Janc, Oliwia A.

[["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.journal","Acta Physiologica"],["dc.bibliographiccitation.volume","213"],["dc.contributor.author","Janc, O."],["dc.contributor.author","Kempkes, B."],["dc.contributor.author","Mueller, M."],["dc.date.accessioned","2018-11-07T09:59:53Z"],["dc.date.available","2018-11-07T09:59:53Z"],["dc.date.issued","2015"],["dc.format.extent","174"],["dc.identifier.isi","000362554200391"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37691"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.issn","1748-1716"],["dc.relation.issn","1748-1708"],["dc.title","Systemic radical scavenger treatment of a mouse model of Rett syndrom"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","102"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neurobiology of Disease"],["dc.bibliographiccitation.lastpage","114"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Grosser, Emanuel"],["dc.contributor.author","Hirt, Ursula"],["dc.contributor.author","Janc, Oliwia A."],["dc.contributor.author","Menzfeld, Christiane"],["dc.contributor.author","Fischer, Marc"],["dc.contributor.author","Kempkes, Belinda"],["dc.contributor.author","Vogelgesang, Steffen"],["dc.contributor.author","Manzke, Till U."],["dc.contributor.author","Opitz, Lennart"],["dc.contributor.author","Salinas-Riester, Gabriela"],["dc.contributor.author","Müller, Michael"],["dc.date.accessioned","2018-09-28T10:18:29Z"],["dc.date.available","2018-09-28T10:18:29Z"],["dc.date.issued","2012"],["dc.description.abstract","Rett syndrome is an X chromosome-linked neurodevelopmental disorder associated with cognitive impairment, motor dysfunction and breathing irregularities causing intermittent hypoxia. Evidence for impaired mitochondrial function is also accumulating. A subunit of complex III is among the potentially dys-regulated genes, the inner mitochondrial membrane is leaking protons, brain ATP levels seem reduced, and Rett patient blood samples confirm increased oxidative damage. We therefore screened for mitochondrial dysfunction and impaired redox balance. In hippocampal slices of a Rett mouse model (Mecp2(-/y)) we detected an increased FAD/NADH baseline-ratio indicating intensified oxidization. Cyanide-induced anoxia caused similar decreases in FAD/NADH ratio and mitochondrial membrane potential in both genotypes, but Mecp2(-/y) mitochondria seemed less polarized. Quantifying cytosolic redox balance with the genetically-encoded optical probe roGFP1 confirmed more oxidized baseline conditions, a more vulnerable redox-balance, and more intense responses of Mecp2(-/y) hippocampus to oxidative challenge and mitochondrial impairment. Trolox treatment improved the redox baseline of Mecp2(-/y) hippocampus and dampened its exaggerated responses to oxidative challenge. Microarray analysis of the hippocampal CA1 subfield did not detect alterations of key mitochondrial enzymes or scavenging systems. Yet, quantitative PCR confirmed a moderate upregulation of superoxide dismutase 1 in Mecp2(-/y) hippocampus, which might be a compensatory response to the increased oxidative burden. Since several receptors and ion-channels are redox-modulated, the mitochondrial and redox changes which already manifest in neonates could contribute to the hyperexcitability and diminished synaptic plasticity in MeCP2 deficiency. Therefore, targeting cellular redox balance might qualify as a potential pharmacotherapeutic approach to improve neuronal network function in Rett syndrome."],["dc.identifier.doi","10.1016/j.nbd.2012.06.007"],["dc.identifier.pmid","22750529"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15855"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1095-953X"],["dc.title","Oxidative burden and mitochondrial dysfunction in a mouse model of Rett syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","698"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","705"],["dc.bibliographiccitation.volume","136"],["dc.contributor.author","Wüstefeld, Liane"],["dc.contributor.author","Winkler, Daniela"],["dc.contributor.author","Janc, Oliwia A."],["dc.contributor.author","Hassouna, Imam"],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Ostmeier, Katrin"],["dc.contributor.author","Müller, Michael"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Wojcik, Sonja M."],["dc.date.accessioned","2017-09-07T11:46:36Z"],["dc.date.available","2017-09-07T11:46:36Z"],["dc.date.issued","2015"],["dc.description.abstract","We have previously shown that treatment with erythropoietin (EPO) improves cognition in patients with neuropsychiatric disorders as well as in healthy mice, and that transgenic expression of a constitutively active form of the EPO receptor (cEPOR) in glutamatergic neurons boosts higher cognitive functions in mice. In the present work, we asked whether selective activation of EPOR signaling in GABAergic neurons would also modulate cognitive performance. We generated transgenic mice that express cEPOR under the control of the vesicular inhibitory amino acid transporter (Viaat) promoter and subjected them to comprehensive behavioral, cognitive and electrophysiological analyses. We demonstrate that transgenic expression of cEPOR in GABAergic neurons alters hippocampal gamma-oscillations and enhances long-term potentiation, but neither impairs nor improves cognition. To conclude, constitutively active EPOR in GABAergic neurons changes hippocampal network properties without affecting cognition, which suggests that the effect of EPO on cognition is dominated by its effect on the glutamatergic system. This article is protected by copyright. All rights reserved."],["dc.identifier.doi","10.1111/jnc.13445"],["dc.identifier.gro","3150552"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7326"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0022-3042"],["dc.title","Selective expression of a constitutively active erythropoietin receptor in GABAergic neurons alters hippocampal network properties without affecting cognition"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]