Steinacker, Petra

[["dc.bibliographiccitation.firstpage","919"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","927"],["dc.bibliographiccitation.volume","114"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Esselmann, Herrmann"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T11:06:56Z"],["dc.date.available","2018-11-07T11:06:56Z"],["dc.date.issued","2007"],["dc.description.abstract","To evaluate variations in amyloid beta (A beta) peptide pattern in cerebrospinal fluid (CSF) in neurodegenerative disorders. A recently estabfished quantitative urea-based A beta-sodium-dodecylsulfate-polyacrylamide-gel-electrophoresis with western immunoblot (AP-SDS-PAGE/immunoblot) revealed a highly conserved A beta peptide (A beta 1-37, 1-38, 1-39, 1-40, 1-42) pattern in CSF. We asked whether the variation might be useful to further elucidate the overlap between or distinctions among neurodegenerative diseases in A beta-processing. We used the A beta-SDS-PAGE/immunoblot to investigate CSF for diseasespecific A beta peptide patterns. CSF samples from 96 patients with mainly clinically diagnosed Alzheimer's disease (n = 15), progressive supranuclear palsy (n = 20), corticobasal degeneration (n =: 12), Parkinson's disease (n = 11), multiple systems atrophy (n = 18), and dementia with Lewy-bodies (n = 20) were analysed as well a comparison group (n = 19). The A beta peptide patterns varied between tauopathies and synucleinopathies and between all diseases and the comparison group, possibly due to the influence of tau and a-synuctein on Ap-processing."],["dc.identifier.doi","10.1007/s00702-007-0629-4"],["dc.identifier.isi","000248001800007"],["dc.identifier.pmid","17318305"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52433"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","0300-9564"],["dc.title","Tauopathies and synucleinopathies: Do cerebrospinal fluid beta-amyloid peptides reflect disease-specific pathogenesis?"],["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.issue","1"],["dc.bibliographiccitation.journal","Alzheimer's Research & Therapy"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Halbgebauer, Steffen"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Riedel, Daniel"],["dc.contributor.author","Oeckl, Patrick"],["dc.contributor.author","Anderl-Straub, Sarah"],["dc.contributor.author","Lombardi, Jolina"],["dc.contributor.author","von Arnim, Christine A. F."],["dc.contributor.author","Nagl, Magdalena"],["dc.contributor.author","Giese, Armin"],["dc.contributor.author","Ludolph, Albert C."],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2022-12-01T08:31:24Z"],["dc.date.available","2022-12-01T08:31:24Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract\n \n Background\n Visinin-like protein 1 (VILIP-1) belongs to the group of emerging biomarkers with the potential to support the early diagnosis of Alzheimer’s disease (AD). However, studies investigating the differential diagnostic potential in cerebrospinal fluid (CSF) are rare and are not available for blood.\n \n \n Methods\n We set up a novel, sensitive single molecule array (Simoa) assay for the detection of VILIP-1 in CSF and serum. In total, paired CSF and serum samples from 234 patients were investigated: 73 AD, 18 behavioral variant frontotemporal dementia (bvFTD), 26 parkinsonian syndromes, 20 amyotrophic lateral sclerosis (ALS), 22 Creutzfeldt-Jakob disease (CJD), and 75 non-neurodegenerative control (Con) patients. The differential diagnostic potential of CSF and serum VILIP-1 was assessed using the receiver operating characteristic curve analysis and findings were compared to core AD biomarkers.\n \n \n Results\n \n CSF and serum VILIP-1 levels correlated weakly (\n r\n =0.32 (CI: 0.20–0.43),\n p\n <0.0001). VILIP-1 concentrations in CSF and serum were elevated in AD compared to Con (\n p\n <0.0001 and\n p\n <0.01) and CJD (\n p\n <0.0001 for CSF and serum), and an increase in CSF was observed already in early AD stages (\n p\n <0.0001). In the discrimination of AD versus Con, we could demonstrate a strong diagnostic potential for CSF VILIP-1 alone (area under the curve (AUC): 0.87), CSF VILIP-1/CSF Abeta 1-42 (AUC: 0.98), and serum VILIP-1/CSF Abeta 1-42 ratio (AUC: 0.89).