Maruschak, Brigitte

[["dc.bibliographiccitation.firstpage","238"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Neuropathology & Experimental Neurology"],["dc.bibliographiccitation.lastpage","246"],["dc.bibliographiccitation.volume","66"],["dc.contributor.author","Kuhlmann, Tanja"],["dc.contributor.author","Remington, Leah"],["dc.contributor.author","Maruschak, Brigitte"],["dc.contributor.author","Owens, Trevor"],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T11:04:36Z"],["dc.date.available","2018-11-07T11:04:36Z"],["dc.date.issued","2007"],["dc.description.abstract","The unambiguous identification of oligodendrocytes in tissue sections, especially in myelinated tracts, is often difficult. Most of the antibodies used to identify oligodendrocytes label the myelin sheath as well. Originally described as an inhibitor of axonal outgrowth, Nogo-A is known to be strongly expressed in mature oligodendrocytes in vivo. In the present investigation we analyzed the expression patterns of Nogo-A in adult mouse and human CNS as well as in demyelinating animal models and multiple sclerosis lesions. Nogo-A expression was compared with that of other frequently used oligodendroglial markers such as CC1, CNP, and in situ hybridization for proteolipid protein mRNA. Nogo-A strongly and reliably labeled oligodendrocytes in the adult CNS as well as in demyelinating lesions and thus represents a valuable tool for the identification of oligodendrocytes in human and mouse CNS tissue."],["dc.identifier.isi","000246852600008"],["dc.identifier.pmid","17356385"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51881"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0022-3069"],["dc.title","Nogo-A is a reliable oligodendroglial marker in adult human and mouse CNS and in demyelinated lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.volume","108"],["dc.contributor.author","Roemer, Shanu"],["dc.contributor.author","Maruschak, B."],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T10:44:55Z"],["dc.date.available","2018-11-07T10:44:55Z"],["dc.date.issued","2004"],["dc.format.extent","367"],["dc.identifier.isi","000224249700075"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47382"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","49th Annual Meeting of the German-Society-of-Neuropathology-and-Neuroanatomy"],["dc.relation.eventlocation","Cologne, GERMANY"],["dc.relation.issn","0001-6322"],["dc.title","Characterization of an immuno-histochemical marker of Wallerian degeneration"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","159"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Brain Research"],["dc.bibliographiccitation.lastpage","164"],["dc.bibliographiccitation.volume","916"],["dc.contributor.author","Siebert, Heike"],["dc.contributor.author","Engelke, Sebastian"],["dc.contributor.author","Maruschak, B."],["dc.contributor.author","Bruck, Wolfgang W."],["dc.date.accessioned","2018-11-07T08:32:21Z"],["dc.date.available","2018-11-07T08:32:21Z"],["dc.date.issued","2001"],["dc.description.abstract","Wallerian degeneration of a peripheral nerve is mainly characterized by axon and myelin degradation and is paralleled by a massive invasion of peripheral macrophages into the nerve. These cells enter the nerve attracted by a cascade of chemokines and cytokines but require proteolytic and enzymatic factors which enables them to cross the blood-nerve barrier. Here we investigated whether U-naphthyl (alpha -NA) esterases - which have been shown to be exclusively expressed in human monocytes - play a role during Wallerian degeneration. These enzymes were blocked by the specific inhibitor bis(4-nitrophenyl)-phosphate (BNPP) in an established in vitro model of Wallerian degeneration. Sciatic nerve segments of mice were co-cultured with peritoneal macrophages and BNPP was added to the cultures in various concentrations and at different timepoints. The macrophage numbers and myelin density in the nerve segments and the myelin load of macrophages were evaluated. After BNPP treatment the macrophage number within the nerve was significantly diminished and the myelin load within the macrophages was decreased, resulting in elevated levels of preserved myelin within the nerves. These experiments clearly showed a double effect of the UNA esterase inhibitor BNPP on macrophages, First, it suggests a role for UNA esterases on the migratory potential of macrophages since their invasion into the nerves was diminished. Second, the reduced myelin uptake is due to the inhibition of phagocytic capacity of these cells by BNPP. The therapeutical use of this inhibitor for treatment of autoimmune diseases such as multiple sclerosis or Guillain-Barre syndrome remains to be investigated. (C) 2001 Elsevier Science B.V. All rights reserved."],["dc.identifier.doi","10.1016/S0006-8993(01)02887-6"],["dc.identifier.isi","000171812300019"],["dc.identifier.pmid","11597603"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17322"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0006-8993"],["dc.title","Concentration-dependent effects of the esterase inhibitor BNPP on macrophage migration and myelin phagocytosis"],["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.firstpage","2558"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","2566"],["dc.bibliographiccitation.volume","125"],["dc.contributor.author","Tschampa, Henriette J."],["dc.contributor.author","Herms, J. W."