Gawinecka, Joanna

[["dc.bibliographiccitation.firstpage","719"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","The World Journal of Biological Psychiatry"],["dc.bibliographiccitation.lastpage","728"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Martins-De-Souza, Daniel"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Gawinecka, Joanna"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Turck, Christoph W."],["dc.date.accessioned","2018-11-07T08:41:14Z"],["dc.date.available","2018-11-07T08:41:14Z"],["dc.date.issued","2010"],["dc.description.abstract","Objectives. To identify proteins differentially expressed in schizophrenia patients, we collected 50 mu l cerebrospinal fluid from 17 first-episode schizophrenia patients and 10 healthy controls. Methods. Their proteins were separated by two-dimensional gel electrophoresis without using any depletion method and identified by mass spectrometry. Results. Approximately 550 spots were detected, six of which had significantly different intensities in schizophrenia compared to control specimens. We were able to validate in individual samples the upregulation of apolipoprotein E, apolipoprotein A1 and prostaglandin-H2 D-isomerase by Western blot analyses and detect the downregulation of transthyretin, TGF-beta receptor type-1 and coiled-coil domain-containing protein 3 precursor. Conclusions. These findings may help to elucidate the disease mechanisms and confirm the hypothesis of disturbed cholesterol and phospholipid metabolism in schizophrenia, and thus reveal the final role players. Moreover, a grouped protein expression analysis of apolipoprotein E, apolipoprotein A-I, and prostaglandin-H2 D-isomerase in cerebrospinal fluid from patients might be a potential diagnostic tool for schizophrenia."],["dc.identifier.doi","10.3109/15622971003758748"],["dc.identifier.isi","000280009300005"],["dc.identifier.pmid","20446881"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19420"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Informa Healthcare"],["dc.relation.issn","1562-2975"],["dc.title","Different apolipoprotein E, apolipoprotein A1 and prostaglandin-H2 D-isomerase levels in cerebrospinal fluid of schizophrenia patients and healthy controls"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1126"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","European Journal of Neurology"],["dc.bibliographiccitation.lastpage","1133"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Gmitterova, Karin"],["dc.contributor.author","Heinemann, U."],["dc.contributor.author","Krasnianski, Anna"],["dc.contributor.author","Gawinecka, Joanna"],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T10:13:56Z"],["dc.date.available","2018-11-07T10:13:56Z"],["dc.date.issued","2016"],["dc.description.abstract","Background and purpose: Cerebrospinal fluid (CSF) analysis supports the clinical diagnosis of sporadic Creutzfeldt-Jakob disease (sCJD) when applied within an adequate clinical context. A diagnostic potential has been attributed to CSF proteins such as 14-3-3, but also tau protein, phosphorylated tau (181P) (p-tau) protein, amyloid beta(1-42), S100B and neuron-specific enolase (NSE). There has been only limited information available about the contribution of CSF analysis in the differentiation of various molecular sCJD subtypes. Methods: The CSF levels of the aforementioned proteins from 73 sCJD patients with distinct molecular subtypes were determined. Results: Differences in tau values were significant amongst the homozygous patients (MM and VV genotype) compared to the heterozygous group (P = 0.07 and P = 0.02 respectively). Significantly higher CSF tau levels (P = 0.003) and NSE (P = 0.02) but lower p-tau/tau ratio (P = 0.01) were observed in MM1 compared to MM2 patients. The p-tau/tau ratio enabled the differentiation of MV genotype with higher levels in PrPsc type 2 (P = 0.04). Elevation of S100B (P < 0.001) and NSE (P = 0.03) was observed in VV2 compared to VV1 subtype. PRNP codon 129 genotype, PrPsc isotype, disease duration and clinical stage influenced the test sensitivity in all proteins. Conclusions: Cerebrospinal fluid protein levels might be useful in the pre-mortem differentiation of molecular sCJD subtypes when the codon 129 genotype is