Escher, Angelika

[["dc.bibliographiccitation.firstpage","2678"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","NeuroImage"],["dc.bibliographiccitation.lastpage","2688"],["dc.bibliographiccitation.volume","59"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Escher, Angelika"],["dc.contributor.author","Dallenga, Tobias"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Tammer, Roland"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2017-09-07T11:44:51Z"],["dc.date.available","2017-09-07T11:44:51Z"],["dc.date.issued","2011"],["dc.description.abstract","Magnetic resonance imaging (MRI) is the gold standard for the detection of multiple sclerosis (MS) lesions. However, current MRI techniques provide little information about the structural features of a brain lesion with inflammatory cell infiltration, demyelination, gliosis, acute axonal damage and axonal loss. To identify methods for a differentiation of demyelination, inflammation, and axonal damage we developed a novel mouse model combining cuprizone-induced demyelination and experimental autoimmune encephalomyelitis. MS-like brain lesions were assessed by T1-weighted, T2-weighted, and magnetization transfer MRI as well as by diffusion tensor imaging (DTI). T2-weighted MRI differentiated control and diseased mice, while T1-weighted MRI better reflected the extent of inflammation and axonal damage. In DTI, axonal damage and cellular infiltration led to a reduction of the axial diffusivity, whereas primary demyelination after cuprizone treatment was reflected by changes in radial but not axial diffusivity. Importantly, alterations in radial diffusivity were less pronounced in mice with demyelination, inflammation, and acute axonal damage, indicating that radial diffusivity may underestimate demyelination in acute MS lesions. In conclusion, the combined information from different DTI parameters allows for a more precise identification of solely demyelinated lesions versus demyelinated and acutely inflamed lesions. These findings are of relevance for offering individualized, stage-adapted therapies for MS patients."],["dc.identifier.doi","10.1016/j.neuroimage.2011.08.051"],["dc.identifier.gro","3150360"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7115"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.issn","1053-8119"],["dc.title","Assessment of lesion pathology in a new animal model of MS by multiparametric MRI and DTI"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Escher, Angelika"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Vollmar, Patrick"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Stadeimann, Christine"],["dc.date.accessioned","2018-11-07T11:11:44Z"],["dc.date.available","2018-11-07T11:11:44Z"],["dc.date.issued","2008"],["dc.format.extent","S79"],["dc.identifier.isi","000259675700247"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53499"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","13th Annual Meeting of the Amer-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis/24th Congress of the European-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis/5th Congress of the Latin-Amer-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis"],["dc.relation.eventlocation","Montreal, CANADA"],["dc.relation.issn","1352-4585"],["dc.title","Experimental autoimmune encephalomyelitis induction in mice with cuprizone-induced demyelination leads to cerebral MS-like lesions"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Escher, Angelika"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T09:22:28Z"],["dc.date.available","2018-11-07T09:22:28Z"],["dc.date.issued","2006"],["dc.format.extent","S53"],["dc.identifier.isi","000241921400174"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29346"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.eventlocation","Madrid, SPAIN"],["dc.relation.issn","1352-4585"],["dc.title","Grey matter pathology induced by immunization with a beta-Synuclein peptide"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.volume","112"],["dc.contributor.author","Escher, Angelika"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T09:16:39Z"],["dc.date.available","2018-11-07T09:16:39Z"],["dc.date.issued","2006"],["dc.format.extent","371"],["dc.identifier.isi","000240061000066"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27980"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.eventlocation","Mannheim, GERMANY"],["dc.relation.issn","0001-6322"],["dc.title","Grey matter pathology induced by immunisation with a beta-Synuclein peptide"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","833"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","European Journal of Immunology"],["dc.bibliographiccitation.lastpage","844"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Berod, Luciana"],["dc.contributor.author","Heinemann, Christina"],["dc.contributor.author","Heink, Sylvia"],["dc.contributor.author","Escher, Angelika"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Drube, Sebastian"],["dc.contributor.author","Wetzker, Reinhard"],["dc.contributor.author","Norgauer, Johannes"],["dc.contributor.author","Kamradt, Thomas"],["dc.date.accessioned","2018-11-07T08:58:44Z"],["dc.date.available","2018-11-07T08:58:44Z"],["dc.date.issued","2011"],["dc.description.abstract","PI3Ks control signal transduction triggered by growth factors and G-protein-coupled receptors and regulate an array of biological processes, including cellular proliferation, differentiation, survival and migration. Herein, we investigated the role of PI3K gamma in the pathogenesis of EAE. We show that, in the absence of PI3K gamma expression, clinical signs of EAE were delayed and mitigated. PI3K gamma-deficient myelin oligodendrocyte glycoprotein (MOG)(35-55)-specific CD4(+) T cells appeared later in the secondary lymphoid organs and in the CNS than their WT counterparts. Transfer of WT CD4(+) cells into PI3K gamma(-/-) mice prior to MOG(35-55) immunisation restored EAE severity to WT levels, supporting the relevance of PI3K gamma expression in Th cells for the pathogenesis of EAE; however, PI3K gamma was dispensable for Th1 and Th17 differentiation, thus excluding an altered expression of these pathogenetically relevant cytokines