Lewczuk, Piotr

[["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","273"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neurobiology of Aging"],["dc.bibliographiccitation.lastpage","281"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Maler, Juan Manuel"],["dc.contributor.author","Reulbach, Udo"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Henkel, Andreas Wolfram"],["dc.contributor.author","Henkel, Maria Kerstin"],["dc.contributor.author","Eikenberg, Oliver"],["dc.contributor.author","Antz, Christof"],["dc.contributor.author","Krause, Wolf-Rainer"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2018-11-07T10:50:56Z"],["dc.date.available","2018-11-07T10:50:56Z"],["dc.date.issued","2004"],["dc.description.abstract","Cerebrospinal fluid (CSF) concentrations of amyloid p peptides ending at positions 42 and 40 (Abeta42 and Abeta40, respectively), and total tau (tTau) protein were measured by ELISA in order to compare their accuracy in discriminating patients with Alzheimer's disease (AD, n = 22), non-Alzheimer dementia (nAD, n = 11) and control subjects (CON, n = 35). As compared to the other groups, the concentrations of Abeta42 and tTau were decreased (P < 0.001) and increased (P < 0.001) in AD, respectively, while Abeta40 did not differ significantly among the groups. Receiver operating characteristic (ROC) analysis was performed to define cut-off values for maximized sensitivity and specificity. For all groups compared the Abeta peptide ratio 42/40 classified more patients correctly, as compared to the concentration of Abeta42 alone: AD versus controls, 94 and 86.7%; AD versus nAD, 90 and 85% and AD versus nAD plus controls, 90.8 and 87%, respectively. The percentage of correctly classified patients was further improved when the Abeta ratio was combined with the analysis of the tTau concentration. Presence of the apolipoprotein E epsilon4 allele, age or degree of mental disability did not significantly influence the parameters studied. (C) 2003 Elsevier Science Inc. All rights reserved."],["dc.identifier.doi","10.1016/S0197-4580(03)00086-1"],["dc.identifier.gro","3151667"],["dc.identifier.isi","000189229600001"],["dc.identifier.pmid","15123331"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48765"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0197-4580"],["dc.title","Neurochemical diagnosis of Alzheimer's dementia by CSF A beta 42, A beta 42/A beta 40 ratio and total tau"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["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","69"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","The World Journal of Biological Psychiatry"],["dc.bibliographiccitation.lastpage","84"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Riederer, Peter"],["dc.contributor.author","Grunblatt, E."],["dc.contributor.author","Hock, C."],["dc.contributor.author","Scheltens, Philip"],["dc.contributor.author","Hampel, Harald"],["dc.contributor.author","Vanderstichele, Hugo"],["dc.contributor.author","Iqbal, K."],["dc.contributor.author","Galasko, D."],["dc.contributor.author","Lannfelt, Lars"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Esselmann, Herrmann"],["dc.contributor.author","Henkel, A. W."],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Blennow, Kaj"],["dc.date.accessioned","2018-11-07T08:49:23Z"],["dc.date.available","2018-11-07T08:49:23Z"],["dc.date.issued","2005"],["dc.description.abstract","Aging of population, and increasing life expectancy result in an increasing number of patients with dementia. This symptom can be a part of a completely curable disease of the central nervous system (e.g, neuro inflammation), or a disease currently considered irreversible (e.g, Alzheimer's disease, AD). In the latter case, several potentially successful treatment approaches are being tested now, demanding reasonable standards of pre-mortem diagnosis. Cerebrospinal fluid and serum analysis (CSF/serum analysis), whereas routinely performed in neuroinflammatory diseases, still requires standardization to be used as an aid to the clinically based diagnosis of AD. Several AD-related CSF parameters (total tau, phosphorylated forms of tau, A beta peptides, ApoE genotype, p97, etc.) tested separately or in a combination provide sensitivity and specificity in the range of 85%, the figure commonly expected from a good diagnostic tool. In this review, recently published reports regarding progress in neurochemical pre-mortem diagnosis of dementias are discussed with a focus