Mollenhauer, Brit

[["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","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","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","238"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Clinical Laboratory Analysis"],["dc.bibliographiccitation.lastpage","245"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Welge, Volker"],["dc.contributor.author","Schmidt, Holger"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2018-11-07T09:15:09Z"],["dc.date.available","2018-11-07T09:15:09Z"],["dc.date.issued","2012"],["dc.description.abstract","Background Blood-based tests for a rapid and valid diagnosis as well as outcome prognosis of acute stroke are desirable. Recently, plasma A beta 40 was suggested as an independent cerebrovascular risk factor candidate. Methods We investigated eight plasma samples of patients with clinical signs of acute cerebral ischemia for derangements of plasma amyloid-beta (A beta) peptide patterns as compared to 13 patients with other neuropsychiatric diseases. For the analysis of plasma, we used immunoprecipitation followed by the quantitative A beta-SDS-PAGE/immunoblot. Results The major outcome was a striking decrease of A beta 140 in plasma paralleled by an increase in the ratio of A beta 138/A beta 140 in two patients with acute stroke. Interestingly, these patients had an onset of symptoms within only 24 hr before venous puncture and there was a strong correlation of A beta 138/A beta 140 levels with the time span between onset of symptoms and venous puncture. Conclusion From these results, we suggest the ratio of plasma A beta 138/A beta 140 as a possible biomarker for the early diagnosis of acute stroke. J. Clin. Lab. Anal. 26:238-245, 2012. (c) 2012 Wiley Periodicals, Inc."],["dc.identifier.doi","10.1002/jcla.21511"],["dc.identifier.isi","000306511500004"],["dc.identifier.pmid","22811355"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27608"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0887-8013"],["dc.title","Plasma Amyloid-BetaPeptides in Acute Cerebral Ischemia: A Pilot Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","671"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","680"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Esselmann, Herrmann"],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Stiens, G."],["dc.contributor.author","Ruether, Eckhart"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, J."],["dc.date.accessioned","2018-11-07T11:01:11Z"],["dc.date.available","2018-11-07T11:01:11Z"],["dc.date.issued","2007"],["dc.description.abstract","Biomarkers for differential diagnosis of the three most frequent degenerative forms of dementia, Alzheimer's disease (AD), dementia with Lewy bodies (DLB) and frontotemporal dementias (FTD), are currently under intensive investigation, but disease-specific biomarkers for FTD and DLB are still lacking. We analyzed 303 cerebrospinal fluid (CSF) samples of 71 AD, 32 DLB and 36 FTD patients in comparison to 93 various other dementias (OD), 20 peripheral neurologic disease (PND) controls, 25 neurodegenerative disorders without dementia (ND) and 26 depressive cognitive complainers (DCC) for distinct CSF amyloid-beta (Ab) peptide patterns, using the quantitative A beta-SDS-PAGE/immunoblot. Additionally, the novel electrochemiluminescence technique (MSD) was used to validate the measures on A beta 1-38. The main outcome measures were a striking decrease of A beta 1-42 in AD ( P = 7.4 x 10(-19)), and most interestingly a pronounced decrease of A beta 1-38 in FTD ( P = 9.6 x 1 0(-7)). Moreover, a novel peptide that most probably represents an oxidized alpha-helical form of A beta 1-40 (A beta 1-40(ox)) displayed a highly significant increase in DLB ( P = 3.7 x 10(-3)) as compared to non-demented disease controls. The overall diagnostic accuracy of percentage Ab peptide abundances (A beta 1-X%) was clearly superior to absolute CSF Ab levels. A beta 1-42% and A beta 1-38% enabled contrasts of 85% or beyond to distinguish AD and FTD, respectively, from all other investigated subjects. A beta 1-40(ox)% yielded a diagnostic sensitivity and specificity of 88 and 73% for the detection of DLB among all other investigated patients. We found a strong correlation between A beta 1-38 levels as measured by the A beta-SDS-PAGE/immunoblot and MSD, respectively. CSF A beta peptides may reflect disease-specific impact of distinct neurodegenerative processes on A beta peptide metabolism and represent a potential diagnostic biomarker for AD, FTD and