Bayer, Thomas A.

[["dc.bibliographiccitation.firstpage","38"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","39"],["dc.bibliographiccitation.volume","110"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Christensen, Ditte Zerlang"],["dc.contributor.author","Bayer, Thomas A."],["dc.date.accessioned","2018-11-07T08:28:16Z"],["dc.date.available","2018-11-07T08:28:16Z"],["dc.date.issued","2009"],["dc.identifier.isi","000266400900098"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16383"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.publisher.place","Malden"],["dc.relation.conference","4th European-Society-for-Neurochemistry Conference on Advances in Molecular Mechanisms of Neurological Disorders"],["dc.relation.eventlocation","Leipzig, GERMANY"],["dc.relation.issn","0022-3042"],["dc.title","Increasing Abeta peptide levels aggravate axonal degeneration in an Alzheimer mouse model"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1153"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Neurobiology of Aging"],["dc.bibliographiccitation.lastpage","1163"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Christensen, Ditte Zerlang"],["dc.contributor.author","Bayer, Thomas A."],["dc.contributor.author","Wirths, Oliver"],["dc.date.accessioned","2018-11-07T08:41:56Z"],["dc.date.available","2018-11-07T08:41:56Z"],["dc.date.issued","2010"],["dc.description.abstract","Loss of cholinergic neurons in the Nucleus Basalis of Meynert in Alzheimer's disease (AD) patients was one of the first discoveries of neuron loss in AD. Despite an intense focus on the cholinergic system in AD, the reason for this cholinergic neuron loss is yet unknown. In the present study we examined A beta-induced pathology and neuron loss in the cholinergic system of the bigenic APP/PS1KI mouse model. Expression of the APP transgene was found in ChAT-positive neurons of motor nuclei accompanied by robust intracellular A beta accumulation, whereas no APP expressing neurons and thus no intracellular A beta accumulation were found in neither the forebrain or pons complexes, nor in the caudate putamen. This expression pattern was used as a model system to study the effect of intra- and extracellular A beta accumulation on neuron loss in the cholinergic system. Stereological quantification revealed a loss of ChAT-positive neurons in APP/PS1KI mice only in the motor nuclei Mo5 and 7N accumulating intracellular A beta. This study supports the hypothesis of intracellular A beta accumulation as an early pathological alteration contributing to cell death in AD. (C) 2008 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.neurobiolaging.2008.07.022"],["dc.identifier.isi","000278438300008"],["dc.identifier.pmid","18771817"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19581"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0197-4580"],["dc.title","Intracellular A beta triggers neuron loss in the cholinergic system of the APP/PS1KI mouse model of 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","116"],["dc.bibliographiccitation.journal","Brain Research"],["dc.bibliographiccitation.lastpage","125"],["dc.bibliographiccitation.volume","1301"],["dc.contributor.author","Christensen, Ditte Zerlang"],["dc.contributor.author","Bayer, Thomas A."],["dc.contributor.author","Wirths, Oliver"],["dc.date.accessioned","2018-11-07T11:22:01Z"],["dc.date.available","2018-11-07T11:22:01Z"],["dc.date.issued","2009"],["dc.description.abstract","The staining protocols so far applied to study intracellular A beta accumulation in human tissue have been inconsistent with varying use of heat and formic acid (FA) for antigen retrieval. Microwave heat treatment has been reported to enhance the staining of intraneuronal A beta as compared to no or enzymatic pretreatment. FA is widely used to increase the staining of plaque pathology in AD, yet the effect of FA on intraneuronal A staining has been reported to be low and similar to the effect of heat or even to counteract the enhancing effect of heat pretreatment on intraneuronal A beta immunohistochemical detection. To overcome these inconsistencies, there is a need for optimization of the staining protocol for intraneuronal. A beta detection and more knowledge is required concerning the effects of the different antigen retrieval methods. in the present work, we optimized the staining protocol for intraneuronal A beta in paraffin-embedded sections in relation to heat and FA using four different mouse models known to accumulate intraneuronal A beta peptides. It was found that FA is essential for the staining of highly aggregated intraneuronal A beta peptides in AD transgenic mouse tissue. (C) 2009 Elsevier B.V. All rights reserved"],["dc.identifier.doi","10.1016/j.brainres.2009.09.014"],["dc.identifier.isi","000272100200013"],["dc.identifier.pmid","19751708"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55907"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0006-8993"],["dc.title","Formic acid is