Bouter, Yvonne

[["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.firstpage","51"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cannabis and Cannabinoid Research"],["dc.bibliographiccitation.lastpage","61"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Bouter, Yvonne"],["dc.contributor.author","Brzózka, Magdalena M."],["dc.contributor.author","Rygula, Rafal"],["dc.contributor.author","Pahlisch, Franziska"],["dc.contributor.author","Leweke, F. Markus"],["dc.contributor.author","Havemann-Reinecke, Ursula"],["dc.contributor.author","Rohleder, Cathrin"],["dc.date.accessioned","2021-04-14T08:27:08Z"],["dc.date.available","2021-04-14T08:27:08Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1089/can.2019.0041"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82180"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","2378-8763"],["dc.relation.issn","2578-5125"],["dc.title","Chronic Psychosocial Stress Causes Increased Anxiety-Like Behavior and Alters Endocannabinoid Levels in the Brain of C57B l /6J Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.contributor.author","Bakrania, Preeti"],["dc.contributor.author","Hall, Gareth"],["dc.contributor.author","Bouter, Yvonne"],["dc.contributor.author","Bouter, Caroline"],["dc.contributor.author","Beindorff, Nicola"],["dc.contributor.author","Cowan, Richard"],["dc.contributor.author","Davies, Sarah"],["dc.contributor.author","Price, Jemma"],["dc.contributor.author","Mpamhanga, Chido"],["dc.contributor.author","Love, Elizabeth"],["dc.contributor.author","Bayer, Thomas A."],["dc.date.accessioned","2021-12-01T09:20:48Z"],["dc.date.available","2021-12-01T09:20:48Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1038/s41380-021-01385-7"],["dc.identifier.pii","1385"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94277"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","1476-5578"],["dc.relation.issn","1359-4184"],["dc.title","Discovery of a novel pseudo β-hairpin structure of N-truncated amyloid-β for use as a vaccine against Alzheimer’s disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","198"],["dc.bibliographiccitation.issue","05"],["dc.bibliographiccitation.journal","Nuklearmedizin"],["dc.bibliographiccitation.lastpage","203"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Bouter, Yvonne"],["dc.contributor.author","Meller, Birgit"],["dc.contributor.author","Sahlmann, Carsten"],["dc.contributor.author","Wolf, Bettina"],["dc.contributor.author","Langer, Laura"],["dc.contributor.author","Bankstahl, Jens"],["dc.contributor.author","Wester, Hans"],["dc.contributor.author","Kropf, Saskia"],["dc.contributor.author","Meller, Johannes"],["dc.contributor.author","Bouter, Caroline"],["dc.date.accessioned","2020-12-10T18:47:26Z"],["dc.date.available","2020-12-10T18:47:26Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.3413/Nukmed-0971-18-04"],["dc.identifier.eissn","2567-6407"],["dc.identifier.issn","0029-5566"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78765"],["dc.language.iso","de"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Immunohistochemical detection of chemokine receptor 4 expression in chronic osteomyelitis confirms specific uptake in 68Ga-Pentixafor-PET/CT"],["dc.title.alternative","Der immunhistochemische Nachweis CXCR4-exprimierender Lymphozyten bei chronischer Osteomyelitis bestätigt einen spezifischen Uptake in der 68Ga-Pentixafor-PET/CT"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","397"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Alzheimer s Disease"],["dc.bibliographiccitation.lastpage","409"],["dc.bibliographiccitation.volume","50"],["dc.contributor.author","Weissmann, Robert"],["dc.contributor.author","Huettenrauch, Melanie"],["dc.contributor.author","Kacprowski, Tim"],["dc.contributor.author","Bouter, Yvonne"],["dc.contributor.author","Pradier, Laurent"],["dc.contributor.author","Bayer, Thomas A."],["dc.contributor.author","Kuss, Andreas W."],["dc.contributor.author","Wirths, Oliver"],["dc.date.accessioned","2018-11-07T10:21:12Z"],["dc.date.available","2018-11-07T10:21:12Z"],["dc.date.issued","2016"],["dc.description.abstract","Alzheimer's disease (AD) is a devastating neurodegenerative disorder characterized by early intraneuronal amyloid-beta (A beta) accumulation, extracellular deposition of A beta peptides, and intracellular hyperphosphorylated tau aggregates. These lesions cause dendritic and synaptic alterations and induce an inflammatory response in the diseased brain. Although the neuropathological characteristics of AD have been known for decades, the molecular mechanisms causing the disease are still under investigation. Studying gene expression changes in postmortem AD brain tissue can yield new insights into the molecular disease mechanisms. To that end, one can employ transgenic AD mouse models and the next-generation sequencing technology. In this study, a whole-brain transcriptome analysis was carried out using the well-characterized APP/PS1KI mouse model for AD. These mice display a robust phenotype reflected byworking memory deficits at 6 months of age, a significant neuron loss in a variety of brain areas including the CA1 region of the hippocampus and a severe amyloid pathology. Based on deep sequencing, differentially expressed