Müller, Michael

[["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Antioxidants"],["dc.bibliographiccitation.volume","11"],["dc.contributor.affiliation","Baroncelli, Laura; 1Institut für Neuro- und Sinnesphysiologie, Universitätsmedizin Göttingen, Georg-August-Universität Göttingen, Humboldtallee 23, D-37073 Göttingen, Germany; laura.baroncelli@in.cnr.it (L.B.); stefanieauel@yahoo.de (S.A.); lena.rinne@gmx.net (L.R.); ak_schuster@web.de (A.-K.S.); victoriabrand@gmx.de (V.B.); bhildeb2@gwdg.de (B.K.); dietrich.katharina85@gmail.com (K.D.)"],["dc.contributor.affiliation","Auel, Stefanie; 1Institut für Neuro- und Sinnesphysiologie, Universitätsmedizin Göttingen, Georg-August-Universität Göttingen, Humboldtallee 23, D-37073 Göttingen, Germany; laura.baroncelli@in.cnr.it (L.B.); stefanieauel@yahoo.de (S.A.); lena.rinne@gmx.net (L.R.); ak_schuster@web.de (A.-K.S.); victoriabrand@gmx.de (V.B.); bhildeb2@gwdg.de (B.K.); dietrich.katharina85@gmail.com (K.D.)"],["dc.contributor.affiliation","Rinne, Lena; 1Institut für Neuro- und Sinnesphysiologie, Universitätsmedizin Göttingen, Georg-August-Universität Göttingen, Humboldtallee 23, D-37073 Göttingen, Germany; laura.baroncelli@in.cnr.it (L.B.); stefanieauel@yahoo.de (S.A.); lena.rinne@gmx.net (L.R.); ak_schuster@web.de (A.-K.S.); victoriabrand@gmx.de (V.B.); bhildeb2@gwdg.de (B.K.); dietrich.katharina85@gmail.com (K.D.)"],["dc.contributor.affiliation","Schuster, Ann-Kathrin; 1Institut für Neuro- und Sinnesphysiologie, Universitätsmedizin Göttingen, Georg-August-Universität Göttingen, Humboldtallee 23, D-37073 Göttingen, Germany; laura.baroncelli@in.cnr.it (L.B.); stefanieauel@yahoo.de (S.A.); lena.rinne@gmx.net (L.R.); ak_schuster@web.de (A.-K.S.); victoriabrand@gmx.de (V.B.); bhildeb2@gwdg.de (B.K.); dietrich.katharina85@gmail.com (K.D.)"],["dc.contributor.affiliation","Brand, Victoria; 1Institut für Neuro- und Sinnesphysiologie, Universitätsmedizin Göttingen, Georg-August-Universität Göttingen, Humboldtallee 23, D-37073 Göttingen, Germany; laura.baroncelli@in.cnr.it (L.B.); stefanieauel@yahoo.de (S.A.); lena.rinne@gmx.net (L.R.); ak_schuster@web.de (A.-K.S.); victoriabrand@gmx.de (V.B.); bhildeb2@gwdg.de (B.K.); dietrich.katharina85@gmail.com (K.D.)"],["dc.contributor.affiliation","Kempkes, Belinda; 1Institut für Neuro- und Sinnesphysiologie, Universitätsmedizin Göttingen, Georg-August-Universität Göttingen, Humboldtallee 23, D-37073 Göttingen, Germany; laura.baroncelli@in.cnr.it (L.B.); stefanieauel@yahoo.de (S.A.); lena.rinne@gmx.net (L.R.); ak_schuster@web.de (A.-K.S.); victoriabrand@gmx.de (V.B.); bhildeb2@gwdg.de (B.K.); dietrich.katharina85@gmail.com (K.D.)"],["dc.contributor.affiliation","Dietrich, Katharina; 1Institut für Neuro- und Sinnesphysiologie, Universitätsmedizin Göttingen, Georg-August-Universität Göttingen, Humboldtallee 23, D-37073 Göttingen, Germany; laura.baroncelli@in.cnr.it (L.B.); stefanieauel@yahoo.de (S.A.); lena.rinne@gmx.net (L.R.); ak_schuster@web.de (A.-K.S.); victoriabrand@gmx.de (V.B.); bhildeb2@gwdg.de (B.K.); dietrich.katharina85@gmail.com (K.D.)"],["dc.contributor.affiliation","Müller, Michael; 1Institut für Neuro- und Sinnesphysiologie, Universitätsmedizin Göttingen, Georg-August-Universität Göttingen, Humboldtallee 23, D-37073 Göttingen, Germany; laura.baroncelli@in.cnr.it (L.B.); stefanieauel@yahoo.de (S.A.); lena.rinne@gmx.net (L.R.); ak_schuster@web.de (A.-K.S.); victoriabrand@gmx.de (V.B.); bhildeb2@gwdg.de (B.K.); dietrich.katharina85@gmail.com (K.D.)"],["dc.contributor.author","Baroncelli, Laura"],["dc.contributor.author","Auel, Stefanie"],["dc.contributor.author","Rinne, Lena"],["dc.contributor.author","Schuster, Ann-Kathrin"],["dc.contributor.author","Brand, Victoria"],["dc.contributor.author","Kempkes, Belinda"],["dc.contributor.author","Dietrich, Katharina"],["dc.contributor.author","Müller, Michael"],["dc.date.accessioned","2022-08-04T08:23:31Z"],["dc.date.available","2022-08-04T08:23:31Z"],["dc.date.issued","2022-07-20"],["dc.date.updated","2022-08-03T09:14:27Z"],["dc.description.abstract","Rett syndrome (RTT) is a severe neurodevelopmental disorder that typically arises from spontaneous germline mutations in the X-chromosomal methyl-CpG binding protein 2 (MECP2) gene. For the first 6–18 months of life, the development of the mostly female patients appears normal. Subsequently, cognitive impairment, motor disturbances, hand stereotypies, epilepsy, and irregular breathing manifest, with previously learned skills being lost. Early mitochondrial impairment and a systemic oxidative burden are part of the complex pathogenesis, and contribute to disease progression. Accordingly, partial therapeutic merits of redox-stabilizing and antioxidant (AO) treatments were reported in RTT patients and Mecp2-mutant mice. Pursuing these findings, we conducted a full preclinical trial