Bouter, Yvonne

[["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.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.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"]]

[["dc.bibliographiccitation.artnumber","107"],["dc.bibliographiccitation.journal","Frontiers in Behavioral Neuroscience"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Wagner, Jannek M."],["dc.contributor.author","Sichler, Marius E."],["dc.contributor.author","Schleicher, Eva M."],["dc.contributor.author","Franke, Timon N."],["dc.contributor.author","Irwin, Caroline"],["dc.contributor.author","Löw, Maximilian Johannes"],["dc.contributor.author","Beindorff, Nicola"],["dc.contributor.author","Bouter, Caroline"],["dc.contributor.author","Bayer, Thomas A."],["dc.contributor.author","Bouter, Yvonne"],["dc.date.accessioned","2019-07-09T11:51:44Z"],["dc.date.available","2019-07-09T11:51:44Z"],["dc.date.issued","2019"],["dc.description.abstract","Alzheimer’s disease (AD) is a neurodegenerative disorder and the most common form of dementia. Hallmarks of AD are memory impairments and cognitive deficits, but non-cognitive impairments, especially motor dysfunctions are also associated with the disease and may even precede classic clinical symptoms. With an aging society and increasing hospitalization of the elderly, motor deficits are of major interest to improve independent activities in daily living. Consistent with clinical findings, a variety of AD mouse models develop motor deficits as well. We investigated the motor function of 3- and 7-month-old Tg4-42 mice in comparison to wild-type controls and 5XFAD mice and discuss the results in context with several other AD mouse model. Our study shows impaired balance and motor coordination in aged Tg4-42 mice in the balance beam and rotarod test, while general locomotor activity and muscle strength is not impaired at 7 months. The cerebellum is a major player in the regulation and coordination of balance and locomotion through practice. Particularly, the rotarod test is able to detect cerebellar deficits. Furthermore, supposed cerebellar impairment was verified by 18F-FDG PET/MRI. Aged Tg4-42 mice showed reduced cerebellar glucose metabolism in the 18F-FDG PET. Suggesting that, deficits in coordination and balance are most likely due to cerebellar impairment. In conclusion, Tg4-42 mice develop motor deficits before memory deficits, without confounding memory test. Thus, making the Tg4-42 mouse model a good model to study the effects on cognitive decline of therapies targeting motor impairments."],["dc.identifier.doi","10.3389/fnbeh.2019.00107"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16180"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59999"],["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","Analysis of Motor Function in the Tg4-42 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.artnumber","5451"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Curdt, Nadine"],["dc.contributor.author","Schmitt, Franziska W."],["dc.contributor.author","Bouter, Caroline"],["dc.contributor.author","Iseni, Trendelina"],["dc.contributor.author","Weile, Hanna C."],["dc.contributor.author","Altunok, Berfin"],["dc.contributor.author","Beindorff, Nicola"],["dc.contributor.author","Bayer, Thomas A."],["dc.contributor.author","Cooke, Matthew B."],["dc.contributor.author","Bouter, Yvonne"],["dc.date.accessioned","2022-05-02T08:02:10Z"],["dc.date.available","2022-05-02T08:02:10Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract Spatial disorientation is one of the earliest symptoms in Alzheimer’s disease and allocentric deficits can already be detected in the asymptomatic preclinical stages of the disease. The Morris Water Maze (MWM) is used to study spatial learning in rodent models. Here we investigated the spatial memory of female 3, 7 and 12 month-old Alzheimer Tg4-42 mice in comparison to wild-type control animals. Conventional behavior analysis of escape latencies and quadrant preference revealed spatial memory and reference memory deficits in female 7 and 12 month-old Tg4-42 mice. In contrast, conventional analysis of the MWM indicated an intact spatial memory in 3 month-old Tg4-42 mice. However, a detailed analysis of the swimming strategies demonstrated allocentric-specific memory deficits in 3 month-old Tg4-42 mice before the onset of severe memory deficits. Furthermore, we could show that the spatial reference memory deficits in aged Tg4-42 animals are caused by the lack of allocentric and spatial strategies. Analyzing search strategies in the MWM allows to differentiate between hippocampus-dependent allocentric and hippocampus-independent egocentric search strategies. The spatial navigation impairments in young Tg4-42 mice are well in line with the hypometabolism and synaptic deficits in the hippocampus. Therefore, analyzing search strategies in the Tg4-42 model can be a powerful tool for preclinical drug testing and identifying early therapeutic successes."