\n \n \n \n Conclusions\n We here report on the successful establishment of a novel Simoa assay for VILIP-1 and illustrate the potential of CSF and serum VILIP-1 in the differential diagnosis of AD with highest levels in CJD."],["dc.description.sponsorship","Intramural funding University of Ulm"],["dc.description.sponsorship","EU Joint Programme-Neurodegenerative Diseases networks Genfi-Prox"],["dc.description.sponsorship","German Federal Ministry of Education and Research"],["dc.description.sponsorship","EU (Moodmarker) program"],["dc.description.sponsorship","German Research Foundation/DFG"],["dc.description.sponsorship","Foundation of the state Baden-Württemberg"],["dc.description.sponsorship","Boehringer Ingelheim Ulm University BioCenter"],["dc.description.sponsorship","Thierry Latran Foundation"],["dc.description.sponsorship","Martin-Luther-Universität Halle-Wittenberg"],["dc.identifier.doi","10.1186/s13195-022-01122-4"],["dc.identifier.pii","1122"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118163"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-621"],["dc.relation.eissn","1758-9193"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Visinin-like protein 1 levels in blood and CSF as emerging markers for Alzheimer’s and other neurodegenerative diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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","387"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Biochemical Society Transactions"],["dc.bibliographiccitation.lastpage","391"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Baxter, H. C."],["dc.contributor.author","Fraser, J. R."],["dc.contributor.author","Liu, W.-G."],["dc.contributor.author","Forster, J. L."],["dc.contributor.author","Clokie, S."],["dc.contributor.author","Steinacker, P."],["dc.contributor.author","Otto, M."],["dc.contributor.author","Bahn, E."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Aitken, A."],["dc.date.accessioned","2017-09-07T11:44:41Z"],["dc.date.available","2017-09-07T11:44:41Z"],["dc.date.issued","2002"],["dc.description.abstract","14-3-3 proteins are involved in signalling processes in neuronal cells. Using isoform-specific antibodies we have examined the variation in 14-3-3 isoform neurolocation in normal and scrapie-infected murine brain and show that in defined areas of the brain there are significant changes associated with the pathology of the disease process. The appearance of 14-3-3 proteins in the cerebrospinal fluid (CSF) is a consequence of neuronal disease and the detection of specific isoforms of the 14-3-3 proteins in the CSF is characteristic of some neurodegenerative diseases. In this study, monitoring specifically for theγ 14-3-3 isoform in the CSF by both Western-blot analysis and ELISA we can show a level of correlation between the assays."],["dc.identifier.doi","10.1042/bst0300387"],["dc.identifier.gro","3151722"],["dc.identifier.pmid","12196100"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8543"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0300-5127"],["dc.title","Specific 14-3-3 isoform detection and immunolocalization in prion diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e10079"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Jesse, Sarah"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Lehnert, Stefan"],["dc.contributor.author","Sdzuj, Martin"],["dc.contributor.author","Cepek, Lukas"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Schmidt, Holger"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T08:44:10Z"],["dc.date.available","2018-11-07T08:44:10Z"],["dc.date.issued","2010"],["dc.description.abstract","Background: The discrimination of bacterial meningitis (BM) versus viral meningitis (VM) shapes up as a problem, when laboratory data are not equivocal, in particular, when Gram stain is negative. Methodology/Principal Findings: With the aim to determine reliable marker for bacterial or viral meningitis, we subjected cerebrospinal fluid (CSF) to a quantitative proteomic screening. By using a recently established 2D-DIGE protocol which was adapted to the individual CSF flow, we compared a small set of patients with proven BM and VM. Thereby, we identified six potential biomarkers out of which Prostaglandin-H2 D-isomerase was already described in BM, showing proof of concept. In the subsequent validation phase on a more comprehensive collective of 80 patients, we could validate that in BM high levels of glial fibrillary acidic protein (GFAP) and low levels of soluble amyloid precursor protein alpha/beta (sAPP alpha/beta) are present as possible binding partner of Fibulin-1. Conclusions/Significance: We conclude that our CSF flow-adapted 2D-DIGE protocol is valid especially in comparing samples with high differences in total protein and suppose that GFAP and sAPP alpha/beta have a high potential as additional diagnostic markers for differentiation of BM from VM. In the clinical setting, this might lead to an improved early diagnosis and to an individual therapy."],["dc.identifier.doi","10.1371/journal.pone.0010079"],["dc.identifier.isi","000276482000014"],["dc.identifier.pmid","20386697"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6922"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20140"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","A Proteomic Approach for the Diagnosis of Bacterial Meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","351"],["dc.bibliographiccitation.issue","5-6"],["dc.bibliographiccitation.journal","Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration"],["dc.bibliographiccitation.lastpage","356"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Feneberg, Emily"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Lehnert, Stefan"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Walther, Paul"],["dc.contributor.author","Thal, Dietmar Rudolf"],["dc.contributor.author","Linsenmeier, Miriam"],["dc.contributor.author","Ludolph, Albert C."],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T09:36:05Z"],["dc.date.available","2018-11-07T09:36:05Z"],["dc.date.issued","2014"],["dc.description.abstract","TAR DNA-binding protein 43 (TDP-43) is one of the neuropathological hallmarks in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). It is present in patients' blood and cerebrospinal fluid (CSF); however, the source and clinical relevance of TDP-43 measurements in body fluids is uncertain. We investigated paired CSF and serum samples, blood lymphocytes, brain urea fractions and purified exosomes from CSF for TDP-43 by one-(1D), and two-dimensional (2D) Western immunoblotting (WB) and quantitative mass spectrometry (MRM) in patients with ALS, FTLD and non-neurodegenerative diseases. By means of 2D-WB we were able to demonstrate a similar isoform pattern of TDP-43 in lymphocytes, serum and CSF in contrast to that of brain urea fractions with TDP-43 pathology. We found that the TDP-43 CSF to blood concentration ratio is about 1:200. As a possible brain specific fraction we found TDP-43 in exosome preparations from CSF by immunoblot and MRM. We conclude that TDP-43 in CSF originates mainly from blood. Measurements of TDP-43 in CSF and blood are of minor importance as a diagnostic tool, but may be important for monitoring therapy effects of TDP-43 modifying drugs."],["dc.identifier.doi","10.3109/21678421.2014.905606"],["dc.identifier.isi","000340827800004"],["dc.identifier.pmid","24834468"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32530"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Informa Healthcare"],["dc.relation.issn","2167-9223"],["dc.relation.issn","2167-8421"],["dc.title","Limited role of free TDP-43 as a diagnostic tool in neurodegenerative diseases"],["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","175628641984605"],["dc.bibliographiccitation.journal","Therapeutic Advances in Neurological Disorders"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Wurster, Claudia D."],["dc.contributor.author","Günther, René"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Dreyhaupt, Jens"],["dc.contributor.author","Wollinsky, Kurt"],["dc.contributor.author","Uzelac, Zeljko"],["dc.contributor.author","Witzel, Simon"],["dc.contributor.author","Kocak, Tugrul"],["dc.contributor.author","Winter, Benedikt"],["dc.contributor.author","Koch, Jan C."],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Petri, Susanne"],["dc.contributor.author","Ludolph, Albert C."],["dc.contributor.author","Hermann, Andreas"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2020-12-10T18:38:37Z"],["dc.date.available","2020-12-10T18:38:37Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1177/1756286419846058"],["dc.identifier.eissn","1756-2864"],["dc.identifier.issn","1756-2864"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16746"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77390"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","Neurochemical markers in CSF of adolescent and adult SMA patients undergoing nusinersen treatment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","36"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","44"],["dc.bibliographiccitation.volume","267"],["dc.contributor.author","Wurster, Claudia D."],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Günther, René"],["dc.contributor.author","Koch, Jan C."],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Uzelac, Zeljko"],["dc.contributor.author","Witzel, Simon"],["dc.contributor.author","Wollinsky, Kurt"],["dc.contributor.author","Winter, Benedikt"],["dc.contributor.author","Osmanovic, Alma"],["dc.contributor.author","Schreiber-Katz, Olivia"],["dc.contributor.author","Al Shweiki, Rami"],["dc.contributor.author","Ludolph, Albert C."],["dc.contributor.author","Petri, Susanne"],["dc.contributor.author","Hermann, Andreas"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2020-12-10T14:10:34Z"],["dc.date.available","2020-12-10T14:10:34Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1007/s00415-019-09547-y"],["dc.identifier.eissn","1432-1459"],["dc.identifier.issn","0340-5354"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70801"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Neurofilament light chain in serum of adolescent and adult SMA patients under treatment with nusinersen"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]