Bibl, Mirko

[["dc.bibliographiccitation.firstpage","366"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Experimental Neurology"],["dc.bibliographiccitation.lastpage","370"],["dc.bibliographiccitation.volume","223"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Vanmechelen, Eugeen"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Heuser, Isabella"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Buerger, Katharina"],["dc.contributor.author","Hampel, Harald"],["dc.contributor.author","Froelich, Lutz"],["dc.contributor.author","Henn, Fritz A."],["dc.contributor.author","Falkai, Peter Gaston"],["dc.contributor.author","Ruether, Eckhart"],["dc.contributor.author","Jahn, Holger"],["dc.contributor.author","Luckhaus, C. H."],["dc.contributor.author","Perneczky, Robert"],["dc.contributor.author","Schmidtke, K."],["dc.contributor.author","Schroeder, J."],["dc.contributor.author","Kessler, H."],["dc.contributor.author","Pantel, Johannes"],["dc.contributor.author","Gertz, H.-J."],["dc.contributor.author","Vanderstichele, Hugo"],["dc.contributor.author","de Meyer, G."],["dc.contributor.author","Shapiro, F."],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Wiltfang, J."],["dc.date.accessioned","2018-11-07T08:42:36Z"],["dc.date.available","2018-11-07T08:42:36Z"],["dc.date.issued","2010"],["dc.description.abstract","We measured concentrations of to peptides 1-42 and 1-40, and their ratio in plasma of patients carefully categorized clinically and neurochemically as having AD or other dementias with a newly commercially available multiplexing assay, characterized by reasonable laboratory performance (intra-assay imprecision in the range of 1.3-3.8% for A beta 1-42, and 1.8-4.1% for A beta 1-40, inter-assay imprecision for A beta 1-42, A beta 1-40, and A beta 1-42/A beta 1-40 concentration ratio in the range of 2.3-11.5%, 2.2-10.4% and 42-9.7%, respectively). Patients with AD or mild cognitive impairment of AD type (MCI-AD) whose clinical diagnosis was supported with CSF biomarkers (n = 193) had significantly lower A beta 1-42 plasma concentrations (p<0.007), and A beta 1-42/1-40 ratios (p<0.003) compared to patients with other dementias and MCI of other types (n = 64). No significant differences between persons with MCI of AD type and patients with early AD were observed, or between MCI of other types versus patients with early dementia of other types. Our findings reconfirm the hypothesis that alterations of biomarker concentrations occur early in a preclinical AD stage and that these alterations are also reflected in plasma. (C) 2009 Published by Elsevier Inc."],["dc.identifier.doi","10.1016/j.expneurol.2009.07.024"],["dc.identifier.isi","000277743700015"],["dc.identifier.pmid","19664622"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19739"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","0014-4886"],["dc.title","Amyloid beta peptides in plasma in early diagnosis of Alzheimer's disease: A multicenter study with multiplexing"],["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","256"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","265"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Schneider, Michael"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Welge, Volker"],["dc.contributor.author","Gross, Martin"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2018-11-07T11:19:48Z"],["dc.date.available","2018-11-07T11:19:48Z"],["dc.date.issued","2008"],["dc.description.abstract","Background/Aims: The study evaluated the patterns of cerebrospinal fluid (CSF), amyloid-beta (A beta) peptides, total tau and phospho-tau among Alzheimer's disease (AD) and vascular dementias (VAD). Methods: A beta-SDS-PAGE immunoblot and commercially available ELISAs were applied to the CSF analysis of 52 patients with probable (n = 21) and possible (n = 16) VAD, AD with cerebrovascular disease (n = 15), 30 patients with probable AD and 30 nondemented disease controls. Results: AD and AD with cerebrovascular disease displayed a similar neurochemical phenotype in contrast to nondemented disease controls and probable VAD with regard to tau, p-tau, A beta-40(ox) and A beta 1-42%. Possible VAD displayed AD-like changes only for A beta 1-40(ox) and A beta 1-42%. Conclusion: CSF neurochemical phenotypes sufficiently discriminate probable AD and VAD from each other, but their diagnostic value is limited in case of no clear-cut clinical appearance, such as possible VAD. Conversely, CSF A beta peptides and p-tau levels may help estimate the involvement of AD-like pathophysiological pathways in VAD subgroups. Copyright (c) 2008 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000115975"],["dc.identifier.isi","000253777500009"],["dc.identifier.pmid","18270488"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9353"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55373"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1420-8008"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Cerebrospinal