Ciesielczyk, Barbara

[["dc.bibliographiccitation.firstpage","139"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neurodegenerative Diseases"],["dc.bibliographiccitation.lastpage","144"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Gawinecka, Joanna"],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Sanchez-Juan, Pascual"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Heinemann, Uta"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:15:34Z"],["dc.date.available","2018-11-07T09:15:34Z"],["dc.date.issued","2012"],["dc.description.abstract","Background:The detection of a 14-3-3 elevated level in cerebrospinal fluid (CSF) is a part of the diagnostic criteria for probable sporadic Creutzfeldt-Jakob disease (sCJD), as defined by the WHO. However, some pathological conditions associated with acute neuronal damage may result in a positive 14-3-3 test and thereby reduce test specificity in sCJD. Objective: Desmoplakin has been previously identified as up-regulated CSF protein in sCJD and these studies aimed to investigate its diagnostic utility and compare it with two known CSF markers, 14-3-3 and tau. Methods and Results: We tested CSF levels of 14-3-3, tau and desmoplakin in 58 sCJD patients and 81 control patients including 45 cases with an elevated 14-3-3 level due to other disease than sCJD. We detected an elevated CSF level of desmoplakin in 78% of the sCJD patients, while 14-3-3 (88%) and tau (91%) showed a higher positive rate. However, the false positive rate of newly tested desmoplakin was significantly lower in comparison to 14-3-3 and tau, and it accounted for only 11% versus 56% and 35%, respectively. Further reduction of false positive rates was achieved by combination of elevated tau level with a positive desmoplakin test. Moreover, in the non-sCJD group, desmoplakin level did not correlate with the level of both above-mentioned CSF markers, whereas a clear correlation was observed in the sCJD group. Conclusion: Desmoplakin showed a low positive rate accompanied by a very low false positive rate. Thus, we conclude that desmoplakin is a promising candidate for supportive CSF marker to rule out 14-3-3 false positive cases in sCJD differential diagnosis. Copyright (C) 2011 S. Karger AG, Basel"],["dc.description.sponsorship","European Commission [KBBE-2007-2-4-06]"],["dc.identifier.doi","10.1159/000334499"],["dc.identifier.isi","000301700600004"],["dc.identifier.pmid","22213780"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9091"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27723"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","S. Karger AG"],["dc.relation.eissn","1660-2862"],["dc.relation.issn","1660-2854"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Desmoplakin as a Potential Candidate for Cerebrospinal Fluid Marker to Rule Out 14-3-3 False Positive Rates in Sporadic Creutzfeldt-Jakob Disease Differential Diagnosis"],["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","263"],["dc.bibliographiccitation.issue","5-6"],["dc.bibliographiccitation.journal","Neurodegenerative Diseases"],["dc.bibliographiccitation.lastpage","269"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Gmitterova, Karin"],["dc.contributor.author","Heinemann, U."],["dc.contributor.author","Gawinecka, Joanna"],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Valkovic, P."],["dc.contributor.author","Benetin, J."],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T08:35:12Z"],["dc.date.available","2018-11-07T08:35:12Z"],["dc.date.issued","2009"],["dc.description.abstract","Background: The 8-hydroxy-2 deoxyguanosine (8-OHdG) is a product of nucleoside oxidation of DNA and a reliable marker of oxidative stress markers. Increased levels of oxidative stress have been reported in the cerebrospinal fluid (CSF) of patients with various neurodegenerative disorders. Objective: In search of a biochemical indicator of Parkinson's disease (PD), we analyzed the levels 8-OHdG in the CSF of 99 patients, using ELISA to assess the differences between various neurodegenerative disorders. Results: Statistically significant higher CSF levels (p = 0.022) of 8-OHdG in non-demented PD patients as compared to the control group were observed. No differences between CSF 8-OHdG levels and age at the time of lumbar puncture, presence or severity of dementia, or gender were found. Conclusions: 8-OHdG levels could be potentially useful in the neurochemically supported diagnosis of PD. Copyright (C) 2009 S. Karger AG, Basel"],["dc.description.sponsorship","European Commission [SP5A-CT-2007-044438]"],["dc.identifier.doi","10.1159/000237221"],["dc.identifier.isi","000274466900008"],["dc.identifier.pmid","19955696"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9327"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18007"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1660-2854"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","8-OHdG in Cerebrospinal Fluid as a Marker of Oxidative Stress in Various Neurodegenerative Diseases"],["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","35"],["dc.bibliographiccitation.journal","BMC Neurology"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Boesenberg-Grosse, Constanze"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Bodemer, Monika"],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Krasnianski, Anna"],["dc.contributor.author","Bartl, Mario"],["dc.contributor.author","Heinemann, Uta"],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Eigenbrod, Sabina"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Green, Alison"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:14:53Z"],["dc.date.available","2018-11-07T09:14:53Z"],["dc.date.issued","2006"],["dc.description.abstract","Background: Brain derived proteins such as 14-3-3, neuron-specific enolase (NSE), S 100b, tau, phosphorylated tau and A beta(1-42) were found to be altered in the cerebrospinal fluid (CSF) in Creutzfeldt-Jakob disease (CJD) patients. The pathogenic mechanisms leading to these abnormalities are not known, but a relation to rapid neuronal damage is assumed. No systematic analysis on brain-derived proteins in the CSF and neuropathological lesion profiles has been performed. Methods: CSF protein levels of brain-derived proteins and the degree of spongiform changes, neuronal loss and gliosis in various brain areas were analyzed in 57 CJD patients. Results: We observed three different patterns of CSF alteration associated with the degree of cortical and subcortical changes. NSE levels increased with lesion severity of subcortical areas. Tau and 14-3-3 levels increased with minor pathological changes, a negative correlation was observed with severity of cortical lesions. Levels of the physiological form of the prion protein (PrPc) and A beta(1-42) levels correlated negatively with cortical pathology, most clearly with temporal and occipital lesions. Conclusion: Our results indicate that the alteration of levels of brain-derived proteins in the CSF does not only reflect the degree of neuronal damage, but it is also modified by the localization on the brain pathology. Brain specific lesion patterns have to be considered when analyzing CSF neuronal proteins."],["dc.identifier.doi","10.1186/1471-2377-6-35"],["dc.identifier.isi","000240991000001"],["dc.identifier.pmid","16989662"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/1372"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27536"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2377"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Brain-derived proteins in the CSF, do they correlate with brain pathology in CJD?"],["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"]]