on male and female mice to define the therapeutic value of an orally administered AO cocktail composed of vitamin E, N-acetylcysteine, and α-lipoic acid. AO treatment ameliorated some of the microcephaly-related aspects. Moreover, the reduced growth, lowered blood glucose levels, and the hippocampal synaptic plasticity of Mecp2−/y mice improved. However, the first-time detected intensified oxidative DNA damage in Mecp2-mutant cortex persisted. The behavioral performance, breathing regularity, and life expectancy of Mecp2-mutant mice did not improve upon AO treatment. Long-term-treated Mecp2+/− mice eventually became obese. In conclusion, the AO cocktail ameliorated a subset of symptoms of the complex RTT-related phenotype, thereby further confirming the potential merits of AO-based pharmacotherapies. Yet, it also became evident that long-term AO treatment may lose efficacy and even aggravate the metabolic disturbances in RTT. This emphasizes the importance of a constantly well-balanced redox balance for systemic well-being."],["dc.description.sponsorship","Cluster of Excellence and Deutsche Forschungsgemeinschaft Research Center Nanoscale Microscopy and Molecular Physiology of the Brain (CNMPB)"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft (DFG, German Research Foundation)"],["dc.description.sponsorship","Umberto Veronesi Foundation"],["dc.description.sponsorship","Georg-August-Universität Göttingen"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.3390/antiox11071406"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112622"],["dc.language.iso","en"],["dc.relation.eissn","2076-3921"],["dc.rights","CC BY 4.0"],["dc.title","Oral Feeding of an Antioxidant Cocktail as a Therapeutic Strategy in a Mouse Model of Rett Syndrome: Merits and Limitations of Long-Term Treatment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","4S_Part_12"],["dc.bibliographiccitation.journal","Alzheimer's & Dementia"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Dietrich, Katharina"],["dc.contributor.author","Bouter, Yvonne"],["dc.contributor.author","Wittnam, Jessica"],["dc.contributor.author","Pillot, Thierry"],["dc.contributor.author","Papot‐Couturier, Sophie"],["dc.contributor.author","Lefebvre, Thomas"],["dc.contributor.author","Sprenger, Frederick"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Janc, Oliwia A."],["dc.contributor.author","Müller, Michael"],["dc.contributor.author","Bayer, Thomas"],["dc.date.accessioned","2021-12-08T12:27:20Z"],["dc.date.available","2021-12-08T12:27:20Z"],["dc.date.issued","2013"],["dc.identifier.doi","10.1016/j.jalz.2013.05.1030"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/95320"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-476"],["dc.relation.eissn","1552-5279"],["dc.relation.issn","1552-5260"],["dc.rights.uri","http://onlinelibrary.wiley.com/termsAndConditions#vor"],["dc.title","P2–381: Tg4–42: A new mouse model of Alzheimer's disease—N‐truncated beta‐amyloid 4–42 affects memory decline and synaptic plasticity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","41"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Antioxidants & Redox Signaling"],["dc.bibliographiccitation.lastpage","58"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Wagener, Kerstin C."],["dc.contributor.author","Kolbrink, Benedikt"],["dc.contributor.author","Dietrich, Katharina"],["dc.contributor.author","Kizina, Kathrin M."],["dc.contributor.author","Terwitte, Lukas S."],["dc.contributor.author","Kempkes, Belinda"],["dc.contributor.author","Bao, Guobin"],["dc.contributor.author","Müller, Michael"],["dc.date.accessioned","2018-09-28T09:52:54Z"],["dc.date.available","2018-09-28T09:52:54Z"],["dc.date.issued","2016"],["dc.description.abstract","Reactive oxygen species (ROS) and downstream redox alterations not only mediate physiological signaling but also neuropathology. For long, ROS/redox imaging was hampered by a lack of reliable probes. Genetically encoded redox sensors overcame this gap and revolutionized (sub)cellular redox imaging. Yet, the successful delivery of sensor-coding DNA, which demands transfection/transduction of cultured preparations or stereotaxic microinjections of each subject, remains challenging. By generating transgenic mice, we aimed to overcome limiting cultured preparations, circumvent surgical interventions, and to extend effectively redox imaging to complex and adult preparations."],["dc.identifier.doi","10.1089/ars.2015.6587"],["dc.identifier.pmid","27059697"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15848"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.eissn","1557-7716"],["dc.title","Redox Indicator Mice Stably Expressing Genetically Encoded Neuronal roGFP: Versatile Tools to Decipher Subcellular Redox Dynamics in