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.1038/s41598-022-09270-1"],["dc.identifier.pii","9270"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107247"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-561"],["dc.relation.eissn","2045-2322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Search strategy analysis of Tg4-42 Alzheimer Mice in the Morris Water Maze reveals early spatial navigation deficits"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","883256"],["dc.bibliographiccitation.journal","Frontiers in Aging Neuroscience"],["dc.bibliographiccitation.volume","14"],["dc.contributor.affiliation","Bouter, Yvonne; 1Department of Psychiatry and Psychotherapy, University Medical Center Göttingen (UMG), Georg-August-University, Göttingen, Germany"],["dc.contributor.affiliation","Bouter, Caroline; 2Department of Nuclear Medicine, University Medical Center Göttingen (UMG), Georg-August-University, Göttingen, Germany"],["dc.contributor.author","Bouter, Yvonne"],["dc.contributor.author","Bouter, Caroline"],["dc.date.accessioned","2022-07-08T07:05:51Z"],["dc.date.available","2022-07-08T07:05:51Z"],["dc.date.issued","2022-06-23"],["dc.date.updated","2022-07-07T10:39:32Z"],["dc.description.abstract","Preclinical studies indicate that selective serotonin reuptake inhibitors (SSRI) have beneficial effects on Alzheimer-related pathologies. Therefore, the aim of this study was to evaluate the influence of SSRI-treatment on amyloid burden in 18F-Florbetapir-positron emission tomography (PET) and on cognition in cognitively normal and cognitively impaired subjects. We included n = 755 cognitively impaired and n = 394 cognitively normal participants from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) that underwent at least one 18F-Florbetapir-PET. Standardized uptake ratios (SUVR) and the Alzheimer Disease Assessment Scale-cognitive subscale (ADAS) scores as well as follow-up results were compared between subgroups with a history of SSRI-treatment (SSRI+) and without SSRI-treatment (SSRI-) as well as in subgroups of SSRI+/Depression+ and SSRI+/Depression- and SSRI-/Depression+ and SSRI-/Depression-. 18F-Florbetapir-PET did not show significant differences of SUVR between the SSRI+ and SSRI- groups in both, cognitively impaired and cognitively normal participants. There were no differences in subgroups of SSRI+/Depression+ and SSRI+/Depression- and SSRI-/Depression+ and SSRI-/Depression-. However, SUVR showed a dose-dependent inverse correlation to the duration of medication in cognitively normal and in cognitively impaired patients. SRRI-treatment did not show an effect on ADAS scores. Furthermore, there was no effect on follow-up SUVR or on follow-up ADAS scores. Overall, SSRI-treatment did not show beneficial effects on amyloid load nor on cognition."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.3389/fnagi.2022.883256"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112404"],["dc.language.iso","en"],["dc.relation.eissn","1663-4365"],["dc.rights","CC BY 4.0"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Selective Serotonin Reuptake Inhibitor-Treatment Does Not Show Beneficial Effects on Cognition or Amyloid Burden in Cognitively Impaired and Cognitively Normal Subjects"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","125"],["dc.bibliographiccitation.journal","Frontiers in Aging Neuroscience"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Bouter, Caroline"],["dc.contributor.author","Henniges, Philipp"],["dc.contributor.author","Franke, Timon N."],["dc.contributor.author","Irwin, Caroline"],["dc.contributor.author","Sahlmann, Carsten Oliver"],["dc.contributor.author","Sichler, Marius E."],["dc.contributor.author","Beindorff, Nicola"],["dc.contributor.author","Bayer, Thomas A."],["dc.contributor.author","Bouter, Yvonne"],["dc.date.accessioned","2019-07-09T11:49:50Z"],["dc.date.available","2019-07-09T11:49:50Z"],["dc.date.issued","2019"],["dc.description.abstract","The evaluation of new therapeutic strategies in Alzheimer’s disease (AD) relies heavily on in vivo imaging and suitable animal models that mimic the pathological changes seen in patients. 18F-Fluorodeoxyglucose (18F-FDG)-positron-emission tomography (PET) is a well-established non-invasive imaging tool for monitoring changes in cerebral brain glucose metabolism in vivo. 18F-FDG-PET is used as a functional biomarker for AD as patients show an early and progressive reduction of cerebral glucose metabolism. However, earlier studies in preclinical models of AD showed conflicting results. The aim of this study was the evaluation of cerebral glucose metabolism in the Tg4–42 mouse model of AD using 18F-FDG-PET/magnetic resonance imaging (MRI). Tg4–42 mice show an age-dependent reduction in glucose metabolism together with severe neuron loss and memory deficits. Similar to AD patients early decrease in 18F-FDG uptake was already detected in young (3 months) Tg4–42 mice. The altered glucose metabolism coupled with age- and disease related cognitive decline of Tg4–42 mice make it a well-suited model for preclinical testing of AD-relevant therapeutics."],["dc.identifier.doi","10.3389/fnagi.2018.00425"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15792"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59642"],["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","18F-FDG-PET Detects Drastic Changes in Brain Metabolism 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"]]