genes (DEGs) between 6-month-old WT or PS1KI and APP/PS1KI were identified and verified by qRT-PCR. Compared to WT mice, 250 DEGs were found in APP/PS1KI mice, while 186 DEGs could be found compared to PS1KI control mice. Most of the DEGs were upregulated in APP/PS1KI mice and belong to either inflammation-associated pathways or lysosomal activation, which is likely due to the robust intraneuronal accumulation of A beta in this mouse model. Our comprehensive brain transcriptome study further highlights APP/PS1KI mice as a valuable model for AD, covering molecular inflammatory and immune responses."],["dc.identifier.doi","10.3233/JAD-150745"],["dc.identifier.isi","000368929200007"],["dc.identifier.pmid","26639971"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42043"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ios Press"],["dc.relation.issn","1875-8908"],["dc.relation.issn","1387-2877"],["dc.title","Gene Expression Profiling in the APP/PS1KI Mouse Model of Familial 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","601"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","603"],["dc.bibliographiccitation.volume","143"],["dc.contributor.author","Bouter, Yvonne"],["dc.contributor.author","Liekefeld, Hendrik"],["dc.contributor.author","Pichlo, Steffen"],["dc.contributor.author","Westhoff, Anna Celine"],["dc.contributor.author","Fenn, Lydia"],["dc.contributor.author","Bakrania, Preeti"],["dc.contributor.author","Bayer, Thomas A."],["dc.date.accessioned","2022-05-02T08:09:41Z"],["dc.date.available","2022-05-02T08:09:41Z"],["dc.date.issued","2022"],["dc.description.sponsorship","Georg-August-Universität Göttingen"],["dc.identifier.doi","10.1007/s00401-022-02418-3"],["dc.identifier.pii","2418"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107436"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-561"],["dc.relation.eissn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Donanemab detects a minor fraction of amyloid-β plaques in post-mortem brain tissue of patients with Alzheimer’s disease and Down syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Journal of Alzheimer's Disease"],["dc.bibliographiccitation.lastpage","11"],["dc.contributor.author","Lio, Chit Tong"],["dc.contributor.author","Kacprowski, Tim"],["dc.contributor.author","Klaedtke, Maik"],["dc.contributor.author","Jensen, Lars R."],["dc.contributor.author","Bouter, Yvonne"],["dc.contributor.author","Bayer, Thomas A."],["dc.contributor.author","Kuss, Andreas W."],["dc.contributor.editor","Leung, Yuk Yee"],["dc.date.accessioned","2022-06-01T09:39:48Z"],["dc.date.available","2022-06-01T09:39:48Z"],["dc.date.issued","2022"],["dc.description.abstract","Background: The Tg4-42 mouse model for sporadic Alzheimer’s disease (AD) has unique features, as the neuronal expression of wild type N-truncated Aβ4–42 induces an AD-typical neurological phenotype in the absence of plaques. It is one of the few models developing neuron death in the CA1 region of the hippocampus. As such, it could serve as a powerful tool for preclinical drug testing and identification of the underlying molecular pathways that drive the pathology of AD. Objective: The aim of this study was to use a differential co-expression analysis approach for analyzing a small RNA sequencing dataset from a well-established murine model in order to identify potentially new players in the etiology of AD. Methods: To investigate small nucleolar RNAs in the hippocampus of Tg4-42 mice, we used RNA-Seq data from this particular tissue and, instead of analyzing the data at single gene level, employed differential co-expression analysis, which takes the comparison to gene pair level and thus affords a new angle to the interpretation of these data. Results: We identified two clusters of differentially correlated small RNAs, including Snord55, Snord57, Snord49a, Snord12, Snord38a, Snord99, Snord87, Mir1981, Mir106b, Mir30d, Mir598, and Mir99b. Interestingly, some of them have been reported to be functionally relevant in AD pathogenesis, as AD biomarkers, regulating tau phosphorylation, TGF-β receptor function or Aβ metabolism. Conclusion: The majority of snoRNAs for which our results suggest a potential role in the etiology of AD were so far not conspicuously implicated in the context of AD pathogenesis and could thus point towards interesting new avenues of research in this field."],["dc.identifier.doi","10.3233/JAD-220110"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/108568"],["dc.notes.intern","DOI-Import GROB-572"],["dc.relation.eissn","1875-8908"],["dc.relation.issn","1387-2877"],["dc.title","Small RNA Sequencing in the Tg4–42 Mouse Model Suggests the Involvement of snoRNAs in the Etiology of Alzheimer’s Disease"],["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","713"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","729"],["dc.bibliographiccitation.volume","130"],["dc.contributor.author","Bouter, Yvonne"],["dc.contributor.author","Noguerola, Jose Socrates Lopez"],["dc.contributor.author","Tucholla, Petra"],["dc.contributor.author","Crespi, Gabriela A. N."],["dc.contributor.author","Parker, Michael W."],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Miles, Luke A."],["dc.contributor.author","Bayer, Thomas