Dietrich, Katharina

[["dc.bibliographiccitation.issue","4S_Part_12"],["dc.bibliographiccitation.journal","Alzheimer's & Dementia"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Bouter, Yvonne"],["dc.contributor.author","Dietrich, Katharina"],["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","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.2013.05.1031"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/95321"],["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","P2–382: Tg4–42: A new mouse model of Alzheimer's disease—N‐truncated amyloid β (Aβ) 4–42 induces severe neuron loss and behavioral deficits"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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","189"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","205"],["dc.bibliographiccitation.volume","126"],["dc.contributor.author","Bouter, Yvonne"],["dc.contributor.author","Dietrich, Katharina"],["dc.contributor.author","Wittnam, Jessica L."],["dc.contributor.author","Rezaei-Ghaleh, Nasrollah"],["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","Zweckstetter, Markus"],["dc.contributor.author","Bayer, Thomas A."],["dc.date.accessioned","2018-11-07T09:21:59Z"],["dc.date.available","2018-11-07T09:21:59Z"],["dc.date.issued","2013"],["dc.description.abstract","N-truncated A beta(4-42) is highly abundant in Alzheimer disease (AD) brain and was the first A beta peptide discovered in AD plaques. However, a possible role in AD aetiology has largely been neglected. In the present report, we demonstrate that A beta(4-42) rapidly forms aggregates possessing a high aggregation propensity in terms of monomer consumption and oligomer formation. Short-term treatment of primary cortical neurons indicated that A beta(4-42) is as toxic as pyroglutamate A beta(3-42) and A beta(1-42). In line with these findings, treatment of wildtype mice using intraventricular A beta injection induced significant working memory deficits with A beta(4-42), pyroglutamate A beta(3-42) and A beta(1-42). Transgenic mice expressing A beta(4-42) (Tg4-42 transgenic line) developed a massive CA1 pyramidal neuron loss in the hippocampus. The hippocampus-specific expression of A beta(4-42) correlates well with age-dependent spatial reference memory deficits assessed by the Morris water maze test. Our findings indicate that N-truncated A beta(4-42) triggers acute and long-lasting behavioral deficits comparable to AD typical memory dysfunction."],["dc.identifier.doi","10.1007/s00401-013-1129-2"],["dc.identifier.isi","000322270200003"],["dc.identifier.pmid","23685882"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10303"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29236"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0001-6322"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","N-truncated amyloid beta (A beta) 4-42 forms stable aggregates and induces acute and long-lasting behavioral deficits"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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"]]

[["dc.bibliographiccitation.journal","Frontiers in Aging Neuroscience"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Bouter, Yvonne"],["dc.contributor.author","Kacprowski, Tim"],["dc.contributor.author","Weissmann, Robert"],["dc.contributor.author","Dietrich, Katharina"],["dc.contributor.author","Borgers, Henning"],["dc.contributor.author","Brauss, Andreas"],["dc.contributor.author","Sperling, Christian"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Albrecht, Mario"],["dc.contributor.author","Jensen, Lars R."],["dc.contributor.author","Kuss, Andreas W."],["dc.contributor.author","Bayer, Thomas A."],["dc.date.accessioned","2018-11-07T09:41:13Z"],["dc.date.available","2018-11-07T09:41:13Z"],["dc.date.issued","2014"],["dc.description.abstract","One of the central research questions on the etiology of Alzheimers disease (AD) is the elucidation of the molecular signatures triggered by the amyloid cascade of pathological events. Next-generation sequencing allows the identification of genes involved in disease processes in an unbiased manner. We have combined this technique with the analysis of two AD mouse models: (1) The 5XFAD model develops early plaque formation, intraneuronal A beta aggregation, neuron loss, and behavioral deficits. (2) The Tg442 model expresses N-truncated A beta 442 and develops neuron loss and behavioral deficits albeit without plaque formation. Our results show that learning and memory deficits in the Morris water maze and fear conditioning tasks in Tg442 mice at 12 months of age are similar to the deficits in 5XFAD animals. This suggested that comparative gene expression analysis between the models would allow the dissection of plaque-related and -unrelated disease relevant factors. Using deep sequencing differentially expressed genes (DEGs) were identified and subsequently verified by quantitative PCR. Nineteen DEGs were identified in pre-symptomatic young 5XFAD mice, and none in young Tg442 mice. In the aged cohort, 131 DEGs were found in 5XFAD and 56 DEGs in Tg442 mice. Many of the DEGs specific to the 5XFAD model belong to neuroinflammatory processes typically associated with plaques. Interestingly, 36 DEGs were identified in both mouse models indicating common disease pathways associated with behavioral deficits and neuron loss."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2014"],["dc.identifier.doi","10.3389/fnagi.2014.00075"],["dc.identifier.isi","000334406800001"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10177"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33683"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Frontiers Research Foundation"],["dc.relation.issn","1663-4365"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Deciphering the molecular profile of plaques, memory decline and neuron loss in two mouse models for Alzheimer's disease by deep sequencing"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]