Degner, Detlef

[["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.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","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","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"]]

[["dc.bibliographiccitation.firstpage","40"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Alcohol and Alcoholism"],["dc.bibliographiccitation.lastpage","44"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Sperling, W."],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Graesel, E."],["dc.contributor.author","Bleich, K."],["dc.contributor.author","Wilhelm, Julia"],["dc.contributor.author","Havemann-Reinecke, Ursula"],["dc.contributor.author","Javaheripour, K."],["dc.contributor.author","Kornhuber, Johannes"],["dc.date.accessioned","2018-11-07T10:41:49Z"],["dc.date.available","2018-11-07T10:41:49Z"],["dc.date.issued","2003"],["dc.description.abstract","Aims and Methods: Magnetic resonance imaging (MRI) of the hippocampus has been extensively studied in both neurological and psychiatric disorders. Furthermore, hippocampal volume reductions on MRI have been reported in patients with chronic alcoholism. The present volumetric MRI study was undertaken to determine whether an association exists between hippocampal volume reduction and first-onset alcohol withdrawal seizure. Until recently, no data as to whether hippocampal volume reductions in alcoholics might serve as a predictor of withdrawal seizures were available. Results: We found the average hippocampal volumes measured by high resolution MRI to be significantly reduced in 52 alcoholics compared with 30 healthy controls. Besides a decrease of hippocampal volume in patients with chronic alcoholism, we could not find any significant correlation between the occurrence of seizures during alcohol withdrawal and the amount of hippocampal volume reduction in these patients. Conclusions: Thus, the alcoholism-related atrophy within the hippocampal formation in patients suffering from chronic alcoholism does not seem to be the source of convulsive activity in these patients. Neither does the amount of atrophy allow the occurrence of first-onset withdrawal seizures to be predicted."],["dc.identifier.doi","10.1093/alcalc/agg017"],["dc.identifier.isi","000181029400008"],["dc.identifier.pmid","12554606"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46628"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0735-0414"],["dc.title","Lack of association between hippocampal volume reduction and first-onset alcohol withdrawal seizure. A volumetric MRI study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Neuropsychopharmacology"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Maler, M."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Bleich, Stefan"],["dc.date.accessioned","2018-11-07T10:36:28Z"],["dc.date.available","2018-11-07T10:36:28Z"],["dc.date.issued","2003"],["dc.format.extent","S406"],["dc.identifier.doi","10.1016/S0924-977X(03)92244-9"],["dc.identifier.isi","000185412300650"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45333"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","16th Congress of the European-College-of-Neuropsychopharmacology"],["dc.relation.eventlocation","PRAGUE, CZECH REPUBLIC"],["dc.relation.issn","0924-977X"],["dc.title","Homocysteine induces cell death of astrocytes in vitro"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2749"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Neuroreport"],["dc.bibliographiccitation.lastpage","2752"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Bandelow, Borwin"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Kornhuber, Johannes"],["dc.date.accessioned","2018-11-07T10:33:14Z"],["dc.date.available","2018-11-07T10:33:14Z"],["dc.date.issued","2000"],["dc.description.abstract","An adaptive consequence of prolonged ethanol consumption is a compensatory up-regulation of NMDA receptors in certain brain areas. Taking into account that homocysteine and its breakdown products (i.e. homocysteic acid) are putative neurotransmitters and agonists at the NMDA receptor, the aim of this study was to assess the influence of levels of homocysteine on alcohol withdrawal seizures. Six patients with chronic alcoholism who suffered from withdrawal seizures had significantly higher levels of homocysteine on admission (84.7 +/- 29.8 mu mol/l) than patients (n = 26) who did not develop seizures (30.2 +/- 23.2 mu mol/l; U = 8.0, p = 0.0007). Furthermore, seizure patients had significantly lower levels of folate and significantly higher blood alcohol concentrations. Using a logistic regression analysis, withdrawal seizures were best predicted by a high homocysteine level on admission (P < 0.01; odds ratio = 1.05). Homocysteine levels on admission may be a useful screening method to identify patients at risk for withdrawal seizures. NeuroReport 11:2749-2752 (C) 2000 Lippincott Williams & Wilkins."],["dc.identifier.doi","10.1097/00001756-200008210-00028"],["dc.identifier.isi","000089003300036"],["dc.identifier.pmid","10976956"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44558"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0959-4965"],["dc.title","Plasma homocysteine is a predictor of alcohol withdrawal seizures"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S420"],["dc.bibliographiccitation.journal","European Neuropsychopharmacology"],["dc.bibliographiccitation.lastpage","S421"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Wilhelm, Julia"],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Sperling, W."],["dc.contributor.author","Kornhuber, Johannes"],["dc.date.accessioned","2018-11-07T10:36:27Z"],["dc.date.available","2018-11-07T10:36:27Z"],["dc.date.issued","2003"],["dc.identifier.doi","10.1016/S0924-977X(03)92282-6"],["dc.identifier.isi","000185412300688"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45331"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","16th Congress of the European-College-of-Neuropsychopharmacology"],["dc.relation.eventlocation","PRAGUE, CZECH REPUBLIC"],["dc.relation.issn","0924-977X"],["dc.title","Apolipoprotein E epsilon 4 is associated with hippocampal volume reduction in females with alcoholism"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","PII S0304-3940(02)01194-1"],["dc.bibliographiccitation.firstpage","179"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","182"],["dc.bibliographiccitation.volume","335"],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Bandelow, Borwin"],["dc.contributor.author","Javaheripour, K."],["dc.contributor.author","Mueller, A."],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Wilhelm, Julia"],["dc.contributor.author","Havemann-Reinecke, Ursula"],["dc.contributor.author","Sperling, W."],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Kornhuber, Johannes"],["dc.date.accessioned","2018-11-07T10:41:44Z"],["dc.date.available","2018-11-07T10:41:44Z"],["dc.date.issued","2003"],["dc.description.abstract","Chronic alcohol consumption can induce brain atrophy, whereby the exact mechanism of brain damage in alcoholics remains unknown. There is evidence that chronic alcoholism is associated with hyperhomocysteinemia. Homocysteine is an excitatory amino acid which markedly enhances the vulnerability of neuronal cells to excitotoxic and oxidative injury in vitro and in vivo. The present volumetric magnetic resonance imaging study included 52 chronic alcoholics and 30 non-drinking healthy controls. Patients were active drinkers and had an established diagnosis of alcohol dependence. We investigated the influence of different variables on the hippocampal volume of patients suffering from chronic alcoholism. We observed that pathological raised levels of plasma homocysteine showed the most significant correlation to hippocampal volume reduction (P < 0.001, multiple regression analysis). Raised plasma levels of homocysteine are associated with hippocampal (brain) atrophy in alcoholism. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/S0304-3940(02)01194-1"],["dc.identifier.isi","000180410900008"],["dc.identifier.pmid","12531462"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46612"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","Hyperhomocysteinemia as a new risk factor for brain shrinkage in patients with alcoholism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","9228"],["dc.bibliographiccitation.journal","The Lancet"],["dc.bibliographiccitation.volume","356"],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Kropp, Silke"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Kornhuber, Johannes"],["dc.date.accessioned","2018-11-07T10:34:03Z"],["dc.date.available","2018-11-07T10:34:03Z"],["dc.date.issued","2000"],["dc.format.extent","512"],["dc.identifier.doi","10.1016/S0140-6736(05)74186-6"],["dc.identifier.isi","000088657700056"],["dc.identifier.pmid","10981920"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44766"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lancet Ltd"],["dc.relation.issn","0140-6736"],["dc.title","Red wine, spirits, beer and serum homocysteine"],["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"]]