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Maruschak, B."],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Jastrow, U."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Steinhoff, B. J."],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.date.accessioned","2018-11-07T09:51:28Z"],["dc.date.available","2018-11-07T09:51:28Z"],["dc.date.issued","2002"],["dc.description.abstract","The pathogenesis underlying the typical findings in Creutzfeldt-Jakob disease (CJD) such as periodic EEG changes or myoclonus is not fully understood. The thalamus possesses a high density of inhibitory neurones and serves as a crucial pacemaker of rhythmic EEG activity. As inhibitory neurones expressing parvalbumin (PV) are reduced in the cerebral cortex and hippocampus in sporadic CJD (sCJD), we studied the distribution and number of PV-immunoreactive neurones in sCJD thalami in order to determine whether damage to them could account for certain clinical findings. Immuno histochemical analysis was performed on the thalami from 21 sCJD patients and five controls. The number of PV+ neurones was counted in the thalamic nuclei and compared with clinical and molecular findings. In sCJD patients, PV+ neurones were significantly reduced in the ventrolateral posterior (VLp), ventrolateral anterior (VLa), anteroventral (AV), lateral dorsal (LD), mediodorsal (MD) and reticular (Re) thalamic nuclei (P < 0.05). The VLp was especially damaged in sCJD patients with homozygosity for methionine at codon 129 and scrapie prion protein (PrPSc) type 1. Patients with typical EEG changes [periodic sharp wave complexes (PSWCs)] and myoclonus had a predominant loss of PV+ cells in the reticular thalamic nucleus. In conclusion, our data support the hypothesis that the damage to PV-immunoreactive neurones determines the generation of certain typical clinical features of CJD, i.e. PSWCs associated with myoclonus."],["dc.identifier.doi","10.1093/brain/awf253"],["dc.identifier.isi","000178834400016"],["dc.identifier.pmid","12390980"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35920"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.title","Clinical findings in sporadic Creutzfeldt-Jakob disease correlate with thalamic pathology"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","185"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Neuroscience Research"],["dc.bibliographiccitation.lastpage","190"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Kuhlmann, T."],["dc.contributor.author","Wendling, U."],["dc.contributor.author","Nolte, C."],["dc.contributor.author","Zipp, Frauke"],["dc.contributor.author","Maruschak, B."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Siebert, Heike"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.date.accessioned","2018-11-07T10:32:35Z"],["dc.date.available","2018-11-07T10:32:35Z"],["dc.date.issued","2002"],["dc.description.abstract","Macrophages/microglia are the key effector cells in myelin removal. Differences exist in the amount and time course of myelin uptake in the central (CNS) and peripheral nervous system (PNS), the basis of this difference, however, is not yet clarified. In the present experiments we studied the phagocytosis rate of CNS or PNS myelin by macrophages and microglia in vitro. Additionally, the effects of intravenous immunoglobulins (IVIg) on this process were investigated. In the PNS experiments, sciatic nerves were cocultured with peritoneal macrophages. Optic nerve fragments were used to characterize the myelin-removing properties of microglia. Cocultures with peritoneal macrophages aimed at investigating the differences in phagocytosis between resident microglia and added macrophages. The myelin phagocytosis in sciatic nerve fragments was higher than in optic nerves, indicating differences in the myelin uptake rate between peripheral macrophages and microglia. IVIg increased the phagocytosis of PNS myelin by macrophages, but not by microglia in optic nerves. The addition of peritoneal macrophages to optic nerve fragments did not lead to an increase in the phagocytosis of CNS myelin either. The IVIg induced phagocytosis of PNS myelin by peripheral macrophages was associated with an increased expression of macrophage Fc receptors measured by FACS. Blocking of Fc receptors by anti-Fc receptor antibody reduced the IVIg induced PNS myelin phagocytosis to basic levels, indicating that the induced but not the basic myelin uptake by macrophages is Fc receptor dependent. In contrast to peripheral macrophages, IVIg did not increase Fc receptor density on microglia. These data indicate that phagocytosis of PNS and CNS myelin by macrophages or microglia is differentially regulated. Local factors within the CNS or PNS may affect this process by modulating the surface receptor profile and activation state of the phagocytic cell or the structure of the myelin sheath. (C) 2002 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/jnr.10104"],["dc.identifier.isi","000173099000006"],["dc.identifier.pmid","11782962"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44382"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0360-4012"],["dc.title","Differential regulation of myelin phagocytosis by macrophages/microglia, involvement of target myelin, Fc receptors and activation by intravenous immunoglobulins"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]