Steinacker, Petra

[["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","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","691"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","697"],["dc.bibliographiccitation.volume","118"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Roeber, Sigrun"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T08:56:27Z"],["dc.date.available","2018-11-07T08:56:27Z"],["dc.date.issued","2011"],["dc.description.abstract","Decreased levels of beta-amyloid (A beta) 1-42 in cerebrospinal fluid (CSF) are characteristic for Alzheimer's disease (AD) and are also evident in Creutzfeldt-Jakob disease (CJD). A beta plaques are thought to be responsible for this decrease in AD patients, whereas such A beta plaques are rarely seen in CJD. To investigate the A beta pattern in brain and CSF of neuropathologically confirmed CJD and AD patients we used an electrophoretic method to investigate A beta peptide fractions which are not accessible to ELISA and immunohistochemistry. We analyzed A beta peptides in the CSF of autopsy-confirmed CJD and AD patients and the corresponding brain homogenates using a quantitative urea-based A beta electrophoresis immunoblot (A beta-SDS-PAGE/immunoblot).The CSF A beta 1-42 decrease correlated with the brain A beta load in AD, but not in CJD. There was no difference in the soluble fractions of brain homogenate in AD and CJD. We therefore conclude that different mechanisms in AD and CJD are responsible for the A beta 1-42 decrease in the CSF."],["dc.identifier.doi","10.1007/s00702-010-0543-z"],["dc.identifier.isi","000290542500006"],["dc.identifier.pmid","21210287"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8052"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23156"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","0300-9564"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Different CSF beta-amyloid processing in Alzheimer's and Creutzfeldt-Jakob disease"],["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.artnumber","e7624"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Linker, Ralf A."],["dc.contributor.author","Brechlin, Peter"],["dc.contributor.author","Jesse, Sarah"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Lee, D. H."],["dc.contributor.author","Asif, Abdul R."],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2019-07-09T11:52:40Z"],["dc.date.available","2019-07-09T11:52:40Z"],["dc.date.issued","2009-10-28"],["dc.description.abstract","The identification of new biomarkers is of high interest for the prediction of the disease course and also for the identification of pathomechanisms in multiple sclerosis (MS). To specify markers of the chronic disease phase, we performed proteome profiling during the later phase of myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalomyelitis (MOG-EAE, day 35 after immunization) as a model disease mimicking many aspects of secondary progressive MS. In comparison to healthy controls, high resolution 2 dimensional gel electrophoresis revealed a number of regulated proteins, among them glial fibrilary acidic protein (GFAP). Phase specific up-regulation of GFAP in chronic EAE was confirmed by western blotting and immunohistochemistry. Protein levels of GFAP were also increased in the cerebrospinal fluid of MS patients with specificity for the secondary progressive disease phase. In a next step, proteome profiling of an EAE model with enhanced degenerative mechanisms revealed regulation of alpha-internexin, syntaxin binding protein 1, annexin V and glutamate decarboxylase in the ciliary neurotrophic factor (CNTF) knockout mouse. The identification of these proteins implicate an increased apoptosis and enhanced axonal disintegration and correlate well the described pattern of tissue injury in CNTF -/- mice which involve oligodendrocyte (OL) apoptosis and axonal injury.In summary, our findings underscore the value of proteome analyses as screening method for stage specific biomarkers and for the identification of new culprits for tissue damage in chronic autoimmune demyelination."],["dc.format.extent","9"],["dc.identifier.doi","10.1371/journal.pone.0007624"],["dc.identifier.fs","544326"],["dc.identifier.pmid","19865482"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5819"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60250"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.subject.ddc","610"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Apoptosis"],["dc.subject.mesh","Axons"],["dc.subject.mesh","Disease Models, Animal"],["dc.subject.mesh","Encephalomyelitis, Autoimmune, Experimental"],["dc.subject.mesh","Gene Expression Profiling"],["dc.subject.mesh","Gene Expression Regulation"],["dc.subject.mesh","Mice"],["dc.subject.mesh","Mice, Inbred C57BL"],["dc.subject.mesh","Mice, Transgenic"],["dc.subject.mesh","Multiple Sclerosis"],["dc.subject.mesh","Oligodendroglia"],["dc.subject.mesh","Proteome"],["dc.subject.mesh","Proteomics"],["dc.subject.mesh","Time Factors"],["dc.title","Proteome profiling in murine models of multiple sclerosis: identification of stage specific markers and culprits for tissue damage."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e48783"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Jesse, Sarah"],["dc.contributor.author","Lehnert, Stefan"],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Parnetti, Lucilla"],["dc.contributor.author","Soininen, Hilkka"],["dc.contributor.author","Herukka, Sanna-Kaisa"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Tawfik, Saskia"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","von Arnim, Christine A. F."],["dc.contributor.author","Neumann, Manuela"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Kulaksiz, Hasan"],["dc.contributor.author","Lenter, Martin"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Ferger, Boris"],["dc.contributor.author","Hengerer, Bastian"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2019-07-09T11:53:59Z"],["dc.date.available","2019-07-09T11:53:59Z"],["dc.date.issued","2012-11-08"],["dc.description.abstract","The prevalence of Parkinson’s disease (PD) increases with age. Up to 50% of PD show cognitive decline in terms of a mild cognitive impairment already in early stages that predict the development of dementia, which can occur in up to 80% of PD patients over the long term, called Parkinson’s disease