DLB."],["dc.identifier.doi","10.1038/sj.mp.4001967"],["dc.identifier.isi","000247619700009"],["dc.identifier.pmid","17339876"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51089"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1359-4184"],["dc.title","Validation of amyloid-beta peptides in CSF diagnosis of neurodegenerative dementias"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","203"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","212"],["dc.bibliographiccitation.volume","116"],["dc.contributor.author","Welge, Volker"],["dc.contributor.author","Fiege, Oliver"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Klafki, Hans-Wolfgang"],["dc.contributor.author","Wolf, Stefanie"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Bibl, Mirko"],["dc.date.accessioned","2018-11-07T08:33:10Z"],["dc.date.available","2018-11-07T08:33:10Z"],["dc.date.issued","2009"],["dc.description.abstract","Cerebrospinal fluid (CSF) concentrations of amyloid-beta (A beta) 1-38, 1-40, 1-42, total-tau and phospho-tau in samples from 156 patients with Alzheimer's disease (AD) (n = 44), depressive cognitive complainers (DCC, n = 25) and various other forms of non-Alzheimer dementias (NAD, n = 87) were analyzed by electrochemiluminescence and enzyme linked immunosorbent assay, respectively. A significant decrease of CSF A beta 1-42 was the most powerful single marker for differentiation of AD from DCC, yielding accuracies of beyond 85%. Increased p-tau and the ratio A beta 1-42/A beta 1-38 yielded accuracies of beyond 80 and 85%, respectively, to discriminate AD versus NAD. Combining p-tau with A beta 1-42/A beta 1-38 resulted in a sensitivity of 94% for detection of AD and 85% specificity for excluding NAD. Decreased CSF A beta 1-42 represents a core biomarker for AD. The lack of specificity for exclusion of NAD can be most effectively compensated by the ratio A beta 1-42/A beta 1-38. The ratio A beta 1-42/A beta 1-38/p-tau powerfully discriminates AD versus NAD and fulfils the accuracy requirements for an applicable screening and differential diagnostic AD biomarker."],["dc.identifier.doi","10.1007/s00702-008-0177-6"],["dc.identifier.isi","000269823900011"],["dc.identifier.pmid","19142572"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17511"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","0300-9564"],["dc.title","Combined CSF tau, p-tau181 and amyloid-beta 38/40/42 for diagnosing Alzheimer's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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.firstpage","192"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Clinical Chemistry and Laboratory Medicine (CCLM)"],["dc.bibliographiccitation.lastpage","195"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Neubert, K."],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T10:21:29Z"],["dc.date.available","2018-11-07T10:21:29Z"],["dc.date.issued","2006"],["dc.description.abstract","The intra vitam diagnosis of different dementias is still based on clinical grounds. So far, no technical investigations have been available to support these diagnoses. For tau protein and beta-amyloid((1-42)) in cerebrospinal fluid (CSF), promising results for the diagnosis of Alzheimer's disease ( AD) have been reported; however, their differential diagnostic spectrum is limited, as was recently shown for dementia with Lewy bodies (DLB) and for AD. Therefore, further marker proteins have to be established to ameliorate, support, and differentiate these clinical diagnoses. We evaluated beta-amyloid((1-40)) and phosphorylated tau protein (181p), in addition to total tau protein and beta-amyloid ((1-42)), in 20 patients with DLB, 34 AD patients, and 20 non- demented neurological controls (NDCs). All markers could differentiate between the dementia groups ( AD, DLB) and the controls. AD and DLB could be differentiated only by levels of total tau protein and by the ratio total tau protein/phosphorylated tau protein. However, values still overlapped markedly. In some cases, tau protein levels in CSF may contribute to the clinical distinction between DLB and AD, but the value of the markers is still limited, especially because of mixed pathology. We conclude that more specific markers have to be established to differentiate between these diseases."],["dc.identifier.doi","10.1515/CCLM.2006.035"],["dc.identifier.isi","000235777200012"],["dc.identifier.pmid","16475906"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42102"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Walter De Gruyter & Co"],["dc.relation.issn","1434-6621"],["dc.title","Total tau