Wirths, Oliver

[["dc.bibliographiccitation.journal","European Neuropsychopharmacology"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Bayer, Thomas A."],["dc.contributor.author","Wirths, Oliver"],["dc.date.accessioned","2018-11-07T11:24:51Z"],["dc.date.available","2018-11-07T11:24:51Z"],["dc.date.issued","2009"],["dc.format.extent","S211"],["dc.identifier.isi","000270312500101"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56500"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","22nd Congress of the European-College-of-Neuropsychopharmacology"],["dc.relation.eventlocation","Istanbul, TURKEY"],["dc.relation.issn","0924-977X"],["dc.title","Paradigm shift in Abeta toxicity"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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.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","849"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Alzheimer's Disease"],["dc.bibliographiccitation.lastpage","858"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Hornung, Karen"],["dc.contributor.author","Zampar, Silvia"],["dc.contributor.author","Engel, Nadine"],["dc.contributor.author","Klafki, Hans"],["dc.contributor.author","Liepold, Thomas"],["dc.contributor.author","Bayer, Thomas A."],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Wirths, Oliver"],["dc.date.accessioned","2020-12-10T18:44:12Z"],["dc.date.available","2020-12-10T18:44:12Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.3233/JAD-181134"],["dc.identifier.eissn","1875-8908"],["dc.identifier.issn","1387-2877"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78365"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","N-Terminal Truncated Aβ4-42 Is a Substrate for Neprilysin Degradation in vitro and in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","101"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Alzheimer s Disease"],["dc.bibliographiccitation.lastpage","110"],["dc.bibliographiccitation.volume","49"],["dc.contributor.author","Savastano, Adriana"],["dc.contributor.author","Klafki, Hans"],["dc.contributor.author","Haussman, Ute"],["dc.contributor.author","Oberstein, Timo Jan"],["dc.contributor.author","Mueller, Petr"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Bayer, Thomas A."],["dc.date.accessioned","2018-11-07T10:21:48Z"],["dc.date.available","2018-11-07T10:21:48Z"],["dc.date.issued","2016"],["dc.description.abstract","According to the modified amyloid hypothesis, the key event in the pathogenesis of Alzheimer's disease (AD) is the deposition of neurotoxic amyloid beta-peptides (A beta s) in plaques and cerebral blood vessels. Additionally to full-length peptides, a great diversity of N-truncated A beta variants is derived from the larger amyloid-beta protein precursor (A beta PP). Vast evidence suggests that A beta(x-42) isoforms play an important role in triggering neurodegeneration due to their high abundance, amyloidogenic propensity and toxicity. Although N-truncated Ap peptides and A beta(x-42) species appear to be the crucial players in AD etiology, the A beta(2-x) isoforms did not receive much attention yet. The present study is the first to show immunohistochemical evidence of A beta(2-x) in cases of AD and its distribution in Al3PP/PS 1KI and 5XFAD transgenic mouse models using a novel antibody pAB77 that has been developed using A132-14 as antigen. Positive plaques and congophilic amyloid angiopathy (CAA) were observed in AD cases and in both mouse models. While in AD cases, abundant CAA and less pronounced plaque pathology was evident, the two mouse models showed predominantly extracellular Ap deposits and minor CAA staining. Western blotting and a capillary isoelectric focusing immunoassay demonstrated the high specificity of the antibody pAb77 against A13-variants starting with the N-terminal Alanine-2."],["dc.identifier.doi","10.3233/JAD-150394"],["dc.identifier.isi","000364409100012"],["dc.identifier.pmid","26529393"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42160"],["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","N-Truncated A beta(2-X) Starting with Position Two in Sporadic Alzheimer's Disease Cases and Two Alzheimer Mouse Models"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","871"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Alzheimer s Disease"],["dc.bibliographiccitation.lastpage","881"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Reinert, Jochim"],["dc.contributor.author","Martens, Henrik"],["dc.contributor.author","Huettenrauch, Melanie"],["dc.contributor.author","Kolbow, Tekla"],["dc.contributor.author","Lannfelt, Lars"],["dc.contributor.author","Ingelsson, Martin"],["dc.contributor.author","Paetau, Anders"],["dc.contributor.author","Verkkoniemi-Ahola, Auli"],["dc.contributor.author","Bayer, Thomas A."],["dc.contributor.author","Wirths, Oliver"],["dc.date.accessioned","2018-11-07T09:46:32Z"],["dc.date.available","2018-11-07T09:46:32Z"],["dc.date.issued","2014"],["dc.description.abstract","The pathogenesis of Alzheimer's disease (AD) is believed to be closely dependent on deposits of neurotoxic amyloid-beta peptides (A beta), which become abundantly present throughout the central nervous system in advanced stages of the disease. The different A beta peptides existing are generated by subsequent cleavage of the amyloid-beta protein precursor (A beta PP) and may vary in length and differ at their C-terminus. Despite extensive studies on the most prevalent species A beta(40) and A beta(42), A beta peptides with other C-termini such as A beta(38) have not received much attention. In the present study, we used a highly specific and sensitive antibody against A beta(38) to analyze the distribution of this A beta species in cases of sporadic and familial AD, as well as in the brains of a series of established transgenic AD mouse models. We found A beta(38) to be present as vascular deposits in the brains of the majority of sporadic AD cases, whereas it is largely absent in non-demented control cases. A beta(38)-positive extracellular plaques were virtually limited to familial cases. Interestingly we observed A beta(38)-positive plaques not only among familial cases due to A beta PP mutations, but also in cases of familial AD caused by presenilin (PSEN) mutations. Furthermore we demonstrate that A beta(38) deposits in the form of extracellular plaques are common in several AD transgenic mouse models carrying either only A beta PP, or combinations of A beta PP, PSEN1, and tau