known."],["dc.identifier.doi","10.1111/ene.12991"],["dc.identifier.isi","000375765000021"],["dc.identifier.pmid","27029507"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40525"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1468-1331"],["dc.relation.issn","1351-5101"],["dc.title","Cerebrospinal fluid markers in the differentiation of molecular subtypes of sporadic 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","1620"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","1628"],["dc.bibliographiccitation.volume","256"],["dc.contributor.author","Ladogana, Anna"],["dc.contributor.author","Sanchez-Juan, Pascual"],["dc.contributor.author","Mitrova, Eva"],["dc.contributor.author","Green, Alison"],["dc.contributor.author","Cuadrado-Corrales, Natividad"],["dc.contributor.author","Sanchez-Valle, Raquel"],["dc.contributor.author","Koscova, Silvia"],["dc.contributor.author","Aguzzi, Adriano"],["dc.contributor.author","Sklaviadis, Theodoros"],["dc.contributor.author","Kulczycki, Jerzy"],["dc.contributor.author","Gawinecka, Joanna"],["dc.contributor.author","Saiz, Albert"],["dc.contributor.author","Calero, Miguel"],["dc.contributor.author","van Duijn, Cornelia M."],["dc.contributor.author","Pocchiari, Maurizio"],["dc.contributor.author","Knight, Richard"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T11:23:52Z"],["dc.date.available","2018-11-07T11:23:52Z"],["dc.date.issued","2009"],["dc.description.abstract","The 14-3-3 protein test has been shown to support the clinical diagnosis of sporadic Creutzfeldt-Jakob disease (CJD) when associated with an adequate clinical context, and a high differential potential for the diagnosis of sporadic CJD has been attributed to other cerebrospinal fluid (CSF) proteins such as tau protein, S100b and neuron specific enolase (NSE). So far there has been only limited information available about biochemical markers in genetic transmissible spongiform encephalopathies (gTSE), although they represent 10-15% of human TSEs. In this study, we analyzed CSF of 174 patients with gTSEs for 14-3-3 (n = 166), tau protein (n = 78), S100b (n = 46) and NSE (n = 50). Levels of brain-derived proteins in CSF varied in different forms of gTSE. Biomarkers were found positive in the majority of gCJD (81%) and insert gTSE (69%), while they were negative in most cases of fatal familial insomnia (13%) and Gerstmann-Straussler-Scheinker syndrome (10%). Disease duration and codon 129 genotype influence the findings in a different way than in sporadic CJD."],["dc.identifier.doi","10.1007/s00415-009-5163-x"],["dc.identifier.isi","000270385400003"],["dc.identifier.pmid","19444528"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6745"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56280"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0340-5354"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Cerebrospinal fluid biomarkers in human genetic transmissible spongiform encephalopathies"],["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","3051"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","3061"],["dc.bibliographiccitation.volume","135"],["dc.contributor.author","Stoeck, Katharina"],["dc.contributor.author","Sanchez-Juan, Pascual"],["dc.contributor.author","Gawinecka, Joanna"],["dc.contributor.author","Green, Alison"],["dc.contributor.author","Ladogana, Anna"],["dc.contributor.author","Pocchiari, Maurizio"],["dc.contributor.author","Sanchez-Valle, Raquel"],["dc.contributor.author","Mitrova, Eva"],["dc.contributor.author","Sklaviadis, Theodor"],["dc.contributor.author","Kulczycki, Jerzy"],["dc.contributor.author","Slivarichova, Dana"],["dc.contributor.author","Saiz, Albert"],["dc.contributor.author","Calero, Miguel"],["dc.contributor.author","Knight, Richard"],["dc.contributor.author","Aguzzi, Adriano"],["dc.contributor.author","Laplanche, Jean-Louis"],["dc.contributor.author","Peoc'h, Katell"],["dc.contributor.author","Schelzke, Gabi"],["dc.contributor.author","Karch, Andre"],["dc.contributor.author","van Duijn, Cornelia M."],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:04:59Z"],["dc.date.available","2018-11-07T09:04:59Z"],["dc.date.issued","2012"],["dc.description.abstract","To date, cerebrospinal fluid analysis, particularly protein 14-3-3 testing, presents an important approach in the identification of Creutzfeldt-Jakob disease cases. However, one special point of criticism of 14-3-3 testing is the