Bayer, Thomas A.

[["dc.bibliographiccitation.firstpage","555"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","566"],["dc.bibliographiccitation.volume","119"],["dc.contributor.author","Christensen, Ditte Zerlang"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Lucassen, Paul J."],["dc.contributor.author","Bayer, Thomas A."],["dc.contributor.author","Wirths, Oliver"],["dc.date.accessioned","2018-11-07T08:43:18Z"],["dc.date.available","2018-11-07T08:43:18Z"],["dc.date.issued","2010"],["dc.description.abstract","In contrast to extracellular plaque and intracellular tangle pathology, the presence and relevance of intraneuronal A beta in Alzheimer's disease (AD) is still a matter of debate. Human brain tissue offers technical challenges such as post-mortem delay and uneven or prolonged tissue fixation that might affect immunohistochemical staining. In addition, previous studies on intracellular A beta accumulation in human brain often used antibodies targeting the C-terminus of A beta and differed strongly in the pretreatments used. To overcome these inconsistencies, we performed extensive parametrical testing using a highly specific N-terminal A beta antibody detecting the aspartate at position 1, before developing an optimal staining protocol for intraneuronal A beta detection in paraffin-embedded sections from AD patients. To rule out that this antibody also detects the beta-cleaved APP C-terminal fragment (beta-CTF, C99) bearing the same epitope, paraffin-sections of transgenic mice overexpressing the C99-fragment were stained without any evidence for cross-reactivity in our staining protocol. The staining intensity of intraneuronal A beta in cortex and hippocampal tissue of 10 controls and 20 sporadic AD cases was then correlated to patient data including sex, Braak stage, plaque load, and apolipoprotein E (ApoE) genotype. In particular, the presence of one or two ApoE4 alleles strongly correlated with an increased accumulation of intraneuronal A beta peptides. Given that ApoE4 is a major genetic risk factor for AD and is involved in neuronal cholesterol transport, it is tempting to speculate that perturbed intracellular trafficking is involved in the increased intraneuronal A beta aggregation in AD."],["dc.identifier.doi","10.1007/s00401-010-0666-1"],["dc.identifier.isi","000276353400003"],["dc.identifier.pmid","20217101"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/4175"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19930"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0001-6322"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Accumulation of intraneuronal A beta correlates with ApoE4 genotype"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]