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.journal","Frontiers in Medicine"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Bouter, Caroline"],["dc.contributor.author","Irwin, Caroline"],["dc.contributor.author","Franke, Timon N."],["dc.contributor.author","Beindorff, Nicola"],["dc.contributor.author","Bouter, Yvonne"],["dc.date.accessioned","2022-01-11T14:06:14Z"],["dc.date.available","2022-01-11T14:06:14Z"],["dc.date.issued","2021"],["dc.description.abstract","Successful back-translating clinical biomarkers and molecular imaging methods of Alzheimer's disease (AD), including positron emission tomography (PET), are very valuable for the evaluation of new therapeutic strategies and increase the quality of preclinical studies. 18 F-Fluorodeoxyglucose (FDG)–PET and 18 F-Florbetaben–PET are clinically established biomarkers capturing two key pathological features of AD. However, the suitability of 18 F-FDG– and amyloid–PET in the widely used 5XFAD mouse model of AD is still unclear. Furthermore, only data on male 5XFAD mice have been published so far, whereas studies in female mice and possible sex differences in 18 F-FDG and 18 F-Florbetaben uptake are missing. The aim of this study was to evaluate the suitability of 18 F-FDG– and 18 F-Florbetaben–PET in 7-month-old female 5XFAD and to assess possible sex differences between male and female 5XFAD mice. We could demonstrate that female 5XFAD mice showed a significant reduction in brain glucose metabolism and increased cerebral amyloid deposition compared with wild type animals, in accordance with the pathology seen in AD patients. Furthermore, we showed for the first time that the hypometabolism in 5XFAD mice is gender-dependent and more pronounced in female mice. Therefore, these results support the feasibility of small animal PET imaging with 18 F-FDG- and 18 F-Florbetaben in 5XFAD mice in both, male and female animals. Moreover, our findings highlight the need to account for sex differences in studies working with 5XFAD mice."],["dc.description.abstract","Successful back-translating clinical biomarkers and molecular imaging methods of Alzheimer's disease (AD), including positron emission tomography (PET), are very valuable for the evaluation of new therapeutic strategies and increase the quality of preclinical studies. 18 F-Fluorodeoxyglucose (FDG)–PET and 18 F-Florbetaben–PET are clinically established biomarkers capturing two key pathological features of AD. However, the suitability of 18 F-FDG– and amyloid–PET in the widely used 5XFAD mouse model of AD is still unclear. Furthermore, only data on male 5XFAD mice have been published so far, whereas studies in female mice and possible sex differences in 18 F-FDG and 18 F-Florbetaben uptake are missing. The aim of this study was to evaluate the suitability of 18 F-FDG– and 18 F-Florbetaben–PET in 7-month-old female 5XFAD and to assess possible sex differences between male and female 5XFAD mice. We could demonstrate that female 5XFAD mice showed a significant reduction in brain glucose metabolism and increased cerebral amyloid deposition compared with wild type animals, in accordance with the pathology seen in AD patients. Furthermore, we showed for the first time that the hypometabolism in 5XFAD mice is gender-dependent and more pronounced in female mice. Therefore, these results support the feasibility of small animal PET imaging with 18 F-FDG- and 18 F-Florbetaben in 5XFAD mice in both, male and female animals. Moreover, our findings highlight the need to account for sex differences in studies working with 5XFAD mice."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3389/fmed.2021.745064"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/97859"],["dc.notes.intern","DOI-Import GROB-507"],["dc.relation.eissn","2296-858X"],["dc.rights","CC BY 4.0"],["dc.title","Quantitative Brain Positron Emission Tomography in Female 5XFAD Alzheimer Mice: Pathological Features and Sex-Specific Alterations"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","269"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Alzheimer's Disease Reports"],["dc.bibliographiccitation.lastpage","278"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Sichler, Marius E."],["dc.contributor.author","Löw, Maximilian J."],["dc.contributor.author","Schleicher, Eva M."],["dc.contributor.author","Bayer, Thomas A."],["dc.contributor.author","Bouter, Yvonne"],["dc.date.accessioned","2021-06-01T10:48:43Z"],["dc.date.available","2021-06-01T10:48:43Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.3233/ADR-190132"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16704"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86031"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2542-4823"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","Reduced Acoustic Startle Response and Prepulse Inhibition in the Tg4-42 Model of Alzheimer’s Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["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.artnumber","94"],["dc.bibliographiccitation.journal","Frontiers in Behavioral Neuroscience"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Schleicher, Eva M."],["dc.contributor.author","Ott, Frederik W."],["dc.contributor.author","Müller, Melanie"],["dc.contributor.author","Silcher, Barbara"],["dc.contributor.author","Sichler, Marius E."],["dc.contributor.author","Löw, Maximilian J."],["dc.contributor.author","Wagner, Jannek M."],["dc.contributor.author","Bouter, Yvonne"],["dc.date.accessioned","2019-07-09T11:51:17Z"],["dc.date.available","2019-07-09T11:51:17Z"],["dc.date.issued","2019"],["dc.description.abstract","The Cannabis plant contains more than 100 currently known phytocannabinoids. Regarding the rising consumption of the non-psychotropic phytocannabinoid cannabidiol (CBD) in people’s everyday life (e.g., beauty products, food and beverages), the importance of studies on the influence of CBD on healthy humans and rodents is evident. Therefore, the behavioral profile of CBD was investigated with a battery of behavioral tests, including motor, anxiety, and memory tests after prolonged CBD treatment. Adult C57Bl/6J wildtype (WT) mice were daily intraperitoneally