fluid neurochemical phenotypes in vascular dementias: Original data and mini-review"],["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","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","812"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Neurobiology of Aging"],["dc.bibliographiccitation.lastpage","818"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Vanderstichele, Hugo"],["dc.contributor.author","Vanmechelen, Eugeen"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Wolf, Stefanie"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Reulbach, Udo"],["dc.contributor.author","Koelsch, Heike"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Schroeder, Johannes"],["dc.contributor.author","Schoenknecht, Peter"],["dc.contributor.author","Hampel, Harald"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Weimer, Erik"],["dc.contributor.author","Perneczky, Robert"],["dc.contributor.author","Jahn, Holger"],["dc.contributor.author","Luckhaus, Christian"],["dc.contributor.author","Lamla, Ulrich"],["dc.contributor.author","Supprian, Tillmann"],["dc.contributor.author","Maler, Juan Manuel"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2018-11-07T11:14:50Z"],["dc.date.available","2018-11-07T11:14:50Z"],["dc.date.issued","2008"],["dc.description.abstract","In this report we evaluated the clinical performance of APOE genotyping and three protein biomarkers (total tau, beta-amyloid(1-42), and tau phosphorylated at threonine 181) in a prospective multicenter study using the INNO-BIA AlzBio3 assay applied on Luminex platform, Concentration of biomarkers of Alzheimer's. disease in cerebrospinal fluid (CSF) was measured with multiplexing technology (n = 223), and compared to the results of ELISA assays in patients with early dementias or mild cognitive impairment (MCI) collected at 12 gerontopsychiatric university departments, and APOE genotyping was performed. Concentrations of A beta(1-42) were statistically significantly lower in MCI-AD subjects compared to MCI-O, and significantly lower in D-AD patients compared to MCI-O. P-tau(181P) concentrations were significantly higher in MCI-AD patients compared to MCI-O, and significantly higher in D-AD patients compared to MCI-O. The total tau concentrations in MCI-AD patients were significantly higher compared to MCI-O, and higher in D-AD compared to MCI-O, moreover, the concentration of total tau was significantly higher in D-AD compared to MCI-AD patients. For the differential diagnosis between D-AD and D-O, the optimal cutoff concentration of A beta(1-42) was 197.7pg/mL, and that for P-tau(181P) was 47.9pg/mL. These cutoff values were also applied to discriminate between MCI-AD and MCI-O subjects. Simultaneous measurement of the biomarkers significantly improves management of the samples and quality control of the assays' performance. (C) 2007 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.neurobiolaging.2006.12.010"],["dc.identifier.isi","000255599700002"],["dc.identifier.pmid","17239996"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54230"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0197-4580"],["dc.title","Multiplexed quantification of dementia biomarkers in the CSF of patients with early dementias and MCI: A multicenter 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","524"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Biological Psychiatry"],["dc.bibliographiccitation.lastpage","530"],["dc.bibliographiccitation.volume","55"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Groemer, Teja Wolfgang"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Maler, Juan Manuel"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2017-09-07T11:44:28Z"],["dc.date.available","2017-09-07T11:44:28Z"],["dc.date.issued","2004"],["dc.description.abstract","The advent of new therapeutic avenues for Alzheimer's disease (AD) calls for an improved early and differential diagnosis. With surface enhanced laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF MS), cerebrospinal fluid from patients with AD (n = 10) and nondemented control subjects (n = 9) was studied. Molecular mass signals were observed corresponding to three novel amyloid beta (Aβ) peptides that have not previously been described, in addition to those previously known, with molecular masses of 4525.1 d, 4846.8 d, and 7755.8 d. The signal-to-noise ratios (S/NR) of Aβ(4525.1) and Aβ(7758.8+2H) were significantly decreased in AD [Aβ(4525.1): median 2.2 and 4.3 in AD and control subjects, respectively, p < .01; Aβ(7758.8+2H): median 1.0 and 14.0 in AD and control subjects, respectively, p < .01], whereas the S/NR of Aβ(4846.8) was significantly increased in AD (median 3.6 and 2.5 in AD and control subjects, respectively, p < .05). The S/NR of two known AD biomarkers, Aβ1-42 and Aβ1-40, expectedly turned out to be significantly decreased (p < .01) and unaltered in