Kornhuber, Johannes

[["dc.bibliographiccitation.firstpage","296"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Alcohol and Alcoholism"],["dc.bibliographiccitation.lastpage","299"],["dc.bibliographiccitation.volume","43"],["dc.contributor.author","Wilhelm, Julia"],["dc.contributor.author","Frieling, Helge"],["dc.contributor.author","Hillemacher, Thomas"],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Bleich, Stefan"],["dc.date.accessioned","2018-11-07T11:15:16Z"],["dc.date.available","2018-11-07T11:15:16Z"],["dc.date.issued","2008"],["dc.description.abstract","Aims: The individual extent of structural brain tissue changes in patients with alcohol dependence is influenced by genetic factors, gender, age and possibly a dose/duration-effect. Aim of the present study was to investigate different types of alcoholic beverages with regard to hippocampal volume loss in patients suffering from alcoholism. Methods: We included 52 patients with alcohol dependence and divided them according to their preferred type of beverage consumption (beer, wine, and spirits). Hippocampal volumes were determined using volumetric high-resolution MR imaging. Results: There was a significant difference in hippocampal volumes between patients consuming different beverages (ANOVA: F = 7.454; df = 2; P = 0.0015) with the smallest volumes in the wine group, followed by the spirits group. Furthermore, patients with a preferred spirits consumption showed significantly higher plasma homocysteine levels (ANOVA: F = 3.39; df = 2; P = 0.042). Linear regression analyses revealed an association of homocysteine and hippocampal volume only in the group of patients preferring spirits (R(2) = 0.364; P = 0.008). Conclusions: Homocysteine-mediated excitotoxicity may be an important pathophysiological mechanism in ethanol-related brain damage, particularly in patients consuming wine and spirits. The extent of brain atrophy in beer consuming patients seems to be more moderate."],["dc.identifier.doi","10.1093/alcalc/agn002"],["dc.identifier.isi","000255756300008"],["dc.identifier.pmid","18238850"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54329"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0735-0414"],["dc.title","Hippocampal volume loss in patients with alcoholism is influenced by the consumed type of alcoholic beverage"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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","379"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","386"],["dc.bibliographiccitation.volume","78"],["dc.contributor.author","Wagner, M."],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Reischies, Friedel M."],["dc.contributor.author","Daerr, M."],["dc.contributor.author","Wolfsgruber, S."],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Popp, J."],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Huell, Michael"],["dc.contributor.author","Froelich, Lutz"],["dc.contributor.author","Hampel, Harald"],["dc.contributor.author","Perneczky, Robert"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Jahn, Holger"],["dc.contributor.author","Luckhaus, C."],["dc.contributor.author","Gertz, H.-J."],["dc.contributor.author","Schroeder, J."],["dc.contributor.author","Pantel, Johannes"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, J."],["dc.date.accessioned","2018-11-07T09:13:50Z"],["dc.date.available","2018-11-07T09:13:50Z"],["dc.date.issued","2012"],["dc.description.abstract","Objective: To compare cued recall measures with other memory and nonmemory tests regarding their association with a biomarker profile indicative of Alzheimer disease (AD) in CSF among patients with mild cognitive impairment (MCI). Methods: Data were obtained by the German Dementia Competence Network. A total of 185 memory clinic patients fulfilling broad criteria for MCI (1 SD deficit in memory tests or in nonmemory tests) were assessed with an extended neuropsychological battery, which included the Free and Cued Selective Reminding Test (FCSRT), the word list learning task from the Consortium to Establish a Registry for Alzheimer's Disease neuropsychological battery (CERAD-NP), and the Logical Memory (LM) paragraph recall test from the Wechsler Memory Scale-Revised. CSF was obtained from all patients. Results: A total of 74 out of 185 subjects with MCI (40%) had a CSF profile consistent with AD (A beta(1-42)/tau ratio; CSF AD + group). FCSRT measures reflecting both free and cued recall discriminated best between CSF AD + and CSF AD - patients, and significantly improved CSF AD classification accuracy, as compared with CERAD delayed recall and LM delayed recall. Conclusions: Cued recall deficits are most closely associated with CSF biomarkers indicative of AD in subjects with MCI. This novel finding complements results from prospective clinical studies and provides further empirical support for cued recall as a specific indicator of prodromal AD, in line with recently proposed research criteria. Neurology (R) 2012; 78: 