Bayer, Thomas A.

[["dc.bibliographiccitation.firstpage","913"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","920"],["dc.bibliographiccitation.volume","116"],["dc.contributor.author","Marcello, Andrea"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Degerman-Gunnarsson, Malin"],["dc.contributor.author","Lannfelt, Lars"],["dc.contributor.author","Bayer, Thomas"],["dc.date.accessioned","2019-07-09T11:52:23Z"],["dc.date.available","2019-07-09T11:52:23Z"],["dc.date.issued","2009"],["dc.description.abstract","It has previously been shown that immune complexes (IC) of a given biomarker with class M immunoglobulins (IgM) provide better performances compared to the unbound biomarker in a number of cancer entities. In the present work, we investigated IC of IgM-Aβ as a potential biomarker for Alzheimer’s disease (AD). Aβ–IgM concentration has been measured in 75 plasma samples from patients with AD, individuals with mild cognitive impairment (MCI), and healthy age- and sex-matched controls (HC). To characterize the fractions associated with Aβ, pooled plasma samples were subjected to gel-filtration analysis. Size-separated fractions were analyzed for the presence of Aβ using a sandwich ELIp. assay. A strong reactivity was observed in the high molecular weight IgM (>500 kDa) and 150 kDa (IgG) fractions indicating that blood Aβ is strongly associated with antibodies. Using an ELISA assay detecting Aβ–IgM complexes, we observed that high levels of Aβ–IgMs were detectable in HC and MCI patients; however, there was no significant difference to the AD group."],["dc.identifier.doi","10.1007/s00702-009-0224-y"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/3557"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60171"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Springer"],["dc.publisher.place","Vienna"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Circulating immune complexes of Aβ and IgM in plasma of patients with Alzheimer’s disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","723782"],["dc.bibliographiccitation.journal","International journal of Alzheimer's disease"],["dc.bibliographiccitation.volume","2010"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Bayer, Thomas A."],["dc.date.accessioned","2019-07-09T11:53:08Z"],["dc.date.available","2019-07-09T11:53:08Z"],["dc.date.issued","2010"],["dc.description.abstract","Since their initial generation in the mid 1990s, transgenic mouse models of Alzheimers's disease (AD) have been proven to be valuable model systems which are indispensable for modern AD research. Whereas most of these models are characterized by extensive amyloid plaque pathology, inflammatory changes and often behavioral deficits, modeling of neuron loss was much less successful. The present paper discusses the current achievements of modeling neuron loss in transgenic mouse models based on APP/Aβ and Tau overexpression and provides an overview of currently available AD mouse models showing these pathological alterations."],["dc.identifier.doi","10.4061/2010/723782"],["dc.identifier.fs","575497"],["dc.identifier.pmid","20871861"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6917"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60349"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2090-0252"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Neuron loss in transgenic 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.firstpage","1651"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","1659"],["dc.bibliographiccitation.volume","115"],["dc.contributor.author","Kessler, Holger"],["dc.contributor.author","Pajonk, Frank-Gerald"],["dc.contributor.author","Bach, Daniela"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Herrmann, Wolfgang"],["dc.contributor.author","Multhaup, Gerd"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Schäfer, Stephanie"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Bayer, Thomas"],["dc.date.accessioned","2019-07-09T11:52:23Z"],["dc.date.available","2019-07-09T11:52:23Z"],["dc.date.issued","2008"],["dc.description.abstract","A plethora of reports suggest that copper (Cu) homeostasis is disturbed in Alzheimer’s disease (AD). In the present report we evaluated the efficacy of oral Cu supplementation on Cp. biomarkers for AD. In a prospective, randomized, double-blind, placebo-controlled phase 2 clinical trial (12 months long) patients with mild AD received either Cu-(II)-orotate-dihydrate (verum group; 8 mg Cu daily) or placebo (placebo group). The primary outcome measures in CSF were Aβ42, Tau and Phospho-Tau. The clinical trial