protein in CSF in the proper clinical context is a reliable diagnostic tool for sporadic CJD. However, the sensitivity varies across molecular CJD subtypes. Objective: We determined the level of the 14-3-3 protein in CSF from 70 sporadic CJD patients with distinct molecular subtypes using an improved enzyme-linked immunosorbent assay (ELISA) protocol technique. Results: The 14-3-3 levels varied markedly across various molecular subtypes. The most elevated levels of 14-3-3 protein were observed in the frequently occurring and classical subtypes, whereas the levels were significantly lower in the subtypes with long disease duration and atypical clinical presentation. PRNP codon 129 genotype, PrPsc isotype, disease stage and clinical subtype influenced the 14-3-3 level and the test sensitivity. Conclusions: The 14-3-3 protein levels differ across molecular subtypes and might be used for their early pre-mortem identification when the codon 129 genotype is known, especially for the less common molecular subtypes such as MV2 and MM2. (C) 2008 Elsevier Inc. All fights reserved."],["dc.identifier.doi","10.1016/j.neurobiolaging.2008.01.007"],["dc.identifier.isi","000270374000013"],["dc.identifier.pmid","18328602"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56099"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","1558-1497"],["dc.relation.issn","0197-4580"],["dc.title","14-3-3 CSF levels in sporadic Creutzfeldt-Jakob disease differ across molecular subtypes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","87"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Prion"],["dc.bibliographiccitation.lastpage","93"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Kiesel, Petra"],["dc.contributor.author","Gibson, Toby J."],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Bodemer, Monika"],["dc.contributor.author","Kaup, Franz-Josef"],["dc.contributor.author","Bodemer, Walter"],["dc.contributor.author","Zischler, Hans"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2022-10-06T13:26:54Z"],["dc.date.available","2022-10-06T13:26:54Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.4161/pri.4.2.11965"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/115196"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.eissn","1933-690X"],["dc.relation.issn","1933-6896"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.title","Transcription of Alu DNA elements in blood cells of sporadic Creutzfeldt-Jakob disease (sCJD)"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]