transgenes."],["dc.identifier.doi","10.3233/JAD-131373"],["dc.identifier.isi","000331842500017"],["dc.identifier.pmid","24305500"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34892"],["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","A beta(38) in the Brains of Patients with Sporadic and Familial Alzheimer's Disease and Transgenic Mouse Models"],["dc.type","journal_article"],["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.artnumber","196.e29"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neurobiology of Aging"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Jawhar, Sadim"],["dc.contributor.author","Trawicka, Anna"],["dc.contributor.author","Jenneckens, Carolin"],["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","In the present report, we extend previous findings in the 5XFAD mouse model and demonstrate that these mice develop an age-dependent motor phenotype in addition to working memory deficits and reduced anxiety levels as demonstrated in an elevated plus maze task. Employing a variety of N- and C-terminal specific A beta antibodies, abundant intraneuronal and plaque-associated pathology, including accumulation of pyroglutamate A beta, was observed as early as the age of 3 months. Using unbiased stereology, we demonstrate that the 5XFAD mice develop a significant selective neuron loss in layer 5 of the cortex, leaving the overall neuron number of the total frontal cortex and hippocampus unaffected. This observation coincides with the accumulation of intraneuronal A beta peptides only in cortical Layer 5, but not in CA1, despite comparable APP expression levels. The motor phenotype correlates with abundant spinal cord pathology, as demonstrated by abundant intraneuronal A beta accumulation and extracellular plaque deposition. In addition, comparable to the APP/PS1KI mouse model, 5XFAD mice develop an age-dependent axonopathy likely contributing to the behavioral deficits. (C) 2012 IBRO All rights reserved."],["dc.identifier.doi","10.1016/j.neurobiolaging.2010.05.027"],["dc.identifier.isi","000297934700025"],["dc.identifier.pmid","20619937"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27877"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0197-4580"],["dc.title","Motor deficits, neuron loss, and reduced anxiety coinciding with axonal degeneration and intraneuronal A beta aggregation in the 5XFAD 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","741"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Alzheimer s Disease"],["dc.bibliographiccitation.lastpage","749"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Hillmann, Antje"],["dc.contributor.author","Pradier, Laurent"],["dc.contributor.author","Haertig, Wolfgang"],["dc.contributor.author","Bayer, Thomas A."],["dc.date.accessioned","2018-11-07T09:29:56Z"],["dc.date.available","2018-11-07T09:29:56Z"],["dc.date.issued","2013"],["dc.description.abstract","N-terminally truncated pyroglutamate amyloid-beta (A beta) starting at position 3 (A beta pE3) represents a major fraction of A beta peptides in Alzheimer's disease (AD). Recently, we have identified low molecular weight A beta(pE3) oligomers, which can be detected by 9D5, a novel mouse monoclonal antibody. In the present study, we analyzed the immunohistochemical staining profile in the brain of patients with AD and in the APP/PS1KI mouse model, as well as in aged rhesus monkeys. 9D5-positive microglia and blood vessels were found in many AD cases, in the transgenic mouse model, and in an aged macaque. The presence of 9D5-immunoreactivity in microglia indicates that low molecular weight A beta(pE3) oligomers may be phagocytosed, since in the APP/ PS1KI model, A beta is exclusively produced in neurons due to neuronal expression of transgenic A beta PP."],["dc.identifier.doi","10.3233/JAD-121945"],["dc.identifier.isi","000319345300008"],["dc.identifier.pmid","23481684"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31178"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ios Press"],["dc.relation.issn","1387-2877"],["dc.title","Oligomeric Pyroglutamate Amyloid-beta is Present in Microglia and a Subfraction of Vessels in Patients with Alzheimer's Disease: Implications for Immunotherapy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","891"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Neurobiology of Aging"],["dc.bibliographiccitation.lastpage","901"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Breyhan, Henning"],["dc.contributor.author","Schaefer, Stephanie"],["dc.contributor.author","Roth, Christian"],["dc.contributor.author","Bayer, Thomas A."],["dc.date.accessioned","2018-11-07T11:14:51Z"],["dc.date.available","2018-11-07T11:14:51Z"],["dc.date.issued","2008"],["dc.description.abstract","The APP/PS1ki mouse model for Alzheimer's disease (AD) exhibits robust brain and spinal cord axonal degeneration and hippocampal CA1 neuron loss starting at 6 months of age. It expresses human mutant APP751 with the Swedish and London mutations together with two FAD-linked knocked-in mutations (PS1 M233T and PS1 L235P) in the murine PS1 gene. The present report covers a phenotypical analysis of this model using either behavioral tests for working memory and motor performance, as well as an analysis of weight development and body shape. At the age of 6 months, a dramatic, age-dependent change in all of these properties and characteristics was observed, accompanied by a significantly reduced ability to perform working memory and motor tasks. The APP/PS1ki mice were smaller and showed development of a thoracolumbar kyphosis, together with an incremental loss of body weight. While 2-month-old APP/PS1ki mice were inconspicuous in all of these tasks and properties, there is a massive age-related impairment in all tested behavioral paradigms. We have previously reported robust axonal degeneration in brain and spinal cord, as well as abundant hippocampal CA1 neuron loss starting at 6 months of age in the APP/PS1ki mouse model, which coincides with the onset of motor and memory deficits described in the present report. (C) 2006 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.neurobiolaging.2006.12.004"],["dc.identifier.isi","000255599700011"],["dc.identifier.pmid","17215062"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54231"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0197-4580"],["dc.title","Deficits in working memory and motor performance in the APP/PS1ki mouse model for Alzheimer's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]