379-386"],["dc.identifier.doi","10.1212/WNL.0b013e318245f447"],["dc.identifier.isi","000300392000007"],["dc.identifier.pmid","22238414"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27260"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","Biomarker validation of a cued recall memory deficit in prodromal Alzheimer disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","872"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Alzheimer's & Dementia"],["dc.bibliographiccitation.lastpage","881"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Louwersheimer, Eva"],["dc.contributor.author","Wolfsgruber, Steffen"],["dc.contributor.author","Espinosa, Ana"],["dc.contributor.author","Lacour, André"],["dc.contributor.author","Heilmann-Heimbach, Stefanie"],["dc.contributor.author","Alegret, Montserrat"],["dc.contributor.author","Hernández, Isabel"],["dc.contributor.author","Rosende-Roca, Maitée"],["dc.contributor.author","Tárraga, Lluís"],["dc.contributor.author","Boada, Mercè"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Frölich, Lutz"],["dc.contributor.author","Hüll, Michael"],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Scherer, Martin"],["dc.contributor.author","Riedel-Heller, Steffi"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Nöthen, Markus M."],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Koene, Ted"],["dc.contributor.author","Scheltens, Philip"],["dc.contributor.author","Holstege, Henne"],["dc.contributor.author","Wagner, Michael"],["dc.contributor.author","Ruiz, Agustín"],["dc.contributor.author","van der Flier, Wiesje M."],["dc.contributor.author","Becker, Tim"],["dc.contributor.author","Ramirez, Alfredo"],["dc.date.accessioned","2017-09-07T11:44:36Z"],["dc.date.available","2017-09-07T11:44:36Z"],["dc.date.issued","2016"],["dc.description.abstract","IntroductionWe evaluated the effect of Alzheimer's disease (AD) susceptibility loci on endophenotypes closely related with AD pathology in patients with mild cognitive impairment (MCI).MethodsWe selected 1730 MCI patients from four independent data sets. Weighted polygenic risk scores (PGS) were constructed of 18 non-apolipoprotein E (APOE) AD risk variants. In addition, we determined APOE genotype. AD endophenotypes were cognitive decline over time and cerebrospinal fluid (CSF) biomarkers (aβ, tau, ptau).ResultsPGS was modestly associated with cognitive decline over time, as measured by mini-mental state examination (MMSE) (β ± SE:−0.24 ± 0.10; P = .012), and with CSF levels of tau and ptau (tau: 1.38 ± 0.36, P = 1.21 × 10−4; ptau: 1.40 ± 0.36, P = 1.02 × 10−4).DiscussionIn MCI, we observed a joint effect of AD susceptibility loci on nonamyloid endophenotypes, suggesting a link of these genetic loci with neuronal degeneration in general rather than with Alzheimer-related amyloid deposition."],["dc.identifier.doi","10.1016/j.jalz.2016.01.006"],["dc.identifier.gro","3151698"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8517"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","1552-5260"],["dc.title","Alzheimer's disease risk variants modulate endophenotypes in mild cognitive impairment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Psychiatry"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Schlautmann, V."],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Bleich, Stefan"],["dc.date.accessioned","2018-11-07T09:29:24Z"],["dc.date.available","2018-11-07T09:29:24Z"],["dc.date.issued","2000"],["dc.format.extent","369S"],["dc.identifier.doi","10.1016/S0924-9338(00)94588-7"],["dc.identifier.isi","000165731700527"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31020"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Editions Scientifiques Medicales Elsevier"],["dc.publisher.place","Paris cedex 15"],["dc.relation.issn","0924-9338"],["dc.title","Thyroid axis alterations in psychoses"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2485"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","2490"],["dc.bibliographiccitation.volume","73"],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Otto, M."],["dc.contributor.author","Baxter, H. C."],["dc.contributor.author","Bodemer, M."],["dc.contributor.author","Steinacker, P."],["dc.contributor.author","Bahn, E."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Kornhuber, J."],["dc.contributor.author","Kretzschmar, H. A."],["dc.contributor.author","Poser, S."],["dc.contributor.author","Rüther, E."],["dc.contributor.author","Aitken, A."],["dc.date.accessioned","2017-09-07T11:44:33Z"],["dc.date.available","2017-09-07T11:44:33Z"],["dc.date.issued","1999"],["dc.description.abstract","Two-dimensional polyacrylamide gel electrophoresis of CSF has been used in the diagnosis of Creutzfeldt-Jakob disease (CJD). One of the two diagnostic protein spots was identified as isoform(s) of the 14-3-3 family of abundant brain proteins. This has led to the development of one-dimensional 14-3-3 sodium dodecyl sulfate polyacrylamide gel electrophoresis immunoblot, which is currently used to support the diagnosis of CJD. In the present study employing western blot analysis, we have identified the panel of 14-3-3 isoforms that appear in the CSF of 10 patients with CJD compared with 10 patients with other dementias. The results clearly show that the 14-3-3 isoforms β, γ, ε, and η are present in the CSF of patients with CJD and can be used to differentiate other dementias. 