on an early and differential diagnosis of AD. Novel perspectives offered by recently introduced technologies, e.g, fluorescence correlation spectroscopy (FCS) and surface enhanced laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF MS) are briefly discussed."],["dc.identifier.doi","10.1080/15622970510029786"],["dc.identifier.isi","000230242300002"],["dc.identifier.pmid","16156480"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21446"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Taylor & Francis Ltd"],["dc.relation.issn","1562-2975"],["dc.title","Consensus paper of the WFSBP Task Force on biological markers of dementia: The role of CSF and blood analysis in the early and differential diagnosis of dementia"],["dc.type","review"],["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"]]

[["dc.bibliographiccitation.firstpage","37"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","44"],["dc.bibliographiccitation.volume","31"],["dc.contributor.affiliation","Bibl, Mirko; aDepartment of Psychiatry, Psychotherapy and Addiction Medicine, Kliniken Essen-Mitte, University of Duisburg-Essen, and bKlinik für Psychiatrie und Psychotherapie der Rheinischen Kliniken Essen, Universität Duisburg-Essen, Essen, cUniversity of Göttingen and Paracelsus-Elena Klinik, Kassel, dDepartment of Psychiatry and Psychotherapy, University of Erlangen-Nuremberg, Erlangen, eDepartment of Psychiatry, University of Göttingen, Göttingen, fInstitute for Neurology, University of Ulm, Ulm, and gDepartment of Psychiatry and Psychotherapy, Ludwig-Maximilian-University of Munich, Munich, Germany"],["dc.contributor.affiliation","Mollenhauer, Brit; aDepartment of Psychiatry, Psychotherapy and Addiction Medicine, Kliniken Essen-Mitte, University of Duisburg-Essen, and bKlinik für Psychiatrie und Psychotherapie der Rheinischen Kliniken Essen, Universität Duisburg-Essen, Essen, cUniversity of Göttingen and Paracelsus-Elena Klinik, Kassel, dDepartment of Psychiatry and Psychotherapy, University of Erlangen-Nuremberg, Erlangen, eDepartment of Psychiatry, University of Göttingen, Göttingen, fInstitute for Neurology, University of Ulm, Ulm, and gDepartment of Psychiatry and Psychotherapy, Ludwig-Maximilian-University of Munich, Munich, Germany"],["dc.contributor.affiliation","Lewczuk, Piotr; aDepartment of Psychiatry, Psychotherapy and Addiction Medicine, Kliniken Essen-Mitte, University of Duisburg-Essen, and bKlinik für Psychiatrie und Psychotherapie der Rheinischen Kliniken Essen, Universität Duisburg-Essen, Essen, cUniversity of Göttingen and Paracelsus-Elena Klinik, Kassel, dDepartment of Psychiatry and Psychotherapy, University of Erlangen-Nuremberg, Erlangen, eDepartment of Psychiatry, University of Göttingen, Göttingen, fInstitute for Neurology, University of Ulm, Ulm, and gDepartment of Psychiatry and Psychotherapy, Ludwig-Maximilian-University of Munich, Munich, Germany"],["dc.contributor.affiliation","Esselmann, Hermann; aDepartment of Psychiatry, Psychotherapy and Addiction Medicine, Kliniken Essen-Mitte, University of Duisburg-Essen, and bKlinik für Psychiatrie und Psychotherapie der Rheinischen Kliniken Essen, Universität Duisburg-Essen, Essen, cUniversity of Göttingen and Paracelsus-Elena Klinik, Kassel, dDepartment of Psychiatry and Psychotherapy, University of Erlangen-Nuremberg, Erlangen, eDepartment of Psychiatry, University of Göttingen, Göttingen, fInstitute for Neurology, University of Ulm, Ulm, and gDepartment of Psychiatry and Psychotherapy, Ludwig-Maximilian-University of Munich, Munich, Germany"],["dc.contributor.affiliation","Wolf, Stefanie; aDepartment of Psychiatry, Psychotherapy and Addiction Medicine, Kliniken Essen-Mitte, University of Duisburg-Essen, and bKlinik für Psychiatrie und Psychotherapie der Rheinischen Kliniken Essen, Universität Duisburg-Essen, Essen, cUniversity of Göttingen and Paracelsus-Elena Klinik, Kassel, dDepartment of Psychiatry and Psychotherapy, University of Erlangen-Nuremberg, Erlangen, eDepartment of Psychiatry, University of Göttingen, Göttingen, fInstitute for Neurology, University of Ulm, Ulm, and gDepartment of Psychiatry and Psychotherapy, Ludwig-Maximilian-University of Munich, Munich, Germany"],["dc.contributor.affiliation","Otto, Markus; aDepartment of Psychiatry, Psychotherapy and Addiction Medicine, Kliniken Essen-Mitte, University of Duisburg-Essen, and bKlinik für Psychiatrie und Psychotherapie der Rheinischen Kliniken Essen, Universität Duisburg-Essen, Essen, cUniversity of Göttingen and