Maler, Juan Manuel

[["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.issue","5"],["dc.bibliographiccitation.journal","Pharmacopsychiatry"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Maler, Juan Manuel"],["dc.contributor.author","Esselmann, Herrmann"],["dc.contributor.author","Dyrks, T."],["dc.contributor.author","Klafki, H."],["dc.contributor.author","Fiszer, M."],["dc.contributor.author","Paul, S."],["dc.contributor.author","Reulbach, Udo"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, J."],["dc.date.accessioned","2018-11-07T10:56:36Z"],["dc.date.available","2018-11-07T10:56:36Z"],["dc.date.issued","2005"],["dc.format.extent","262"],["dc.identifier.isi","000232591900164"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50051"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.publisher.place","Stuttgart"],["dc.relation.conference","24th Symposium of the Arbeitsgemeinschaft-fur-Neuropsychopharmakologie-und-Pharmakopsychiatrie (AGNP)"],["dc.relation.eventlocation","Munich, GERMANY"],["dc.relation.issn","0176-3679"],["dc.title","Specific inhibition of beta-amyloid peptide secretion by ZK808762 mimicks the effect of non-steroidal antiinflammatory drugs"],["dc.type","conference_abstract"],["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","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","156"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Brain Research"],["dc.bibliographiccitation.lastpage","162"],["dc.bibliographiccitation.volume","1052"],["dc.contributor.author","Maler, Juan Manuel"],["dc.contributor.author","Esselmann, Herrmann"],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Kunz, N."],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Reulbach, Udo"],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Kornhuber, Johannes"],["dc.date.accessioned","2018-11-07T10:56:49Z"],["dc.date.available","2018-11-07T10:56:49Z"],["dc.date.issued","2005"],["dc.description.abstract","The present study examined the effect of memantine, an uncompetitive NMDA receptor antagonist, on ethanol-induced NMDA receptor up-regulation. Primary glutamatergic rat hippocampal neurons were exposed to ethanol and memantine for 5 days. The ethanol-sensitive NMDA receptor subunits NR1, NR2A and NR213 were quantified by Western immunoblot analysis. Fxposure to ethanol (50 mM) caused an increase in the levels of NRI (137 +/- 11 % of untreated control, P = 0.009), NR2A (128 +/- 14 %. P 0.022) and N213 (136 +/- 119 %, P = 0.012). Coincubation with memantine (10 mu M) completely blocked the ethanol-induced up-regulation of NR1 (102, 4 %) NR2A (95 +/- 7 %) and NR2B (105 +/- 13 %). No effect of memantine on NR subunit expression was observable, except for NR2A, where a decrease (79 +/- 6 %, P = 0.034) was noted. Neither ethanol nor memantine alone or in combination were toxic in the concentrations tested. These results may provide a molecular explanation for beneficial effects of memantine on ethanol-induced glutamatergic hyperexcitability reflected in the ethanol withdrawal syndrome and on the development of ethanol dependence. (c) 2005 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.brainres.2005.06.017"],["dc.identifier.isi","000231493000005"],["dc.identifier.pmid","16009352"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50105"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0006-8993"],["dc.title","Mernantine inhibits ethanol-induced NMDA receptor up-regulation in rat hippocampal neurons"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","236"],["dc.bibliographiccitation.issue","4-5"],["dc.bibliographiccitation.journal","Neurodegenerative Diseases"],["dc.bibliographiccitation.lastpage","241"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Maler, J. M."],["dc.contributor.author","Kunz, N."],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Paul, S."],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2017-09-07T11:44:27Z"],["dc.date.available","2017-09-07T11:44:27Z"],["dc.date.issued","2004"],["dc.description.abstract","We studied endogenous amyloid precursor protein (APP) processing and amyloid beta (Aβ) peptide formation in primary chicken telencephalic neurons, because their Aβ peptide sequence is identical to humans. As detected by quantitative Aβ-SDS-PAGE/immunoblot, Aβ peptides 1–40/42 and three additional C-truncated species, namely Aβ1–37/38/39 were regularly