AD, respectively. A moderate and highly significant correlation was observed between S/NR of Aβ1-42 and Aβ42 concentration as measured with enzyme-linked immunosorbent assay (R = .67, p < .01). We report evidence of three novel amyloid β peptides that might play an important role in the diagnosis and pathophysiology of Alzheimer's disease."],["dc.identifier.doi","10.1016/j.biopsych.2003.10.014"],["dc.identifier.gro","3151663"],["dc.identifier.pmid","15023581"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8480"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0006-3223"],["dc.title","Amyloid β peptides in cerebrospinal fluid as profiled with surface enhanced laser desorption/ionization time-of-flight mass spectrometry: evidence of novel biomarkers in Alzheimer's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["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","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"]]

[["dc.bibliographiccitation.firstpage","1177"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","1187"],["dc.bibliographiccitation.volume","129"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Esselmann, Herrmann"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Klafki, H. W."],["dc.contributor.author","Sparbier, Katrin"],["dc.contributor.author","Smirnov, Alexey"],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Wiltfang, J."],["dc.date.accessioned","2018-11-07T09:51:06Z"],["dc.date.available","2018-11-07T09:51:06Z"],["dc.date.issued","2006"],["dc.description.abstract","As the differential diagnosis of dementias based on established clinical criteria is often difficult, biomarkers for applicable diagnostic testing are currently under intensive investigation. Amyloid plaques deposited in the brain of patients suffering from Alzheimer's disease, dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD) mainly consist of carboxy-terminally elongated forms of amyloid-beta (A beta) peptides, such as A beta 1-42. Absolute A beta 1-42 levels in CSF have shown diagnostic value for the diagnosis of Alzheimer's disease, but the discrimination among Alzheimer's disease, DLB and PDD was poor. A recently established quantitative urea-based A beta-sodium-dodecylsulphate-polyacrylamide-gel-electrophoresis with Western immunoblot (A beta-SDS-PAGE/immunoblot) revealed a highly conserved A beta peptide pattern of the carboxy-terminally truncated A beta peptides 1-37, 1-38, 1-39 in addition to 1-40 and 1-42 in human CSF. We used the A beta-SDS-PAGE/immunoblot to investigate the CSF of 23 patients with Alzheimer's disease, 21 with DLB, 21 with PDD and 23 non-demented disease controls (NDC) for disease-specific alterations of the A beta peptide patterns in its absolute and relative quantities. The diagnostic groups were matched for age and severity of dementia. The present study is the first attempt to evaluate the meaning of A beta peptide patterns in CSF for differential diagnosis of the three neurodegenerative diseases-Alzheimer's disease, DLB and PDD. The A beta peptide patterns displayed disease-specific variations and the ratio of the differentially altered A beta 1-42 to the A beta 1-37 levels subsequently discriminated all diagnostic groups from each other at a highly significant level, except DLB from PDD. Additionally, a novel peptide with A beta-like immunoreactivity was observed constantly in the CSF of all 88 investigated patients. The pronounced percentage increase of this peptide in DLB allowed a highly significant discrimination from PDD. Using a cut-off point of 0.954%, this marker yielded a diagnostic sensitivity and specificity of 81 and 71%, respectively. From several lines of indication, we consider this peptide to represent an oxidized alpha-helical form of A beta 1-40 (A beta 1-40( )). The increased abundance of A beta 1-40( ) probably reflects a disease-specific alteration of the A beta 1-40 metabolism in DLB. We conclude that A beta peptide patterns reflect disease-specific pathophysiological pathways of different dementia syndromes as distinct neurochemical phenotypes. Although A beta peptide patterns failed to fulfil the requirements for a sole biomarker, their combined evaluation with other biomarkers is promising in neurochemical dementia diagnosis. It is noteworthy that DLB and PDD exhibit distinct clinical temporal courses, despite their similar neuropathological appearance. Their distinct molecular phenotypes support the view of different pathophysiological pathways for each of these neurodegenerative diseases."],["dc.identifier.doi","10.1093/brain/awl063"],["dc.identifier.isi","000236998000012"],["dc.identifier.pmid","16600985"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35846"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.title","CSF amyloid-beta-peptides in Alzheimer's disease, dementia with Lewy bodies and Parkinson's disease dementia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]