Paracelsus-Elena Klinik, Kassel, dDepartment of Psychiatry and Psychotherapy, University of Erlangen-Nuremberg, Erlangen, eDepartment of Psychiatry, University of Göttingen, Göttingen, fInstitute for Neurology, University of Ulm, Ulm, and gDepartment of Psychiatry and Psychotherapy, Ludwig-Maximilian-University of Munich, Munich, Germany"],["dc.contributor.affiliation","Kornhuber, Johannes; aDepartment of Psychiatry, Psychotherapy and Addiction Medicine, Kliniken Essen-Mitte, University of Duisburg-Essen, and bKlinik für Psychiatrie und Psychotherapie der Rheinischen Kliniken Essen, Universität Duisburg-Essen, Essen, cUniversity of Göttingen and Paracelsus-Elena Klinik, Kassel, dDepartment of Psychiatry and Psychotherapy, University of Erlangen-Nuremberg, Erlangen, eDepartment of Psychiatry, University of Göttingen, Göttingen, fInstitute for Neurology, University of Ulm, Ulm, and gDepartment of Psychiatry and Psychotherapy, Ludwig-Maximilian-University of Munich, Munich, Germany"],["dc.contributor.affiliation","Rüther, Eckart; aDepartment of Psychiatry, Psychotherapy and Addiction Medicine, Kliniken Essen-Mitte, University of Duisburg-Essen, and bKlinik für Psychiatrie und Psychotherapie der Rheinischen Kliniken Essen, Universität Duisburg-Essen, Essen, cUniversity of Göttingen and Paracelsus-Elena Klinik, Kassel, dDepartment of Psychiatry and Psychotherapy, University of Erlangen-Nuremberg, Erlangen, eDepartment of Psychiatry, University of Göttingen, Göttingen, fInstitute for Neurology, University of Ulm, Ulm, and gDepartment of Psychiatry and Psychotherapy, Ludwig-Maximilian-University of Munich, Munich, Germany"],["dc.contributor.affiliation","Wiltfang, Jens; aDepartment of Psychiatry, Psychotherapy and Addiction Medicine, Kliniken Essen-Mitte, University of Duisburg-Essen, and bKlinik für Psychiatrie und Psychotherapie der Rheinischen Kliniken Essen, Universität Duisburg-Essen, Essen, cUniversity of Göttingen and Paracelsus-Elena Klinik, Kassel, dDepartment of Psychiatry and Psychotherapy, University of Erlangen-Nuremberg, Erlangen, eDepartment of Psychiatry, University of Göttingen, Göttingen, fInstitute for Neurology, University of Ulm, Ulm, and gDepartment of Psychiatry and Psychotherapy, Ludwig-Maximilian-University of Munich, Munich, Germany"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Wolf, Stefanie"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Rüther, Eckart"],["dc.date.accessioned","2018-11-07T09:01:05Z"],["dc.date.available","2018-11-07T09:01:05Z"],["dc.date.issued","2011"],["dc.date.updated","2022-02-09T13:23:15Z"],["dc.description.abstract","Background/Aims: We determined cerebrospinal fluid (CSF) concentrations of amyloid-beta(A beta)(1-38), A beta(1-40), A beta(1-42), total tau and phospho-tau (p-tau) in order to study their differential expression in frontotemporal dementia (FTD, n = 25) and primary progressive aphasia (PPA, n = 12) as compared to Alzheimer's dementia (AD, n = 25) and nondemented controls (n = 20). Methods: Commercially available ELISA and electrochemiluminescence methods were applied. Results: High CSF p-tau and low ratios of A beta(1-42)/A beta(1-40) and A beta(1-42)/A beta(1-38), respectively, were specific for AD. CSF A beta(1-38) was reduced in FTD as compared to each of the other diagnostic groups, including PPA. CSF tau and p-tau levels were elevated in PPA as compared to FTD. Conclusion: This is the first detailed report on biomarker patterns in PPA, indicating distinct CSF biomarker patterns in FTD and PPA as major subgroups of frontotemporal lobar degeneration. The diagnostic and pathophysiological implications of our results warrant further studies on larger and neuropathologically diagnosed patient populations. Copyright (C) 2010 S. Karger AG, Basel"],["dc.description.sponsorship","EU [LSHM-CT-2007-037950, LSHB-CT-2006-037953]"],["dc.identifier","21135556"],["dc.identifier.doi","10.1159/000322370"],["dc.identifier.eissn","1421-9824"],["dc.identifier.isi","000286425500005"],["dc.identifier.issn","1420-8008"],["dc.identifier.pmid","21135556"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9096"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24332"],["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","1421-9824"],["dc.relation.issn","1420-8008"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Cerebrospinal Fluid Tau, p-Tau 181 and Amyloid-β38/40/42 in Frontotemporal Dementias and Primary Progressive Aphasias"],["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"]]