released into the supernatant. The highly conserved Aβ quintet strongly resembles the pattern of Aβ peptides found in human cerebrospinal fluid. Furthermore, the C-terminally shorter Aβ peptides 1–33/34 could be readily detected. Recent evidence indicates that lithium specifically inhibits secretion of the amyloidogenic Aβ1–42 peptide in cultured permanent cells transfected with human APP. We therefore investigated the effect of lithium on Aβ peptide secretion as well as intracellular Aβ peptides in our untransfected primary cell culture system. Our data shows that lithium leads to a dose-dependent reduction of Aβ1–37/38/39/40/42 secretion. Surprisingly, intracellular analysis revealed that lithium specifically increases a band comigrating with synthetic Aβ1–38 while Aβ1–40 and Aβ1–42 remained almost unaffected. These results demonstrate for the first time that lithium treatment decreases Aβ peptide secretion in primary chicken neuronal cells but specifically elevates intracellular Aβ1–38. Therefore, we conclude that there are two independent mechanisms of lithium in intra- and extracellular Aβ peptide production."],["dc.identifier.doi","10.1159/000080992"],["dc.identifier.gro","3151670"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8488"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","chake"],["dc.relation.issn","1660-2854"],["dc.title","Lithium Decreases Secretion of Aβ1–42 and C-Truncated Species Aβ1–37/38/39/40 in Chicken Telencephalic Cultures but Specifically Increases Intracellular Aβ1–38"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Pharmacopsychiatry"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Esselmann, Herrmann"],["dc.contributor.author","Maler, Juan Manuel"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, J."],["dc.date.accessioned","2018-11-07T10:56:35Z"],["dc.date.available","2018-11-07T10:56:35Z"],["dc.date.issued","2005"],["dc.format.extent","260"],["dc.identifier.isi","000232591900153"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50049"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.publisher.place","Stuttgart"],["dc.relation.conference","24th Symposium of the Arbeitsgemeinschaft-fur-Neuropsychopharmakologie-und-Pharmakopsychiatrie (AGNP)"],["dc.relation.eventlocation","Munich, GERMANY"],["dc.relation.issn","0176-3679"],["dc.title","The concentrations of amyloid beta 1-42, total Tau and phospho-Tau181 in the CSF of patients with early dementia and MCI as measured with multiplexing technology"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","332"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Clinical Chemistry"],["dc.bibliographiccitation.lastpage","334"],["dc.bibliographiccitation.volume","52"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Beck, G."],["dc.contributor.author","Esselmann, Herrmann"],["dc.contributor.author","Bruckmoser, R."],["dc.contributor.author","Zimmermann, R."],["dc.contributor.author","Fiszer, M."],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Maler, Juan Manuel"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, J."],["dc.date.accessioned","2018-11-07T10:21:27Z"],["dc.date.available","2018-11-07T10:21:27Z"],["dc.date.issued","2006"],["dc.identifier.doi","10.1373/clinchem.2005.058776"],["dc.identifier.isi","000235069600030"],["dc.identifier.pmid","16449222"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42091"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Clinical Chemistry"],["dc.relation.issn","0009-9147"],["dc.title","Effect of sample collection tubes on cerebrospinal fluid concentrations of tau proteins and amyloid beta peptides"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","115"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Molecular Neuroscience"],["dc.bibliographiccitation.lastpage","122"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Esselmann, Herrmann"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Beck, G."],["dc.contributor.author","Maler, Juan Manuel"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, L."],["dc.date.accessioned","2018-11-07T10:52:49Z"],["dc.date.available","2018-11-07T10:52:49Z"],["dc.date.issued","2004"],["dc.description.abstract","Cerebrospinal fluid (CSF) concentrations of total Tau and Tau phosphorylated at threonine (position 181 [pTau181]) were studied with ELISA in a group of carefully selected patients with a neurochemically supported