specificity in the differential diagnosis of rapid dementia. The constant observation of increased cerebrospinal fluid referrals in the national surveillance centres over the last years raises the concern of declining specificity due to higher number of cerebrospinal fluid tests performed in various neurological conditions. Within the framework of a European Community supported longitudinal multicentre study ('cerebrospinal fluid markers') we analysed the spectrum of rapid progressive dementia diagnoses, their potential influence on 14-3-3 specificity as well as results of other dementia markers (tau, phosphorylated tau and amyloid-beta(1-42)) and evaluated the specificity of 14-3-3 in Creutzfeldt-Jakob disease diagnosis for the years 1998-2008. A total of 29 022 cerebrospinal fluid samples were analysed for 14-3-3 protein and other cerebrospinal fluid dementia markers in patients with rapid dementia and suspected Creutzfeldt-Jakob disease in the participating centres. In 10 731 patients a definite diagnosis could be obtained. Protein 14-3-3 specificity was analysed for Creutzfeldt-Jakob disease with respect to increasing cerebrospinal fluid tests per year and spectrum of differential diagnosis. Ring trials were performed to ensure the comparability between centres during the reported time period. Protein 14-3-3 test specificity remained high and stable in the diagnosis of Creutzfeldt-Jakob disease during the observed time period across centres (total specificity 92%; when compared with patients with definite diagnoses only: specificity 90%). However, test specificity varied with respect to differential diagnosis. A high 14-3-3 specificity was obtained in differentiation to other neurodegenerative diseases (95-97%) and non-neurological conditions (91-97%). We observed lower specificity in the differential diagnoses of acute neurological diseases (82-87%). A marked and constant increase in cerebrospinal fluid test referrals per year in all centres did not influence 14-3-3 test specificity and no change in spectrum of differential diagnosis was observed. Cerebrospinal fluid protein 14-3-3 detection remains an important test in the diagnosis of Creutzfeldt-Jakob disease. Due to a loss in specificity in acute neurological events, the interpretation of positive 14-3-3 results needs to be performed in the clinical context. The spectrum of differential diagnosis of rapid progressive dementia varied from neurodegenerative dementias to dementia due to acute neurological conditions such as inflammatory diseases and non-neurological origin."],["dc.description.sponsorship","European Commission [QLG3-CT-2002-81606, 222887, 01ED1201A]"],["dc.identifier.doi","10.1093/brain/aws238"],["dc.identifier.isi","000310156700015"],["dc.identifier.pmid","23012332"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8382"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25223"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Cerebrospinal fluid biomarker supported diagnosis of Creutzfeldt-Jakob disease and rapid dementias: a longitudinal multicentre study over 10 years"],["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","758"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of neuropathology and experimental neurology"],["dc.bibliographiccitation.lastpage","767"],["dc.bibliographiccitation.volume","72"],["dc.contributor.author","Wemheuer, Wiebke M."],["dc.contributor.author","Wrede, Arne"],["dc.contributor.author","Gawinecka, Joanna"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.date.accessioned","2015-11-18T10:28:52Z"],["dc.date.accessioned","2021-10-27T13:20:22Z"],["dc.date.available","2015-11-18T10:28:52Z"],["dc.date.available","2021-10-27T13:20:22Z"],["dc.date.issued","2013-08-01"],["dc.description.abstract","In brain biopsies taken from patients with rapidly progressive dementia, the first differential diagnoses to be ruled out are prion diseases. For safe diagnostic processing of tissue and instruments, a rapid, highly sensitive, and specific analysis for prion aggregates is necessary. Here, we examined 16 brain biopsies and brain samples (frontal cortex and cerebellum) from 65 autopsies by Western blot, paraffin-embedded tissue (PET) blot, immunohistochemistry, and the recently described membrane adsorption assay (MAA) for their suitability to detect pathologic prion protein. In