14-3-3η also gave a baseline signal in all patients with other dementias, including six patients with Alzheimer's disease. The presence of 14-3-3η in the CSF of a patient with herpes simplex encephalitis was particularly noteworthy. This study has determined that isoform-specific 14-3-3 antibodies against β, γ, and ε should be considered for the neurochemical differentiation of CJD from other neurodegenerative diseases."],["dc.identifier.doi","10.1046/j.1471-4159.1999.0732485.x"],["dc.identifier.gro","3151688"],["dc.identifier.pmid","10582609"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8506"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0022-3042"],["dc.title","Isoform Pattern of 14-3-3 Proteins in the Cerebrospinal Fluid of Patients with Creutzfeldt-Jakob Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1005"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Alzheimer's Disease"],["dc.bibliographiccitation.lastpage","1015"],["dc.bibliographiccitation.volume","76"],["dc.contributor.author","Fuentes, Manuel"],["dc.contributor.author","Klostermann, Arne"],["dc.contributor.author","Kleineidam, Luca"],["dc.contributor.author","Bauer, Chris"],["dc.contributor.author","Schuchhardt, Johannes"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Frölich, Lutz"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Klöppel, Stefan"],["dc.contributor.author","Schieting, Vera"],["dc.contributor.author","Teipel, Stefan J."],["dc.contributor.author","Wagner, Michael"],["dc.contributor.author","Peters, Oliver"],["dc.date.accessioned","2021-04-14T08:27:21Z"],["dc.date.available","2021-04-14T08:27:21Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.3233/JAD-200230"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82256"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1875-8908"],["dc.relation.issn","1387-2877"],["dc.title","Identification of a Cascade of Changes in Activities of Daily Living Preceding Short-Term Clinical Deterioration in Mild Alzheimer’s Disease Dementia via Lead-Lag Analysis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","227"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Neuropsychiatry"],["dc.bibliographiccitation.lastpage","231"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Kropp, Silke"],["dc.contributor.author","Kern, V."],["dc.contributor.author","Lange, K."],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Hajak, Goran"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Emrich, H. M."],["dc.contributor.author","Schneider, Udo"],["dc.contributor.author","Bleich, Stefan"],["dc.date.accessioned","2018-11-07T11:20:37Z"],["dc.date.available","2018-11-07T11:20:37Z"],["dc.date.issued","2005"],["dc.description.abstract","Neurotoxicity of first-generation antipsychotics: (FGAs) may be involved in lipid peroxidation, which is the pathogenesis of extrapyramidal symptoms, including tardive dyskinesia (TD). Blood samples at day 0, 7, and 21 drawn from patients taking antipsychotics were analyzed for malondialdehyde (MDA) in plasma, a marker of lipid peroxidation, by high-performance liquid chromatography. Of 115 patients enrolled, 92 patients completed the study. Most MDA levels were within normal ranges (<1.0 mu mol/liter). Malondialdehyde levels in patients receiving clozapine (p = 0.002), quetiapine (p = 0.003), amisulpride (p = 0.008), and risperidone (p = 0.008) were significantly lower than within the first generation antipsychotic group. The authors conclude that lipid peroxidation is significantly higher in treatment with FGAs."],["dc.identifier.doi","10.1176/appi.neuropsych.17.2.227"],["dc.identifier.isi","000229541000014"],["dc.identifier.pmid","15939978"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55581"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Psychiatric Publishing, Inc"],["dc.publisher.place","Arlington"],["dc.relation.conference","Annual Meeting of the Nordic-Association-for-Psychiatric-Epidemiology"],["dc.relation.eventlocation","REYKJAVIK, ICELAND"],["dc.relation.issn","1545-7222"],["dc.relation.issn","0895-0172"],["dc.title","Oxidative stress during treatment with first- and second-generation antipsychotics"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","68"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","71"],["dc.bibliographiccitation.volume","440"],["dc.contributor.author","Koelsch, Heike"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Dichgans, Martin"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Froelich, Lutz"],["dc.contributor.author","Heuser, Isabella"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Schulz, Joerg B."],["dc.contributor.author","Schwab, Sibylle G."],["dc.contributor.author","Maier, Wolfgang"],["dc.date.accessioned","2018-11-07T11:12:54Z"],["dc.date.available","2018-11-07T11:12:54Z"],["dc.date.issued","2008"],["dc.description.abstract","SORL1 gene variants were described as risk factors of