Poser, Sigrid

[["dc.bibliographiccitation.firstpage","731"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","43"],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T10:28:17Z"],["dc.date.available","2018-11-07T10:28:17Z"],["dc.date.issued","2002"],["dc.identifier.doi","10.1007/s00108-002-0616-7"],["dc.identifier.isi","000176551100004"],["dc.identifier.pmid","12426728"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43393"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0020-9554"],["dc.title","Clinical aspects, diagnosis and some treatments of human prion diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","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","312"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","DMW - Deutsche Medizinische Wochenschrift"],["dc.bibliographiccitation.lastpage","317"],["dc.bibliographiccitation.volume","127"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Ruge, D."],["dc.contributor.author","Krause, G."],["dc.contributor.author","Mehnert, W. H."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Poser, Sigrid"],["dc.date.accessioned","2018-11-07T10:31:53Z"],["dc.date.available","2018-11-07T10:31:53Z"],["dc.date.issued","2002"],["dc.description.abstract","Objective: Analogous to prospective studies in other countries, prevalance and symptoms of sporadic Creutzfeldt-Jakob disease (CJD) were recorded in order to assess irregularities in the incidence of the disease in Germany since the onset of bovine spongioform encephalopathy (BSE). Patients and methods: Since 1993 all suspected case of CJD reported in the Federal Republic of Germany have been analysed by a unified schema and classified by standardised criteria. In addition to voluntary reporting two other systems were accessed: (1) compulsory reporting to the Robert Koch Institute via the appropriate Health Department and (2) cause of death statistics of the Federal Office of Statistics. Results: Between June 1993 and May 2001, a total of 1247 patients with suspected CJD, obtained by the >>Study of the epidemiology and early diagnosis of human spongioform encephalopathies<< at Gottingen University, were examined. The suspected disease was confirmed by autopsy in 404 cases, the diagnosis of probable CJD was made in 369 cases on the basis of clinical data and additional investigation. At the beginning of the Gottingen Study in 1993 the incidence in Germany was 0.7 per mill. population, while in the year 2000 it had risen to 1.3 per mill. population. Corresponding increases in the number of cases since 1993 have been noted also by the Robert Koch Institute and the Federal Office of Statistics. Conclusions: The increased incidence can be explained primarily by a decrease in previously unknown cases. Concerted action as part of the Gottingen Study has increased the cooperation of associated clinics. In addition to sporadic cases of CJD, genetic and, more rarely, iatrogenic forms have been seen in Germany. But no cases of new variant CJD have been reported so far."],["dc.identifier.doi","10.1055/s-2002-20150"],["dc.identifier.isi","000173968100002"],["dc.identifier.pmid","11845386"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44217"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","0012-0472"],["dc.title","Epidemiology and clinical symptomatology 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","2348"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","2359"],["dc.bibliographiccitation.volume","127"],["dc.contributor.author","Pocchiari, Mauricio"],["dc.contributor.author","Puopolo, M."],["dc.contributor.author","Croes, E. A."],["dc.contributor.author","Budka, H."],["dc.contributor.author","Gelpi, Elena"],["dc.contributor.author","Collins, S."],["dc.contributor.author","Lewis, V."],["dc.contributor.author","Sutcliffe, T."],["dc.contributor.author","Guilivi, A."],["dc.contributor.author","Delasnerie-Laupretre, N."],["dc.contributor.author","Brandel, Jean-Philippe"],["dc.contributor.author","Alperovitch, Annick"],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Ladogana, Anna"],["dc.contributor.author","Rietvald, I."],["dc.contributor.author","Mitrova, Eva"],["dc.contributor.author","Martinez-Martin, P."],["dc.contributor.author","de Pedro-Cuesta, Jesus"],["dc.contributor.author","Glatzel, Markus"],["dc.contributor.author","Aguzzi, A."],["dc.contributor.author","Cooper, S."],["dc.contributor.author","Mackenzie, Jan"],["dc.contributor.author","van Duijn, C. M."],["dc.contributor.author","Will, Robert G."],["dc.date.accessioned","2018-11-07T10:45:02Z"],["dc.date.available","2018-11-07T10:45:02Z"],["dc.date.issued","2004"],["dc.description.abstract","A collaborative study of human transmissible spongiform encephalopathies has been carried out from 1993 to 2000 and includes data from 10 national registries, the majority in Western Europe. In this study, we present analyses of predictors of survival in sporadic (n = 2304), iatrogenic (n = 106) and variant Creutzfeldt-Jakob disease (n = 86) and in cases associated with mutations of the prion protein gene (n = 278), including Gerstmann-Straussler-Scheinker syndrome (n = 24) and fatal familial insomnia (n = 41). Overall survival for each disease type was assessed by the Kaplan-Meier method and the multivariate analyses by the Cox proportional hazards model. In sporadic disease, longer survival was correlated with younger age at onset of illness, female gender, codon 129 heterozygosity, presence of CSF 14-3-3 protein and type 2a prion protein type. The ability to predict survival based on patient covariates is important for diagnosis and counselling, and the characterization of the survival distributions, in the absence of therapy, will be an important starting point for the assessment of potential therapeutic agents in the future."],["dc.identifier.doi","10.1093/brain/awh249"],["dc.identifier.isi","000224082400020"],["dc.identifier.pmid","15361416"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47403"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.title","Predictors of survival in sporadic Creutzfeldt-Jakob disease and other human transmissible spongiform encephalopathies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","747"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Journal of Clinical