A."],["dc.date.accessioned","2017-09-07T11:44:26Z"],["dc.date.available","2017-09-07T11:44:26Z"],["dc.date.issued","2015"],["dc.description.abstract","Solanezumab and Crenezumab are two humanized antibodies targeting Amyloid-β (Aβ) which are currently tested in multiple clinical trials for the prevention of Alzheimer’s disease. However, there is a scientific discussion ongoing about the target engagement of these antibodies. Here, we report the immunohistochemical staining profiles of biosimilar antibodies of Solanezumab, Crenezumab and Bapineuzumab in human formalin-fixed, paraffin-embedded tissue and human fresh frozen tissue. Furthermore, we performed a direct comparative immunohistochemistry analysis of the biosimilar versions of the humanized antibodies in different mouse models including 5XFAD, Tg4-42, TBA42, APP/PS1KI, 3xTg. The staining pattern with these humanized antibodies revealed a surprisingly similar profile. All three antibodies detected plaques, cerebral amyloid angiopathy and intraneuronal Aβ in a similar fashion. Remarkably, Solanezumab showed a strong binding affinity to plaques. We also reaffirmed that Bapineuzumab does not recognize N-truncated or modified Aβ, while Solanezumab and Crenezumab do detect N-terminally modified Aβ peptides Aβ4–42 and pyroglutamate Aβ3–42. In addition, we compared the results with the staining pattern of the mouse NT4X antibody that recognizes specifically Aβ4–42 and pyroglutamate Aβ3–42, but not full-length Aβ1–42. In contrast to the biosimilar antibodies of Solanezumab, Crenezumab and Bapineuzumab, the murine NT4X antibody shows a unique target engagement. NT4X does barely cross-react with amyloid plaques in human tissue. It does, however, detect cerebral amyloid angiopathy in human tissue. In Alzheimer mouse models, NT4X detects intraneuronal Aβ and plaques comparable to the humanized antibodies. In conclusion, the biosimilar antibodies Solanezumab, Crenezumab and Bapineuzumab strongly react with amyloid plaques, which are in contrast to the NT4X antibody that hardly recognizes plaques in human tissue. Therefore, NT4X is the first of a new class of therapeutic antibodies."],["dc.identifier.doi","10.1007/s00401-015-1489-x"],["dc.identifier.gro","3151656"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8472"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0001-6322"],["dc.title","Abeta targets of the biosimilar antibodies of Bapineuzumab, Crenezumab, Solanezumab in comparison to an antibody against N-truncated Abeta in sporadic Alzheimer disease cases and mouse models"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1617"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Alzheimer's Disease"],["dc.bibliographiccitation.lastpage","1630"],["dc.bibliographiccitation.volume","53"],["dc.contributor.author","Jakobsen, Jannik E."],["dc.contributor.author","Johansen, Marianne G."],["dc.contributor.author","Schmidt, Mette"],["dc.contributor.author","Liu, Ying"],["dc.contributor.author","Li, Rong"],["dc.contributor.author","Callesen, Henrik"],["dc.contributor.author","Melnikova, Margarita"],["dc.contributor.author","Habekost, Mette"],["dc.contributor.author","Matrone, Carmela"],["dc.contributor.author","Bouter, Yvonne"],["dc.contributor.author","Bayer, Thomas A."],["dc.contributor.author","Nielsen, Anders Lade"],["dc.contributor.author","Duthie, Monika"],["dc.contributor.author","Fraser, Paul E."],["dc.contributor.author","Holm, Ida E."],["dc.contributor.author","Jørgensen, Arne Lund"],["dc.date.accessioned","2020-12-10T18:44:10Z"],["dc.date.available","2020-12-10T18:44:10Z"],["dc.date.issued","2016"],["dc.description.abstract","Mutations in the amyloid-beta protein precursor gene (A beta PP), the presenilin 1 gene (PSEN1) or the presenilin 2 gene (PSEN2) that increase production of the A beta PP-derived peptide A beta(42) cause early-onset Alzheimer's disease. Rodent models of the disease show that further increase in A beta(42) production and earlier brain pathology can be obtained by coexpressing A beta PP and PSEN1 mutations. To generate such elevated A beta(42) level in a large animal model, we produced Gottingen minipigs carrying in their genome one copy of a human PSEN1 cDNA with the Met146Ile (PSEN1M146I) mutation and three copies of a human A beta PP695 cDNA with the Lys670Asn/Met671Leu (A beta PPsw) double-mutation. Both transgenes were expressed in fibroblasts and in the brain, and their respective proteins were processed normally. Immunohistochemical staining with A beta(42)-specific antibodies detected intraneuronal accumulation of A beta(42) in brains from a 10- and an 18-month-old pig. Such accumulation may represent an early event in the pathogenesis of Alzheimer's disease."],["dc.identifier.doi","10.3233/JAD-160408"],["dc.identifier.eissn","1875-8908"],["dc.identifier.isi","000383149600033"],["dc.identifier.issn","1387-2877"],["dc.identifier.pmid","27540966"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78350"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ios Press"],["dc.relation.issn","1875-8908"],["dc.relation.issn","1387-2877"],["dc.title","Expression of the Alzheimer’s Disease Mutations AβPP695sw and PSEN1M146I in Double-Transgenic Göttingen Minipigs"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]