Dallenga, Tobias

[["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.firstpage","976"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Brain Pathology"],["dc.bibliographiccitation.lastpage","985"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Dziedzic, Tomasz"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Dallenga, Tobias"],["dc.contributor.author","Koenig, Fatima Barbara"],["dc.contributor.author","Mueller, Sven"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T08:39:34Z"],["dc.date.available","2018-11-07T08:39:34Z"],["dc.date.issued","2010"],["dc.description.abstract","Axonal loss is a major component of the pathology of multiple sclerosis (MS) and the morphological basis of permanent clinical disability. It occurs in demyelinating plaques but also in the so-called normal-appearing white matter (NAWM). However, the contribution of Wallerian degeneration to axonal pathology is not known. Here, we analyzed the extent of Wallerian degeneration and axonal pathology in periplaque white matter (PPWM) and lesions in early multiple sclerosis biopsy tissue from 63 MS patients. Wallerian degeneration was visualized using an antibody against the neuropeptide Y receptor Y1 (NPY-Y1R). The number of SMI-32-positive axons with non-phosphorylated neurofilaments was significantly higher in both PPWM and plaques compared to control white matter. APP-positive, acutely damaged axons were found in significantly higher numbers in plaques compared to PPWM. Strikingly, the number of NPY-Y1R-positive axons undergoing Wallerian degeneration was significantly higher in PPWM and plaques than in control WM. NPY-Y1R-positive axons in PPWM were strongly correlated to those in the lesions. Our results show that Wallerian degeneration is a major component of axonal pathology in the periplaque white matter in early MS. It may contribute to radiological changes observed in early MS and most likely plays a major role in the development of disability."],["dc.identifier.doi","10.1111/j.1750-3639.2010.00401.x"],["dc.identifier.isi","000280629400010"],["dc.identifier.pmid","20477831"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19027"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1015-6305"],["dc.title","Wallerian Degeneration: A Major Component of Early Axonal Pathology in Multiple Sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","57"],["dc.bibliographiccitation.journal","Journal of Neuroinflammation"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Singh, Shailender"],["dc.contributor.author","Dallenga, Tobias"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Roemer, Shanu"],["dc.contributor.author","Maruschak, Brigitte"],["dc.contributor.author","Siebert, Heike"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T10:26:08Z"],["dc.date.available","2018-11-07T10:26:08Z"],["dc.date.issued","2017"],["dc.description.abstract","Background: Axonal damage and loss substantially contribute to the incremental accumulation of clinical disability in progressive multiple sclerosis. Here, we assessed the amount of Wallerian degeneration in brain tissue of multiple sclerosis patients in relation to demyelinating lesion activity and asked whether a transient blockade of Wallerian degeneration decreases axonal loss and clinical disability in a mouse model of inflammatory demyelination. Methods: Wallerian degeneration and acute axonal damage were determined immunohistochemically in the periplaque white matter of multiple sclerosis patients with early actively demyelinating lesions, chronic active lesions, and inactive lesions. Furthermore, we studied the effects of Wallerian degeneration blockage on clinical severity, inflammatory pathology, acute axonal damage, and long-term axonal loss in experimental autoimmune encephalomyelitis using Wallerian degeneration slow (WldS) mutant mice. Results: The highest numbers of axons undergoing Wallerian degeneration were found in the perilesional white matter of multiple sclerosis patients early in the disease course and with actively demyelinating lesions. Furthermore, Wallerian degeneration was more abundant in patients harboring chronic active as compared to chronic inactive lesions. No co-localization of neuropeptide Y-Y1 receptor, a bona fide immunohistochemical marker of Wallerian degeneration, with amyloid precursor protein, frequently used as an indicator of acute axonal transport disturbance, was observed in human and mouse tissue, indicating distinct axon-degenerative processes. Experimentally, a delay of Wallerian degeneration, as observed in WldS mice, did not result in a reduction of clinical disability or acute axonal damage in experimental autoimmune encephalomyelitis, further supporting that acute axonal damage as reflected by axonal transport disturbances does not share common molecular mechanisms with Wallerian degeneration. Furthermore, delaying Wallerian degeneration did not result in a net rescue of axons in late lesion stages of experimental autoimmune encephalomyelitis. Conclusions: Our data indicate that in multiple sclerosis, ongoing demyelination in focal lesions is associated with axonal degeneration in the perilesional white matter, supporting a role for focal pathology in diffuse white matter damage. Also, our results suggest that interfering with Wallerian degeneration in inflammatory demyelination does not suffice to prevent acute axonal damage and finally axonal loss."],["dc.identifier.doi","10.1186/s12974-017-0831-8"],["dc.identifier.isi","000397153100002"],["dc.identifier.pmid","28302146"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14381"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42975"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1742-2094"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Relationship of acute axonal damage, Wallerian degeneration, and clinical disability in multiple sclerosis"],["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"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.volume","118"],["dc.contributor.author","Dallenga, Tobias"],["dc.contributor.author","Bittner, A."],["dc.contributor.author","Jaeger, W."],["dc.contributor.author","Vollmar, Patrick"],["dc.contributor.author","Oertel, Wolfgang Hermann"],["dc.contributor.author","Sommer, N."],["dc.contributor.author","Moeller, J. C."],["dc.contributor.author","Hemmer, Bernhard"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Nessler, S."],["dc.date.accessioned","2018-11-07T11:24:24Z"],["dc.date.available","2018-11-07T11:24:24Z"],["dc.date.issued","2009"],["dc.format.extent","436"],["dc.identifier.isi","000268421800026"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56397"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","54th Annual Meeting of the German-Society-of-Neuropathology-and-Neuroanatomy"],["dc.relation.eventlocation","Dusseldorf, GERMANY"],["dc.relation.issn","0001-6322"],["dc.title","Increased axonal damage in p75(NTR)-knockout mice after induction of experimental autoimmune encephalomyelitis by adoptive transfer"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]