Epidemiology"],["dc.bibliographiccitation.lastpage","754"],["dc.bibliographiccitation.volume","53"],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Brandel, Jean-Philippe"],["dc.contributor.author","Masullo, C."],["dc.contributor.author","Wientjens, D."],["dc.contributor.author","de Silva, Rohan"],["dc.contributor.author","Zeidler, M."],["dc.contributor.author","Granieri, E."],["dc.contributor.author","Sampaolo, S."],["dc.contributor.author","van Duijn, Cornelia M."],["dc.contributor.author","Delasnerie-Laupretre, N."],["dc.contributor.author","Will, Rainer"],["dc.contributor.author","Poser, Sigrid"],["dc.date.accessioned","2018-11-07T10:41:33Z"],["dc.date.available","2018-11-07T10:41:33Z"],["dc.date.issued","2000"],["dc.description.abstract","Medical risk factors for Creutzfeldt-Jakob disease (CJD) were analyzed in a prospective ongoing case-control study based on European CJD surveillance. Detailed data on past and recent medical history were analyzed in 405 cases and controls matched by sex, age, and hospital. Data were correlated with polymorphism at codon 129 of the prion protein gene. Our analysis did not support a number of previously reported associations and failed to identify any common medical risk factor for CJD. Although not statistically significant, brain surgery was associated with an increased risk of CJD. A detailed medical history should be obtained in every suspected CJD case in order to identify iatrogenic sources of CJD. (C) 2000 Elsevier Science Inc. All rights reserved."],["dc.identifier.doi","10.1016/S0895-4356(99)00207-3"],["dc.identifier.isi","000088519500013"],["dc.identifier.pmid","10941953"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46565"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","0895-4356"],["dc.title","European surveillance on Creutzfeldt-Jakob disease: a case-control study for medical risk factors"],["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","699"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","705"],["dc.bibliographiccitation.volume","249"],["dc.contributor.author","Henkel, K."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Hertel, A."],["dc.contributor.author","Gratz, K. F."],["dc.contributor.author","Schroter, A."],["dc.contributor.author","Tschampa, Henriette J."],["dc.contributor.author","Bihl, H."],["dc.contributor.author","Bull, U."],["dc.contributor.author","Grunwald, F."],["dc.contributor.author","Drzezga, A."],["dc.contributor.author","Spitz, J."],["dc.contributor.author","Poser, Sigrid"],["dc.date.accessioned","2018-11-07T10:29:01Z"],["dc.date.available","2018-11-07T10:29:01Z"],["dc.date.issued","2002"],["dc.description.abstract","The aim of this study was to explore the sites of metabolic changes with [F-18]2-fluoro-2-desoxy-D-glucose (FDG) and positron emission tomography (PET) in patients with Creutzfeldt-Jakob disease and to correlate the findings with clinical symptoms. Static [F-18]FDG-PET studies of eight patients with the diagnosis of confirmed or probable CJD were retrospectively analysed by two physicians from departments of nuclear medicine independently with a strong interrater agreement (kappa=0,98). The clinical data of the patients, based on a standardized evaluation by physicians from the German Creutzfeldt-Jakob disease surveillance study, was correlated with the PET findings. [F-18]FDG-PET shows widespread hypometabolism in CJD. All patients had a reduction of cerebral glucose metabolism in at least one temporal or parietal region. Additionally in 7 of our own 8 cases and 3 of 4 cases from the literature the occipital lobe, the cerebellum or the basal ganglia were involved. These findings differ from typical patterns of hypometabolism in Alzheimer's disease and other neurodegenerative disorders. In two thirds of the cases the distribution was markedly asymmetric. Myoclonus was present in five out of our eight own cases. Our data suggest that myoclonus might correlate with metabolic impairment of contralateral parietal and temporal lobes. In three of four patients with visual symptoms FDG uptake was reduced in the visual cortex bilaterally. Typical hyperintensities on MRI were only found in two of the eight cases at the time of PET-studies. Our results demonstrate that [F-18]FDG-PET appears to be a sensitive investigation in CJD and could be useful to differentiate CJD from other neuro degenerative disorders."],["dc.identifier.doi","10.1007/s00415-002-0695-3"],["dc.identifier.isi","000176407100008"],["dc.identifier.pmid","12111302"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43553"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0340-5354"],["dc.title","Positron emission tomography with [F-18]FDG in the diagnosis of Creutzfeldt-Jakob disease (CJD)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","91"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Der Nervenarzt"],["dc.bibliographiccitation.lastpage","95"],["dc.bibliographiccitation.volume","71"],["dc.contributor.author","Kropp, Silke"],["dc.contributor.author","Finkenstaedt, M."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Schroter, A."],["dc.contributor.author","Poser, Sigrid"],["dc.date.accessioned","2018-11-07T10:44:49Z"],["dc.date.available","2018-11-07T10:44:49Z"],["dc.date.issued","2000"],["dc.description.abstract","Today the diagnosis of Creutzfeldt-Jakob disease (UD) is proven only postmortem or by evidence of neuropathology. During the patient's lifetime EEG recordings or cerebrospinal fluid analysis may support the diagnosis. In most cases, T2-MRI scans show hyperintensities of the basal ganglia. A new imaging technique called diffusion-weighted MRI (DWI) has recently been established. The sensitivity of DWI was evaluated in five patients suspected of CJD. All five cases showed hyperintense signal changes in the basal ganglia on DWI sequences. These findings were more pronounced in DWI than in T2, FLAIR, or PD-weighted images. Thus, DWI seems to be the most sensitive sequence for detecting changes in patients with suspected UD. Moreover, its short scanning time ensures that fewer artifacts occur, especially in the case of myoclonus."],["dc.identifier.doi","10.1007/s001150070001"],["dc.identifier.isi","000085384700004"],["dc.identifier.pmid","10703009"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47357"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0028-2804"],["dc.title","Diffusion-weighted MRI in 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","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"]]