injected with 20 mg/kg CBD for 6 weeks starting at two different points of ages (3 months and 5 months) to compare the influence of prolonged CBD treatment with a washout period (former group) to the effects of long term CBD treatment (current group). Our results show that CBD treatment does not influence motor performance on an accelerating Rotarod test, while it also results in a lower locomotor activity in the open field (OF). No influence of CBD on spatial learning and long term memory in the Morris Water Maze (MWM) was observed. Memory in the Novel Object Recognition test (NORT) was unaffected by CBD treatment. Two different anxiety tests revealed that CBD does not affect anxiety behavior in the Dark-Light Box (DLB) and OF test. Although, anxiety is altered by current CBD treatment in the Elevated Plus Maze (EPM). Moreover, CBDtreated C57Bl/6J mice showed an unaltered acoustic startle response (ASR) compared to vehicle-treated mice. However, current CBD treatment impairs prepulse inhibition (PPI), a test to analyze sensorimotor gating. Furthermore, prolonged CBD treatment did not affect the hippocampal neuron number. Our results demonstrate that prolonged CBD treatment has no negative effect on the behavior of adult C57Bl/6J mice."],["dc.identifier.doi","10.3389/fnbeh.2019.00094"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16095"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59917"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Prolonged Cannabidiol Treatment Lacks on Detrimental Effects on Memory, Motor Performance and Anxiety in C57BL/6J Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["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.journal","Frontiers in Medicine"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Franke, Timon N."],["dc.contributor.author","Irwin, Caroline"],["dc.contributor.author","Bayer, Thomas A."],["dc.contributor.author","Brenner, Winfried"],["dc.contributor.author","Beindorff, Nicola"],["dc.contributor.author","Bouter, Caroline"],["dc.contributor.author","Bouter, Yvonne"],["dc.date.accessioned","2021-04-14T08:32:38Z"],["dc.date.available","2021-04-14T08:32:38Z"],["dc.date.issued","2020"],["dc.description.abstract","Imaging biomarkers of Alzheimer's disease (AD) that are able to detect molecular changes in vivo and transgenic animal models mimicking AD pathologies are essential for the evaluation of new therapeutic strategies. Positron-emission tomography (PET) using either 18F-Fluorodeoxyglucose (18F-FDG) or amyloid-tracers is a well-established, non-invasive tool in the clinical diagnostics of AD assessing two major pathological hallmarks. 18F-FDG-PET is able to detect early changes in cerebral glucose metabolism and amyloid-PET shows cerebral amyloid load. However, the suitability of 18F-FDG- and amyloid-PET in the widely used 5XFAD mouse model of AD is unclear as only a few studies on the use of PET biomarkers are available showing some conflicting results. The aim of this study was the evaluation of 18F-FDG-PET and amyloid-PET in 5XFAD mice in comparison to neurological deficits and neuropathological changes. Seven- and 12-month-old male 5XFAD mice showed a significant reduction in brain glucose metabolism in 18F-FDG-PET and amyloid-PET with 18F-Florbetaben demonstrated an increased cerebral amyloid deposition (n = 4–6 per group). Deficits in spatial reference memory were detected in 12-month-old 5XFAD mice in the Morris Water Maze (n = 10–12 per group). Furthermore, an increased plaque load and gliosis could be proven immunohistochemically in 5XFAD mice (n = 4–6 per group). PET biomarkers 18F-FDG and 18F-Florbetaben detected cerebral hypometabolism and increased plaque load even before the onset of severe memory deficits. Therefore, the 5XFAD mouse model of AD is well-suited for in vivo monitoring of AD pathologies and longitudinal testing of new therapeutic approaches."],["dc.identifier.doi","10.3389/fmed.2020.00529"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17550"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83972"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","2296-858X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","In vivo Imaging With 18F-FDG- and 18F-Florbetaben-PET/MRI Detects Pathological Changes in the Brain of the Commonly Used 5XFAD Mouse Model of Alzheimer's Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["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.journal","Frontiers in Medicine"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Bouter, Caroline"],["dc.contributor.author","Bouter, Yvonne"],["dc.date.accessioned","2020-12-10T18:44:26Z"],["dc.date.available","2020-12-10T18:44:26Z"],["dc.date.issued","2019"],["dc.description.abstract","Suitable animal models and in vivo biomarkers are essential for development and evaluation of new therapeutic strategies in Alzheimer's disease (AD). 18F-Fluorodeoxyglucose (18F-FDG)-positron-emission tomography (PET) is an imaging biomarker that allows the assessment of cerebral glucose metabolism in vivo. While 18F-FDG-PET/CT is an established tool in the evaluation of AD patients, its role in preclinical studies with AD mouse models remains unclear. Here, we want to review available studies on 18F-FDG-PET/CT in AD mouse models in order to evaluate the method and its impact in preclinical AD research. Only a limited number of studies using 18F-FDG-PET in AD mice were carried out so far showing contradictory findings in cerebral FDG uptake. Methodological differences as well as underlying pathological features of used mouse models seem to be accountable for those varying results. However, 18F-FDG-PET can be a valuable tool in longitudinal in vivo therapy monitoring with a lot of potential for future studies."],["dc.identifier.doi","10.3389/fmed.2019.00071"],["dc.identifier.eissn","2296-858X"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17582"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78450"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","2296-858X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","18F-FDG-PET in Mouse Models of Alzheimer's Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]