Neuropathophysiology"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","266"],["dc.bibliographiccitation.journal","Frontiers in Cellular Neuroscience"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Janc, Oliwia A."],["dc.contributor.author","Hüser, Marc A."],["dc.contributor.author","Dietrich, Katharina"],["dc.contributor.author","Kempkes, Belinda"],["dc.contributor.author","Menzfeld, Christiane"],["dc.contributor.author","Hülsmann, Swen"],["dc.contributor.author","Müller, Michael"],["dc.date.accessioned","2018-09-28T09:49:07Z"],["dc.date.available","2018-09-28T09:49:07Z"],["dc.date.issued","2016"],["dc.description.abstract","Rett syndrome (RTT) is a severe neurodevelopmental disorder typically arising from spontaneous mutations in the X-chromosomal methyl-CpG binding protein 2 (MECP2) gene. The almost exclusively female Rett patients show an apparently normal development during their first 6-18 months of life. Subsequently, cognitive- and motor-impairment, hand stereotypies, loss of learned skills, epilepsy and irregular breathing manifest. Early mitochondrial impairment and oxidative challenge are considered to facilitate disease progression. Along this line, we recently confirmed in vitro that acute treatment with the vitamin E-derivative Trolox dampens neuronal hyperexcitability, reinstates synaptic plasticity, ameliorates cellular redox balance and improves hypoxia tolerance in male MeCP2-deficient (Mecp2-/y ) mouse hippocampus. Pursuing these promising findings, we performed a preclinical study to define the merit of systemic Trolox administration. Blinded, placebo-controlled in vivo treatment of male mice started at postnatal day (PD) 10-11 and continued for ~40 days. Compounds (vehicle only, 10 mg/kg or 40 mg/kg Trolox) were injected intraperitoneally every 48 h. Detailed phenotyping revealed that in Mecp2-/y mice, blood glucose levels, lipid peroxidation, synaptic short-term plasticity, hypoxia tolerance and certain forms of environmental exploration were improved by Trolox. Yet, body weight and size, motor function and the rate and regularity of breathing did not improve. In conclusion, in vivo Trolox treatment partially ameliorated a subset of symptoms of the complex Rett phenotype, thereby confirming a partial merit of the vitamin E-derivative based pharmacotherapy. Yet, it also became evident that frequent animal handling and the route of drug administration are critical issues to be optimized in future trials."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2016"],["dc.identifier.doi","10.3389/fncel.2016.00266"],["dc.identifier.pmid","27895554"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13968"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15847"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Systemic Radical Scavenger Treatment of a Mouse Model of Rett Syndrome: Merits and Limitations of the Vitamin E Derivative Trolox"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","718"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Molecules"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Dietrich, Katharina"],["dc.contributor.author","Bouter, Yvonne"],["dc.contributor.author","Müller, Michael"],["dc.contributor.author","Bayer, Thomas A."],["dc.date.accessioned","2018-09-28T09:40:32Z"],["dc.date.available","2018-09-28T09:40:32Z"],["dc.date.issued","2018"],["dc.description.abstract","This commentary reviews the role of the Alzheimer amyloid peptide Aβ on basal synaptic transmission, synaptic short-term plasticity, as well as short- and long-term potentiation in transgenic mice, with a special focus on N-terminal truncated Aβ4-42. Aβ4-42 is highly abundant in the brain of Alzheimer's disease (AD) patients. It demonstrates increased neurotoxicity compared to full length Aβ, suggesting an important role in the pathogenesis of AD. Transgenic Tg4-42 mice, a model for sporadic AD, express human Aβ4-42 in Cornu Ammonis (CA1) neurons, and develop age-dependent hippocampal neuron loss and neurological deficits. In contrast to other transgenic AD mouse models, the Tg4-42 model exhibits synaptic hyperexcitability, altered synaptic short-term plasticity with no alterations in short- and long-term potentiation. The outcomes of this study are discussed in comparison with controversial results from other AD mouse models."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2018"],["dc.identifier.doi","10.3390/molecules23040718"],["dc.identifier.pmid","29561816"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15107"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15845"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.publisher","MDPI"],["dc.relation.eissn","1420-3049"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Synaptic Alterations in Mouse Models for Alzheimer Disease-A Special Focus on N-Truncated Abeta 4-42"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]