essential for immunohistochemical detection of aggregated intraneuronal A beta peptides in mouse models of 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","647"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","655"],["dc.bibliographiccitation.volume","116"],["dc.contributor.author","Christensen, Ditte Zerlang"],["dc.contributor.author","Kraus, Sophie Luise"],["dc.contributor.author","Flohr, Antonius"],["dc.contributor.author","Cotel, Marie-Caroline"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Bayer, Thomas A."],["dc.date.accessioned","2018-11-07T11:08:15Z"],["dc.date.available","2018-11-07T11:08:15Z"],["dc.date.issued","2008"],["dc.description.abstract","The accumulation of beta-amyloid (A beta) plaques and neurofibrillary tangles consisting of hyperphosphorylated tau protein are pathological features of Alzheimer's disease (AD) commonly modeled in mice using known human familial mutations; however, the loss of neurons also found to occur in AD is rarely observed in such models. The mechanism of neuron degeneration remains unclear but is of great interest as it is very likely an important factor for the onset of adverse memory deficits occurring in individuals with AD. The role of A beta in the neuronal degeneration is a matter of controversial debates. In the present study we investigated the impact of extracellular plaque A beta versus intraneuronal A beta on neuronal cell death. The thalamus and the frontal cortex of the APP/PS1KI mouse model were chosen for stereological quantification representing regions with plaques only (thalamus) or plaques as well as intraneuronal A beta (frontal cortex). A loss of neurons was found in the frontal cortex at the age of 6 months coinciding with the decrease of intraneuronal immunoreactivity, suggesting that the neurons with early intraneuronal A beta accumulation were lost. Strikingly, no neuron loss was observed in the thalamus despite the development of abundant plaque pathology with levels comparable to the frontal cortex. This study suggests that plaques have no effect on neuron death whereas accumulation of intraneuronal A beta may be an early transient pathological event leading to neuron loss in AD."],["dc.identifier.doi","10.1007/s00401-008-0451-6"],["dc.identifier.isi","000261025200007"],["dc.identifier.pmid","18974993"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52731"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0001-6322"],["dc.title","Transient intraneuronal A beta rather than extracellular plaque pathology correlates with neuron loss in the frontal cortex of APP/PS1KI mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","96"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neurobiology of Aging"],["dc.bibliographiccitation.lastpage","107"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Cotel, Marie-Caroline"],["dc.contributor.author","Jawhar, Sadim"],["dc.contributor.author","Christensen, Ditte Zerlang"],["dc.contributor.author","Bayer, Thomas A."],["dc.contributor.author","Wirths, Oliver"],["dc.date.accessioned","2018-11-07T09:16:11Z"],["dc.date.available","2018-11-07T09:16:11Z"],["dc.date.issued","2012"],["dc.description.abstract","Environmental enrichment has been used in a variety of transgenic mouse models of Alzheimer's disease (AD), however, with conflicting results. Here we studied the influence of environmental enrichment in a severely affected AD mouse model, showing a multiplicity of pathological alterations including hippocampal neuron loss. APP/PS1KI and wild type (WT) control mice were housed under standard conditions or in enriched cages equipped with various objects and running wheels. Amyloid plaque load, motor and working memory performance, axonopathy, as well as CA1 neuron number and hippocampal neurogenesis were assessed. Although a partial improvement in motor performance was observed, 4 months of enriched housing showed no beneficial effects in terms of working memory, A beta plaque pathology, or neuron loss in APP/PS1KI mice. In addition, no changes in hippocampal neurogenesis and even an aggravation of the axonal phenotype were detected with a tendency toward a premature death. The APP/PS1KI model represents a model for mild to severe AD showing early behavioral deficits starting at 2 months of age with fast deterioration. Therefore our data might suggest that physical activity and enriched environment might be more beneficial in patients with mild cognitive impairment than in patients with incipient AD. (C) 2012 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.neurobiolaging.2010.02.012"],["dc.identifier.isi","000297934700010"],["dc.identifier.pmid","20359774"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27876"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","1558-1497"],["dc.relation.issn","0197-4580"],["dc.title","Environmental enrichment fails to rescue working memory deficits, neuron loss, and neurogenesis in APP/PS1KI mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]