our hands, the PET blot method provided the highest sensitivity in prion detection (biopsies, 100%; all autopsy sections, 96.3%), closely followed by the MAA (biopsies, 100%; all autopsy samples, 96%) and Western blot analysis (biopsies, 100%; all autopsy samples, 92%). Conventional immunohistochemistry is the least sensitive method (biopsies, 50%; all autopsy sections, 80%) and also gave 1 false-positive biopsy result. Consequently, our standard diagnostic protocol is to use the MAA as a first step for detecting or excluding a prion disease, followed by the PET blot for the prion deposition pattern, Western blotting for prion typing, and immunohistochemistry for differential diagnoses. With this standard and the availability of unfixed tissue, a diagnosis was possible in all 16 biopsies examined."],["dc.description.sponsorship","VolkswagenStiftung [VWZ2168]; Prionscreen [FP6-2005-SSP-5A]"],["dc.format.extent","19"],["dc.identifier.doi","10.1097/NEN.0b013e31829d2799"],["dc.identifier.isi","000330383600005"],["dc.identifier.pmid","23860029"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12445"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/91960"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1554-6578"],["dc.relation.issn","0022-3069"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.mesh","Alzheimer Disease"],["dc.subject.mesh","Biopsy"],["dc.subject.mesh","Brain"],["dc.subject.mesh","Cell Membrane"],["dc.subject.mesh","Dementia"],["dc.subject.mesh","Female"],["dc.subject.mesh","Filtration"],["dc.subject.mesh","Frontotemporal Lobar Degeneration"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Male"],["dc.subject.mesh","Parkinson Disease"],["dc.subject.mesh","Positron-Emission Tomography"],["dc.subject.mesh","PrPSc Proteins"],["dc.subject.mesh","Prion Diseases"],["dc.subject.mesh","Prions"],["dc.subject.mesh","Sensitivity and Specificity"],["dc.title","Filtration of protein aggregates increases the accuracy for diagnosing prion diseases in brain biopsies."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","submitted_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","232"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Acta Neurologica Belgica"],["dc.bibliographiccitation.lastpage","236"],["dc.bibliographiccitation.volume","111"],["dc.contributor.author","Gabelic, Tereza"],["dc.contributor.author","Habek, Mario"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Gawinecka, Joanna"],["dc.contributor.author","Pavlisa, Goran"],["dc.contributor.author","Brinar, Vesna V."],["dc.date.accessioned","2018-11-07T08:52:01Z"],["dc.date.available","2018-11-07T08:52:01Z"],["dc.date.issued","2011"],["dc.description.abstract","Creutzfeld-Jacob disease (CJD) is a degenerative, invariably fatal brain disorder. Multiple sclerosis (MS) is a chronic, potentially disabling, immune-mediated inflammatory demyelinating disease of the central nervous system. Here, we report a 50-year-old woman who, two years after the diagnosis of relapsing remitting MS, developed altered consciousness, dystonic posture of the left hand and myoclonic jerks. Repeated brain MRI showed hyperintensities on T2 sequences in basal ganglia bilaterally and diffusion restriction in these areas, and, since typical EEG and CSF features were present, the diagnosis of CJD was made. To the best of our knowledge, this is the first report of a glatiramer acetate-treated MS patient who developed sporadic CJD. This combination is interesting in the light of recent data suggesting that CJD and MS may share similar mechanisms of \"molecular mimicry\" and autoimmunity. This case also emphasizes the importance of critically assessing every new symptom even in a patient with an established diagnosis of MS."],["dc.identifier.isi","000296995800014"],["dc.identifier.pmid","22141291"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22070"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Acta Medica Belgica"],["dc.relation.issn","0300-9009"],["dc.title","Sporadic CJD in a patient with relapsing-remitting multiple sclerosis on an immunomodulatory treatment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Prion"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Nowak, Martin"],["dc.contributor.author","Gawinecka, Joanna"],["dc.contributor.author","Carimalo, Julie"],["dc.contributor.author","Schutz-Schaeffer, Walter"],["dc.contributor.author","Asif, Abdul