protein, phosphorylated tau (181p) protein, beta-amyloid(1-42), and beta-amyloid(1-40) in cerebrospinal fluid of patients with dementia with Lewy bodies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","22"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","28"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Cepek, Lukas"],["dc.contributor.author","Brechlin, Peter"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Klingebiel, Enrico"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T11:06:25Z"],["dc.date.available","2018-11-07T11:06:25Z"],["dc.date.issued","2007"],["dc.description.abstract","So far, only the detection of 14-3-3 proteins in cerebrospinal fluid (CSF) has been accepted as diagnostic criterion for Creutzfeldt-Jakob disease (CJD). However, this assay cannot be used for screening because of the high rate of false-positive results, whereas patients with variant CJD are often negative for 14-3-3 proteins. The aim of this study was to compare the spot patterns of CSF by 2-dimensional polyacrylamide gel electrophoresis (2D-PAGE) to search for a CJD-specific spot pattern. We analyzed the CSF of 28 patients [11 CJD, 9 Alzheimer's disease ( AD), 8 nondemented controls (NDC)] employing 2D-PAGE which was optimized for minimal volumes of CSF (0.1 ml; 7-cm strips). All samples were run at least three times, gels were silver stained and analyzed by an analysis software and manually revised. We could consistently match 268 spots which were then compared between all groups. By the use of 5 spots, we were able to differentiate CJD from AD or NDC with a sensitivity of 100%. CJD could also be distinguished from both groups by using a heuristic clustering algorithm of 2 spots. We conclude that this proteomic approach can differentiate CJD from other diseases and may serve as a model for other neurodegenerative diseases. Copyright (C) 2007 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000096589"],["dc.identifier.isi","000242167700003"],["dc.identifier.pmid","17068393"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52307"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1420-8008"],["dc.title","Proteomic analysis of the 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","467"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","474"],["dc.bibliographiccitation.volume","103"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Weniger, Godehard"],["dc.contributor.author","Welge, Volker"],["dc.contributor.author","Liess, Michael"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Schulz, Joerg B."],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2018-11-07T10:58:12Z"],["dc.date.available","2018-11-07T10:58:12Z"],["dc.date.issued","2007"],["dc.description.abstract","Blood-based tests for the differential diagnosis of Alzheimer's disease (AD) are under intensive investigation and have shown promising results with regard to A beta 40 and A beta 42 peptide species in incipient AD. Moreover, plasma A beta 40 was suggested as an independent cerebrovascular risk factor candidate. These considerations prompted us to analyse a total of 72 plasma samples in vascular dementias (VAD, n = 15), AD with cerebrovascular disease (AD with CVD, n = 7), AD (n = 15), Parkinson's disease and Parkinson's disease dementia (PD/PDD, n = 20) and 15 patients with depression that served as controls (DC) for distinct plasma amyloid-beta (A beta) peptide patterns. For the analysis of plasma we used immunoprecipitation followed by the quantitative ApSDS-PAGE/immunoblot. For comparison, CSF tau and A beta 1 -42 analyses were performed. The major outcome was an increase in A beta 1-40 in plasma of VAD paralleled by a decrease in the ratio of A beta 1-38/A beta 1-40. The ratio A beta 1-38/A beta-1-40 in plasma enabled contrasts of beyond 85% and 80% for discriminating VAD from DC and all other patients, respectively. In CSF, we confirmed the typical CSF biomarker constellation of increased tau and diminished A beta 1-42 levels for AD. The diagnostic accuracy of plasma A beta 1-38/A beta 1-40 for VAD resembled the accuracy of CSF biomarkers for AD. From the presented results, we consider the ratio of plasma A beta 1-38/ A beta 1-40 peptides to be a blood-based biomarker candidate for VAD."],["dc.identifier.doi","10.1111/j.1471-4159.2007.04763.x"],["dc.identifier.isi","000250384500004"],["dc.identifier.pmid","17662050"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.relation.issn","0022-3042"],["dc.title","Blood-based neurochemical diagnosis of vascular dementia: A pilot study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]