Merkler, Doron

[["dc.bibliographiccitation.firstpage","277"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Cell"],["dc.bibliographiccitation.lastpage","290"],["dc.bibliographiccitation.volume","156"],["dc.contributor.author","Snaidero, Nicolas"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Czopka, Tim"],["dc.contributor.author","Hekking, Liesbeth H. P."],["dc.contributor.author","Mathisen, Cliff"],["dc.contributor.author","Verkleij, Dick"],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Edgar, Julia M."],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Lyons, David A."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Simons, Mikael"],["dc.date.accessioned","2018-11-07T09:45:05Z"],["dc.date.available","2018-11-07T09:45:05Z"],["dc.date.issued","2014"],["dc.description.abstract","Central nervous system myelin is a multilayered membrane sheath generated by oligodendrocytes for rapid impulse propagation. However, the underlying mechanisms of myelin wrapping have remained unclear. Using an integrative approach of live imaging, electron microscopy, and genetics, we show that new myelin membranes are incorporated adjacent to the axon at the innermost tongue. Simultaneously, newly formed layers extend laterally, ultimately leading to the formation of a set of closely apposed paranodal loops. An elaborated system of cytoplasmic channels within the growing myelin sheath enables membrane trafficking to the leading edge. Most of these channels close with ongoing development but can be reopened in adults by experimentally raising phosphatidylinositol-(3,4,5)-triphosphate levels, which reinitiates myelin growth. Our model can explain assembly of myelin as a multilayered structure, abnormal myelin outfoldings in neurological disease, and plasticity of myelin biogenesis observed in adult life."],["dc.identifier.doi","10.1016/j.cell.2013.11.044"],["dc.identifier.isi","000329912200027"],["dc.identifier.pmid","24439382"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34540"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.relation.issn","1097-4172"],["dc.relation.issn","0092-8674"],["dc.title","Myelin Membrane Wrapping of CNS Axons by PI(3,4,5) P3-Dependent Polarized Growth at the Inner Tongue"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","13275"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Romanelli, Elisa"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Mezydlo, Aleksandra"],["dc.contributor.author","Weil, Marie-Theres"],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Nikic, Ivana"],["dc.contributor.author","Potz, Stephanie"],["dc.contributor.author","Meinl, Edgar"],["dc.contributor.author","Matznick, Florian E. H."],["dc.contributor.author","Kreutzfeldt, Mario"],["dc.contributor.author","Ghanem, Alexander"],["dc.contributor.author","Conzelmann, Karl-Klaus"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Routh, Matthew"],["dc.contributor.author","Simons, Mikael"],["dc.contributor.author","Bishop, Derron"],["dc.contributor.author","Misgeld, Thomas"],["dc.contributor.author","Kerschensteiner, Martin"],["dc.date.accessioned","2018-11-07T10:05:43Z"],["dc.date.available","2018-11-07T10:05:43Z"],["dc.date.issued","2016"],["dc.description.abstract","Oligodendrocyte damage is a central event in the pathogenesis of the common neuro-inflammatory condition, multiple sclerosis (MS). Where and how oligodendrocyte damage is initiated in MS is not completely understood. Here, we use a combination of light and electron microscopy techniques to provide a dynamic and highly resolved view of oligodendrocyte damage in neuroinflammatory lesions. We show that both in MS and in its animal model structural damage is initiated at the myelin sheaths and only later spreads to the oligodendrocyte cell body. Early myelin damage itself is characterized by the formation of local myelin out-foldings-'myelinosomes'-, which are surrounded by phagocyte processes and promoted in their formation by anti-myelin antibodies and complement. The presence of myelinosomes in actively demyelinating MS lesions suggests that oligodendrocyte damage follows a similar pattern in the human disease, where targeting demyelination by therapeutic interventions remains a major open challenge."],["dc.identifier.doi","10.1038/ncomms13275"],["dc.identifier.isi","000387837900001"],["dc.identifier.pmid","27848954"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13963"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38953"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","2041-1723"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Myelinosome formation represents an early stage of oligodendrocyte damage in multiple sclerosis and its animal model"],["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","756"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Nature Medicine"],["dc.bibliographiccitation.lastpage","761"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Lang, Philipp A."],["dc.contributor.author","Contaldo, Claudio"],["dc.contributor.author","Georgiev, Panco"],["dc.contributor.author","El-Badry, Ashraf Mohammad"],["dc.contributor.author","Recher, Mike"],["dc.contributor.author","Kurrer, Michael O."],["dc.contributor.author","Cervantes-Barragan, Luisa"],["dc.contributor.author","Ludewig, Burkhard"],["dc.contributor.author","Calzascia, Thomas"],["dc.contributor.author","Bolinger, Beatrice"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Odermatt, Bernhard"],["dc.contributor.author","Bader, Michael"],["dc.contributor.author","Graf, Rolf"],["dc.contributor.author","Clavien, Pierre-Alain"],["dc.contributor.author","Hegazy, Ahmed