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","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","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","1498"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","1501"],["dc.bibliographiccitation.volume","251"],["dc.contributor.author","Bitsch, Annette"],["dc.contributor.author","Dressel, Alexander"],["dc.contributor.author","Meier, K."],["dc.contributor.author","Bogumil, T."],["dc.contributor.author","Deisenhammer, Florian"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Kitze, Bernd"],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Weber, F."],["dc.date.accessioned","2018-11-07T10:43:31Z"],["dc.date.available","2018-11-07T10:43:31Z"],["dc.date.issued","2004"],["dc.description.abstract","We conducted an open-labeled clinical trial of interferon beta-1b (IFNB) treatment in 20 patients with primary progressive multiple sclerosis (PPMS) and longitudinally monitored autoantibodies against double-stranded DNA (dsDNA), thyroid peroxidase (TPO),myelin basic protein (MBP), myelin oligodendrocyte glycoprotein (MOG), synapsin and S-100B. Before treatment, one patient had elevated TPO antibodies, four patients had elevated antibodies against S-100B, two patients against MOG or synapsin and one patient against MBP. In two patients we observed a continuous increase of dsDNA or TPO antibodies above the normal range. This rise paralleled IFNB treatment. In addition, 11 of 20 patients developed neutralizing antibodies against IFNB. There was no increase of autoantibodies directed against central nervous system antigens. Like patients with relapsing remitting or secondary progressive multiple sclerosis, PPMS patients may be at risk of an autoimmune response during IFNB treatment."],["dc.identifier.doi","10.1007/s00415-004-0580-3"],["dc.identifier.isi","000226302000010"],["dc.identifier.pmid","15645350"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47070"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0340-5354"],["dc.title","Autoantibody synthesis in primary progressive multiple sclerosis patients treated with interferon beta-1b"],["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","1224"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","1228"],["dc.bibliographiccitation.volume","250"],["dc.contributor.author","Yushchenko, M."],["dc.contributor.author","Mader, M."],["dc.contributor.author","Elitok, E."],["dc.contributor.author","Bitsch, Annette"],["dc.contributor.author","Dressel, Alexander"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Bogumil, T."],["dc.contributor.author","Kitze, Bernd"],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Weber, F."],["dc.date.accessioned","2018-11-07T10:35:52Z"],["dc.date.available","2018-11-07T10:35:52Z"],["dc.date.issued","2003"],["dc.description.abstract","Recent reports have shown that matrix-metalloproteinases (MMPs) facilitate T-cell migration into the CNS and play a role in disruption of the blood-brain-barrier and myelin breakdown. An increase of MMP-9 serum levels predicts disease activity in relapsing remitting multiple sclerosis (RRMS). Interferon-beta (IFN-beta), which is an established treatment for RRMS, inhibits T-cell migration in vitro in parallel with the downregulation of MMP expression. Only limited data are available for primary progressive multiple sclerosis (PPMS) which differs in demographic and immunological aspects as well as in MRI criteria from RRMS. In this study, 19 patients with laboratory-supported definite PPMS were treated with 8 x 10(6) IU IFN-beta1b (Betaferon(R)) subcutaneously every other day. Serum was collected before treatment and on months 1, 2, 3,6 and 9 during treatment. Levels of MMP-9 and of its natural inhibitor known as tissue-inhibitor of matrix-metalloproteinase-1 (TIMP-1) were quantified by ELISA. In addition MMP-2 serum levels were determined by zymography. 19 healthy volunteers served as controls. Before treatment serum levels of MMP-9 were elevated in patients with PPMS compared with controls, whereas there was no difference in TIMP-1 serum levels. During treatment with IFN-beta1b the concentration of MMP-9 in the serum of 18 out of 19 PPMS patients decreased, whereas serum levels of MMP-2 and TIMP-1 remained nearly unaffected. Our results demonstrate that the MMP-9 to TIMP-1 ratio in patients with PPMS is elevated in comparison with healthy controls. The suppression of MMP-9 by IFN-beta1b indicates that this drug is immunomodulatory active in PPMS patients. Further studies are necessary to test if IFN-beta exerts a beneficial effect in PPMS."],["dc.identifier.doi","10.1007/s00415-003-0191-4"],["dc.identifier.isi","000186231900015"],["dc.identifier.pmid","14586607"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45190"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0340-5354"],["dc.title","Interferon-beta-1b decreased matrix metalloproteinase-9 serum levels in primary progressive multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]