R."],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T08:42:00Z"],["dc.date.available","2018-11-07T08:42:00Z"],["dc.date.issued","2010"],["dc.format.extent","177"],["dc.identifier.isi","000285872300169"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19599"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.publisher.place","Austin"],["dc.relation.issn","1933-6896"],["dc.title","Proteomic Analysis of Synaptosomes from Patients with Sporadic Creutzfeldt-Jakob Disease"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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","461"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","470"],["dc.bibliographiccitation.volume","270"],["dc.contributor.author","Gmitterová, Karin"],["dc.contributor.author","Gawinecka, Joanna"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Varges, Daniela"],["dc.contributor.author","Valkovič, Peter"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2020-12-10T14:10:31Z"],["dc.date.available","2020-12-10T14:10:31Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1007/s00406-018-0928-9"],["dc.identifier.eissn","1433-8491"],["dc.identifier.issn","0940-1334"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70785"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Cerebrospinal fluid markers analysis in the differential diagnosis of dementia with Lewy bodies and Parkinson’s disease dementia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1640"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Neuroscience"],["dc.bibliographiccitation.lastpage","1650"],["dc.bibliographiccitation.volume","169"],["dc.contributor.author","Weiss, Elisabeth"],["dc.contributor.author","Ramljak, Sanja"],["dc.contributor.author","Asif, Abdul Rahman"],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Schmitz, M."],["dc.contributor.author","Gawinecka, Joanna"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Behrens, C."],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T08:39:11Z"],["dc.date.available","2018-11-07T08:39:11Z"],["dc.date.issued","2010"],["dc.description.abstract","The definite physiological role of the cellular prion protein (PrPc) remains elusive. There is ample in vitro and in vivo evidence suggesting a neuroprotective role for PrPc. On the other hand, several in vitro and in vivo studies demonstrated detrimental effects of PrPc overexpression through activation of a p53 pathway. Recently, we reported that transient overexpression of PrPc in human embryonic kidney 293 cells elicits proteome expression changes which point to deregulation of proteins involved in energy metabolism and cellular homeostasis. Here we report proteome expression changes following stable PrPc overexpression in human neuronal SH-SY5Y cells. In total 18 proteins that are involved in diverse biological processes were identified as differentially regulated. The majority of these proteins is involved in cell signaling, cytoskeletal organization and protein folding. Annexin V exhibited a several fold up-regulation following stable PrPc overexpression in SH-SY5Y cells. This finding has been reproduced in alternative, mouse N2a and human SK-N-LO neuroblastoma cell lines transiently overexpressing PrPc. Annexin V plays an important role in maintenance of calcium homeostasis which when disturbed can activate a p53-dependent cell death. Although we did not detect changes in p53 expression between PrPc overexpressing SH-SY5Y and control cells, deregulation of several proteins including annexin V, polyglutamine tract-binding protein-1, spermine synthase and transgelin 2 indicates disrupted cellular equilibrium. We conclude that stable PrPc overexpression in SH-SY5Y cells is sufficient to perturb cellular balance but insufficient to affect p53 expression. (C) 2010 IBRO. Published by Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.neuroscience.2010.06.013"],["dc.identifier.isi","000281050600016"],["dc.identifier.pmid","20547212"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18932"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","0306-4522"],["dc.title","CELLULAR PRION PROTEIN OVEREXPRESSION DISTURBS CELLULAR HOMEOSTASIS IN SH-SY5Y NEUROBLASTOMA CELLS BUT DOES NOT ALTER p53 EXPRESSION: A PROTEOMIC STUDY"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]