dementia (PDD). So far, diagnosis of PD/PDD is made according to clinical and neuropsychological examinations while laboratory data is only used for exclusion of other diseases. The aim of this study was the identification of possible biomarkers in cerebrospinal fluid (CSF) of PD, PDD and controls (CON) which predict the development of dementia in PD. For this, a proteomic approach optimized for CSF was performed using 18 clinically well characterized patients in a first step with subsequent validation using 84 patients. Here, we detected differentially sialylated isoforms of Serpin A1 as marker for differentiation of PD versus PDD in CSF. Performing 2Dimmunoblots, all PDD patients could be identified correctly (sensitivity 100%). Ten out of 24 PD patients showed Serpin A1 isoforms in a similar pattern like PDD, indicating a specificity of 58% for the test-procedure. In control samples, no additional isoform was detected. On the basis of these results, we conclude that differentially sialylated products of Serpin A1 are an interesting biomarker to indicate the development of a dementia during the course of PD."],["dc.format.extent","10"],["dc.identifier.doi","10.1371/journal.pone.0048783"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8304"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60545"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Differential Sialylation of Serpin A1 in the Early Diagnosis of Parkinson’s Disease Dementia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","33"],["dc.bibliographiccitation.journal","Cortex"],["dc.bibliographiccitation.lastpage","40"],["dc.bibliographiccitation.volume","117"],["dc.contributor.author","Albrecht, Franziska"],["dc.contributor.author","Mueller, Karsten"],["dc.contributor.author","Ballarini, Tommaso"],["dc.contributor.author","Lampe, Leonie"],["dc.contributor.author","Diehl-Schmid, Janine"],["dc.contributor.author","Fassbender, Klaus"],["dc.contributor.author","Fliessbach, Klaus"],["dc.contributor.author","Jahn, Holger"],["dc.contributor.author","Jech, Robert"],["dc.contributor.author","Kassubek, Jan"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Landwehrmeyer, Bernhard"],["dc.contributor.author","Lauer, Martin"],["dc.contributor.author","Ludolph, Albert C."],["dc.contributor.author","Lyros, Epameinondas"],["dc.contributor.author","Prudlo, Johannes"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Synofzik, Matthis"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Danek, Adrian"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Schroeter, Matthias L."],["dc.contributor.author","Anderl-Straub, Sarah"],["dc.contributor.author","Brüggen, Katharina"],["dc.contributor.author","Fischer, Marie"],["dc.contributor.author","Förstl, Hans"],["dc.contributor.author","Hammer, Anke"],["dc.contributor.author","Homola, György"],["dc.contributor.author","Just, Walter"],["dc.contributor.author","Levin, Johannes"],["dc.contributor.author","Marroquin, Nicolai"],["dc.contributor.author","Marschhauser, Anke"],["dc.contributor.author","Nagl, Magdalena"],["dc.contributor.author","Oberstein, Timo"],["dc.contributor.author","Polyakova, Maryna"],["dc.contributor.author","Pellkofer, Hannah"],["dc.contributor.author","Richter-Schmidinger, Tanja"],["dc.contributor.author","Rossmeier, Carola"],["dc.contributor.author","Schuemberg, Katharina"],["dc.contributor.author","Semler, Elisa"],["dc.contributor.author","Spottke, Annika"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Thöne-Otto, Angelika"],["dc.contributor.author","Uttner, Ingo"],["dc.contributor.author","Zech, Heike"],["dc.date.accessioned","2020-12-10T14:23:17Z"],["dc.date.available","2020-12-10T14:23:17Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.cortex.2019.02.015"],["dc.identifier.issn","0010-9452"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16567"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71890"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Unraveling corticobasal syndrome and alien limb syndrome with structural brain imaging"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Halbgebauer, Steffen"],["dc.contributor.author","Nagl, Magdalena"],["dc.contributor.author","Klafki, Hans"],["dc.contributor.author","Haußmann, Ute"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Oeckl, Patrick"],["dc.contributor.author","Kassubek, Jan"],["dc.contributor.author","Pinkhardt, Elmar"],["dc.contributor.author","Ludolph, Albert C."],["dc.contributor.author","Soininen, Hilkka"],["dc.contributor.author","Herukka, Sanna-Kaisa"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2017-09-07T11:44:30Z"],["dc.date.available","2017-09-07T11:44:30Z"],["dc.date.issued","2016"],["dc.description.abstract","Early detection of dementia in Parkinson disease is a prerequisite for preventive therapeutic approaches. Modified serpinA1 in cerebrospinal fluid (CSF) was suggested as an early biomarker for differentiation between Parkinson patients with (PDD) or without dementia (PD). Within this study we aimed to further explore the diagnostic value of serpinA1. We applied a newly developed nanoscale method for the detection of serpinA1 based on automated capillary isoelectric focusing (CIEF). A clinical sample of 102 subjects including neurologically healthy controls (CON), PD and PDD patients was investigated. Seven serpinA1 isoforms of different charge were detected in CSF from all three diagnostic groups. The mean CSF signals of the most acidic serpinA1 isoform differed significantly (p < 0.01) between PDD (n = 29) and PD (n = 37) or CON (n = 36). Patients above the cut-off of 6.4 have a more than six times higher risk for an association with dementia compared to patients below the cut off. We propose this serpinA1 CIEF-immunoassay as a novel tool in predicting cognitive impairment in PD patients and therefore for patient stratification in therapeutic trials."],["dc.identifier.doi","10.1038/srep26145"],["dc.identifier.gro","3151674"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13360"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8492"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","public"],["dc.notes.submitter","chake"],["dc.relation.issn","2045-2322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Modified serpinA1 as risk marker for Parkinson’s disease dementia: Analysis of baseline data"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]