Alzheimer's disease (AD). We investigated the association of four SORL1 variants with CSF levels of A beta(42) and A beta(40) in 153 AD patients recruited from a multicenter study of the German Competence Net Dementias. Only one SORL1 SNP was associated with altered A beta(42) levels in the single marker analysis (SNP21: p = 0.011), the other SNPs did not show an association with A beta(42) orA beta(40) CSF levels. Haplotype analysis identified a three marker SORL1 haplotype consisting of SNP19 T-allele, SNP21 G-allele and SNP23 A-allele (T/G/A) which was associated with reduced A beta(42) CSF levels in AD patients (p = 0.003). A beta(40) levels were also lower in carriers of this haplotype; however, this did not reach statistical significance (p = 0.15). We found a SORL1 haplotype which was associated with CSF levels of amyloid-P cleavage products, measured as altered levels of A beta(42). Thus our data suggest that: SORL1 gene variants might influence AD pathology. (C) 2008 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.neulet.2008.05.049"],["dc.identifier.isi","000257640200016"],["dc.identifier.pmid","18541377"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53768"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","Influence of SORL1 gene variants: Association with CSF amyloid-beta products in probable 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","466"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Fortschritte der Neurologie · Psychiatrie"],["dc.bibliographiccitation.lastpage","475"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Maler, Manuel"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Rüther, Eckart"],["dc.date.accessioned","2017-09-07T11:44:45Z"],["dc.date.available","2017-09-07T11:44:45Z"],["dc.date.issued","2008"],["dc.description.abstract","The spectrum of action of flupirtine includes analgesic, muscle-relaxant and neuroprotective properties. The substance's mechanism of action has yet to be fully explained. Over the past few years, however, evidence has accumulated that flupirtine interacts with the glutamatergic N-Methyl-D-Aspartate (NMDA) receptor. Although it was not possible to demonstrate a direct effect on the NMDA receptor, all of the findings pointed to an indirect influence on the NMDA receptor in the sense of a functional NMDA antagonism. It was thus postulated that a site of action \"up- or downstream\" of the NMDA receptor is influenced. Such a site of action proved to be the G-protein-activated inwardly rectifying K+ channels (GIRK), the opening of which leads to a stabilisation of the resting membrane potential of neuronal cells and thus causes an indirect inhibition of the NMDA receptor. At therapeutically relevant concentrations, flupirtine is a neuronal potassium channel opener. This mechanism may explain the spectrum of action of flupirtine. Selective neuronal potassium channel opening (SNEPCO) thus proves to be a new principle of action, making flupirtine the prototype of a new substance class with analgesic, muscle-relaxant and neuroprotective properties. The experimental basis for this working hypothesis and the resulting model concepts are presented from the perspective of a four-stage approach."],["dc.description.abstract","Das Wirkspektrum von Flupirtin umfaßt analgetische, muskelentspannende und neuroprotektive Eigenschaften. Der Wirkmechanismus der Substanz war bislang unzureichend bekannt. In den letzten Jahren verdichteten sich jedoch Hinweise auf eine Interaktion von Flupirtin mit dem glutamatergen N-Methyl-D-Aspartat (NMDA)-Rezeptor. Obwohl eine direkte Wirkung am NMDA-Rezeptor nicht nachweisbar war. sprachen alle Befunde für eine indirekte Beeinflussung des NMDA-Rezeptors im Sinne eines funktionellen NMDA-Antagonismus. Es wurde somit postuliert, daß ein Wirkort ,,up- oder downstream\" vom NMDA-Rezeptor beeinflußt wird. Als solcher erwiesen sich die G-Protein gesteuerten einwärts gleichrichtenden K\"-Kanale (GIRK), deren Öffnung zu einer Stabilisierung des Ruhemembranpotentials neuronaler Zellen führt und dadurch eine indirekte Hemmung des NMDA-Rezeptors bewirkt. Flupirtin ist in therapeutisch relevanten Konzentrationen ein neuronaler K'-Kanalöffner (neuronal potassium Channel opener). Dieser Mechanismus vermag das Wirkspektrum von Flupirtin zu erklären. Damit erweist sich die selektive neuronale K+-Kanaloffnung (SNEPCO) als ein neues Wirkprinzip und Flupirtin als Prototyp einer neuen Substanzklasse mit analgetischen, muskelrelaxierenden und neuroprotektiven Eigenschaften. Die experimentellen Grundlagen dieser Arbeitshypothese und der daraus resultierenden Modellvorstellungen werden in einer vierstufigen Betrachtungsebene vorgestellt."],["dc.identifier.doi","10.1055/s-2007-994997"],["dc.identifier.gro","3151740"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8561"],["dc.language.iso","de"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0720-4299"],["dc.title","Neuronale Kaliumkanalöffnung durch Flupirtin"],["dc.title.subtitle","Opening of Neuronal K+ Channels by Flupirtine"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]