demonstrates that long-term oral intake of 8 mg Cu can be excluded as a risk factor for AD based on CSF biomarker analysis. Cu intake had no effect on the progression of Tau and Phospho-Tau levels in CSF. While Aβ42 levels declined by 30% in the placebo group (P = 0.001), they decreased only by 10% (P = 0.04) in the verum group. Since decreased CSF Aβ42 is a diagnostic marker for AD, this observation may indicate that Cu treatment had a positive effect on a relevant AD biomarker. Using mini-mental state examination (MMSE) and Alzheimer disease assessment scale-cognitive subscale (ADAS-cog) we have previously demonstrated that there are no Cu treatment effects on cognitive performance, however. Finally, CSF Aβ42 levels declined significantly in both groups within 12 months supporting the notion that CSF Aβ42 may be valid not only for diagnostic but also for prognostic purposes in AD."],["dc.identifier.doi","10.1007/s00702-008-0136-2"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/3561"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60172"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Springer"],["dc.publisher.place","Vienna"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Effect of copper intake on CSF parameters in patients with mild Alzheimer’s disease: a pilot phase 2 clinical trial"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","64"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Frontiers in aging neuroscience"],["dc.bibliographiccitation.lastpage","12"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Lopez-Noguerola, Jose S."],["dc.contributor.author","Giessen, Nicolai M. E."],["dc.contributor.author","Ueberück, Maximilian"],["dc.contributor.author","Meißner, Julius N."],["dc.contributor.author","Pelgrim, Charlotte E."],["dc.contributor.author","Adams, Johnathan"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Bouter, Yvonne"],["dc.contributor.author","Bayer, Thomas A."],["dc.date.accessioned","2019-07-09T11:45:17Z"],["dc.date.available","2019-07-09T11:45:17Z"],["dc.date.issued","2018"],["dc.description.abstract","The N-terminally truncated pyroglutamate Aβ3-42 (AβpE3-42) and Aβ4-42 peptides are known to be highly abundant in the brain of Alzheimer's disease (AD) patients. Both peptides show enhanced aggregation and neurotoxicity in comparison to full-length Aβ, suggesting that these amyloid peptides may play an important role in the pathogenesis of AD. The aim of the present work was to study the direct effect of the combination of AβpE3-42 and Aβ4-42 on ongoing AD-related neuron loss, pathology, and neurological deficits in transgenic mice. Bigenic mice were generated by crossing the established TBA42 and Tg4-42 mouse models expressing the N-truncated Aβ peptides AβpE3-42 and Aβ4-42, respectively. After generation of the bigenic mice, detailed phenotypical characterization was performed using either immunostainings to evaluate amyloid pathology or quantification of neuron numbers using design-based stereology. The elevated plus maze was used to study anxiety levels. In order to evaluate sensori-motor deficits, the inverted grid, the balance beam and the string suspension tasks were applied. We could demonstrate that co-expression of AβpE3-42 and Aβ4-42 accelerates neuron loss in the CA1 pyramidal layer of young bigenic mice as seen by reduced neuron numbers in comparison to single transgenic homozygous mice expressing either AβpE3-42 or Aβ4-42. This observation coincides with the robust intraneuronal Aβ accumulation observed in the bigenic mice. In addition, loss of anxiety and motor deficits were enhanced in an age-dependent manner. The sensori-motor deficits correlate with the abundant spinal cord pathology, as demonstrated by robust intracellular Aβ accumulation within motor neurons and extracellular Aβ deposition. Our observations demonstrate that a combination of AβpE3-42 and Aβ4-42 has a stronger effect on ongoing AD pathology than the peptides alone. Therefore, AβpE3-42 and Aβ4-42 might represent excellent potential therapeutic targets and diagnostic markers for AD."],["dc.identifier.doi","10.3389/fnagi.2018.00064"],["dc.identifier.pmid","29568268"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15099"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59203"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1663-4365"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Synergistic Effect on Neurodegeneration by N-Truncated Aβ4-42 and Pyroglutamate Aβ3-42 in a 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","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"]]