diagnosis of Alzheimer's disease (AD, n = 9; age range, 51-89 yr) and in a group of sex- and age-matched non-demented controls (n = 9; age range, 52-81 yr). The concentration of both biomarkers is increased significantly in the AD group (total Tau, p < 0.0008; pTau181, p < 0.008). A significant correlation between CSF concentrations of both biomarkers is observed (R = 0.897; P < 0.001). Neither total Tau nor pTau181 correlates with age or degree of memory impairment, and only a tendency is observed between the concentrations of total Tau and Abeta42 in the CSF. Our results further confirm a possible role of pTau181 as a diagnostic tool in AD. The current literature regarding the physiological and pathological role of phosphorylated Tau proteins is reviewed, as well as the role of these proteins as promising biomarkers in the diagnosis of neurodegenerative disorders."],["dc.identifier.doi","10.1385/JMN:23:1-2:115"],["dc.identifier.isi","000221487600012"],["dc.identifier.pmid","15126697"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49202"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Humana Press Inc"],["dc.publisher.place","Totowa"],["dc.relation.conference","Symposium on Novel Therapeutic Opportunities for Neuodegenerative Disease"],["dc.relation.eventlocation","Univ Aveiro, Aveiro, PORTUGAL"],["dc.relation.issn","0895-8696"],["dc.title","Tau protein phosphorylated at threonine 181 in CSF as a neurochemical biomarker in Alzheimer's disease - Original data and review of the literature"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","613"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Alzheimer s Disease"],["dc.bibliographiccitation.lastpage","622"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Klafki, Hans-Wolfgang"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Kamrowski-Kruck, Heike"],["dc.contributor.author","Maler, Juan Manuel"],["dc.contributor.author","Mueller, Katharina"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Heuser, Isabella"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Popp, Julius"],["dc.contributor.author","Froelich, Lutz"],["dc.contributor.author","Wolf, Stefanie"],["dc.contributor.author","Prinz, Berit"],["dc.contributor.author","Luckhaus, Christian"],["dc.contributor.author","Schroeder, Johannes"],["dc.contributor.author","Pantel, Johannes"],["dc.contributor.author","Gertz, Hermann-Josef"],["dc.contributor.author","Koelsch, Heike"],["dc.contributor.author","Mueller, Bernhard W."],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2018-11-07T08:34:46Z"],["dc.date.available","2018-11-07T08:34:46Z"],["dc.date.issued","2009"],["dc.description.abstract","The clinical diagnosis of neurodegenerative disorders can be supported by soluble biomarkers in cerebrospinal fluid (CSF), such as tau protein, phospho-tau, and amyloid-beta peptides. In particular, increased CSF levels of phospho-tau in Alzheimer's disease appear to reflect disease specific pathological processes. We report here evidence for the presence of soluble MAP-kinase ERK1/2 in a small set of human CSF samples from patients with Alzheimer's disease, frontotemporal degeneration, and mild cognitive impairment. The level of total ERK1/2 in CSF as measured by electrochemiluminescent assay was correlated with that of total tau and phospho-tau. A small fraction of ERK1/2 in a pooled CSF sample was found to be in the doubly phosphorylated (activated) state. Our findings suggest that i) MAP kinase ERK1/2 is apparently released under neurodegenerative conditions in parallel with tau and phospho-tau and ii) in the future, it might be possible to find in CSF samples evidence for disease related alterations in brain kinase signaling pathways by use of highly sensitive and activation-state specific anti-kinase antibodies."],["dc.identifier.doi","10.3233/JAD-2009-1167"],["dc.identifier.isi","000272860100013"],["dc.identifier.pmid","19625747"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17898"],["dc.notes.claim","Wed Nov 07 12:36:41 UTC 2018:dc_contributor_author:Hallo Sabine, das ist nicht mein Artikel.... :-)"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ios Press"],["dc.relation.issn","1387-2877"],["dc.title","Measurement of ERK 1/2 in CSF from Patients with Neuropsychiatric Disorders and Evidence for the Presence of the Activated Form"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]