as the cause for ameliorated EAE in PI3K gamma(-/-) mice. These findings demonstrate that PI3K gamma contributes to the development of autoimmune CNS inflammation."],["dc.identifier.doi","10.1002/eji.201040504"],["dc.identifier.isi","000288097700028"],["dc.identifier.pmid","21287545"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23714"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0014-2980"],["dc.title","PI3K gamma deficiency delays the onset of experimental autoimmune encephalomyelitis and ameliorates its clinical outcome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","NEURON GLIA BIOLOGY"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Escher, Angelika"],["dc.contributor.author","Merlder, Doron"],["dc.contributor.author","Rohde, Anna"],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Stadelman, Christine"],["dc.date.accessioned","2018-11-07T11:07:11Z"],["dc.date.available","2018-11-07T11:07:11Z"],["dc.date.issued","2007"],["dc.format.extent","S104"],["dc.identifier.isi","000251708800321"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52496"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cambridge Univ Press"],["dc.publisher.place","New york"],["dc.relation.issn","1740-925X"],["dc.title","MS-like grey matter lesions in beta-synuclein(93)-111 immunized Lewis rats"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","E169"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","E170"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Kunz, Pierre"],["dc.contributor.author","Escher, Angelika"],["dc.contributor.author","Barrantes-Freer, Alonso"],["dc.contributor.author","Nessler, S."],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Stadelmann-Nessler, Christine"],["dc.date.accessioned","2018-11-07T09:54:19Z"],["dc.date.available","2018-11-07T09:54:19Z"],["dc.date.issued","2015"],["dc.identifier.isi","000356386700296"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36510"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.eventlocation","Bilbao, SPAIN"],["dc.relation.issn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","Influence of autoimmune inflammation on remyelination in cuprizone-induced demyelination"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.volume","116"],["dc.contributor.author","Escher, Angelika"],["dc.contributor.author","Nessler, S."],["dc.contributor.author","Vollmar, Patrick"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Reichardt, Heike"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T11:11:01Z"],["dc.date.available","2018-11-07T11:11:01Z"],["dc.date.issued","2008"],["dc.format.extent","342"],["dc.identifier.isi","000258235200023"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53334"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","53rd Annual Meeting of the German-Society-of-Neuropathology-and-Neuroanatomy"],["dc.relation.eventlocation","Wurzburg, GERMANY"],["dc.relation.issn","0001-6322"],["dc.title","Immunization of cuprizone-treated mice leads to cerebral inflammatory pathology"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2992"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","3005"],["dc.bibliographiccitation.volume","129"],["dc.contributor.author","Capetillo-Zarate, Estibaliz"],["dc.contributor.author","Staufenbiel, Matthias"],["dc.contributor.author","Abramowski, Dorothee"],["dc.contributor.author","Haass, Christian"],["dc.contributor.author","Escher, Angelika"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Yamaguchi, Haruyasu"],["dc.contributor.author","Wiestler, Otmar D."],["dc.contributor.author","Thal, Dietmar Rudolf"],["dc.date.accessioned","2018-11-07T08:59:50Z"],["dc.date.available","2018-11-07T08:59:50Z"],["dc.date.issued","2006"],["dc.description.abstract","The amyloid beta-protein (A beta) is the main component of Alzheimer's disease-related senile plaques. Although A beta is associated with the development of Alzheimer's disease, it has not been shown which forms of A beta induce neurodegeneration in vivo and which types of neurons are vulnerable. To address these questions, we implanted DiI crystals into the left frontocentral cortex of APP23 transgenic mice overexpressing mutant human APP (amyloid precursor protein gene) and of littermate controls. Traced commissural neurons in layer III of the right frontocentral cortex were quantified in 3-, 5-, 11- and 15-month-old mice. Three different types of commissural neurons were traced. At 3 months of age no differences in the number of labelled commissural neurons were seen in APP23 mice compared with wild-type mice. A selective reduction of the heavily ramified type of neurons was observed in APP23 mice compared with wild-type animals at 5, 11 and 15 months of age, starting when the first A beta-deposits occurred in the frontocentral cortex at 5 months. The other two types of commissural neurons did not show alterations at 5 and 11 months. At 15 months, the number of traced sparsely ramified pyramidal neurons was reduced in addition to that of the heavily ramified neurons in APP23 mice compared with wild-type mice. At this time A beta-deposits were seen in the neo- and allocortex as well as in the basal ganglia and the thalamus. In summary, our results show that A beta induces progressive degeneration of distinct types of commissural neurons. Degeneration of the most vulnerable neurons starts in parallel with the occurrence of the first fibrillar A beta-deposits in the neocortex, that is, with the detection of aggregated A beta. The involvement of additional neuronal subpopulations is associated with the expansion of A beta-deposition into further brain regions. The vulnerability of different types of neurons to A beta, thereby, is presumably related to the complexity of their dendritic morphology."],["dc.identifier.doi","10.1093/brain/awl176"],["dc.identifier.isi","000241783800020"],["dc.identifier.pmid","16844716"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24002"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.title","Selective vulnerability of different types of commissural neurons for amyloid beta-protein-induced neurodegeneration in APP23 mice correlates with dendritic tree morphology"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]