N."],["dc.contributor.author","Loehning, Max"],["dc.contributor.author","Harris, Nicola L."],["dc.contributor.author","Ohashi, Pamela S."],["dc.contributor.author","Hengartner, Hans"],["dc.contributor.author","Zinkernagel, Rolf M."],["dc.contributor.author","Lang, Karl S."],["dc.date.accessioned","2018-11-07T11:13:43Z"],["dc.date.available","2018-11-07T11:13:43Z"],["dc.date.issued","2008"],["dc.description.abstract","More than 500 million people worldwide are persistently infected with hepatitis B virus or hepatitis C virus(1). Although both viruses are poorly cytopathic, persistence of either virus carries a risk of chronic liver inflammation, potentially resulting in liver steatosis, liver cirrhosis, end-stage liver failure or hepatocellular carcinoma. Virus-specific T cells are a major determinant of the outcome of hepatitis, as they contribute to the early control of chronic hepatitis viruses, but they also mediate immunopathology during persistent virus infection(1-4). We have analyzed the role of platelet-derived vasoactive serotonin during virus-induced CD8(+) T cell-dependent immunopathological hepatitis in mice infected with the noncytopathic lymphocytic choriomeningitis virus. After virus infection, platelets were recruited to the liver, and their activation correlated with severely reduced sinusoidal microcirculation, delayed virus elimination and increased immunopathological liver cell damage. Lack of platelet-derived serotonin in serotonin-deficient mice normalized hepatic microcirculatory dysfunction, accelerated virus clearance in the liver and reduced CD8(+) T cell-dependent liver cell damage. In keeping with these observations, serotonin treatment of infected mice delayed entry of activated CD8(+) T cells into the liver, delayed virus control and aggravated immunopathological hepatitis. Thus, vasoactive serotonin supports virus persistence in the liver and aggravates virus-induced immunopathology."],["dc.identifier.doi","10.1038/nm1780"],["dc.identifier.isi","000257452700023"],["dc.identifier.pmid","18516052"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53962"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1078-8956"],["dc.title","Aggravation of viral hepatitis by platelet-derived serotonin"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Journal of Neurology"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Schirmer, Lucas"],["dc.contributor.author","Koenig, Fatima Barbara"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T08:39:40Z"],["dc.date.available","2018-11-07T08:39:40Z"],["dc.date.issued","2010"],["dc.format.extent","657"],["dc.identifier.isi","000293331101589"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19052"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Malden"],["dc.relation.eventlocation","Geneva, SWITZERLAND"],["dc.relation.issn","1351-5101"],["dc.title","Comparative study of neuronal and axonal pathology in early multiple sclerosis and CNS trauma lesions"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","34594"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Bjarnadottir, Kristbjorg"],["dc.contributor.author","Benkhoucha, Mahdia"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Payne, Natalie L."],["dc.contributor.author","Bernard, Claude C. A."],["dc.contributor.author","Molnarfi, Nicolas"],["dc.contributor.author","Lalive, Patrice H."],["dc.date.accessioned","2018-11-07T10:07:11Z"],["dc.date.available","2018-11-07T10:07:11Z"],["dc.date.issued","2016"],["dc.description.abstract","Studies in experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis (MS), have shown that regulatory B cells modulate the course of the disease via the production of suppressive cytokines. While data indicate a role for transforming growth factor (TGF)-beta 1 expression in regulatory B cell functions, this mechanism has not yet been tested in autoimmune neuroinflammation. Transgenic mice deficient for TGF-beta 1 expression in B cells (B-TGF-beta 1(-/-)) were tested in EAE induced by recombinant mouse myelin oligodendrocyte glycoprotein (rmMOG). In this model, B-TGF-beta 1(-/-) mice showed an earlier onset of neurologic impairment compared to their littermate controls. Exacerbated EAE susceptibility in B-TGF-beta 1(-/-) mice was associated with augmented CNS T helper (Th) 1/17 responses. Moreover, selective B cell TGF-beta 1-deficiency increased the frequencies and activation of myeloid dendritic cells, potent professional antigen-presenting cells (APCs), suggesting that B cell-derived TGF-beta 1 can constrain Th1/17 responses through inhibition of APC activity. Collectively our data suggest that B cells can down-regulate the function of APCs, and in turn encephalitogenic Th1/17 responses, via TGF-beta 1, findings that may be relevant to B cell-targeted therapies."],["dc.identifier.doi","10.1038/srep34594"],["dc.identifier.isi","000384762700001"],["dc.identifier.pmid","27708418"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13812"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39233"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","2045-2322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","B cell-derived transforming growth factor-beta 1 expression limits the induction phase of autoimmune neuroinflammation"],["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","1316"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Nature Medicine"],["dc.bibliographiccitation.lastpage","1323"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Recher, Mike"],["dc.contributor.author","Lang, Karl S."],["dc.contributor.author","Navarini, Alexander"],["dc.contributor.author","Hunziker, Lukas E."],["dc.contributor.author","Lang, Philipp A."],["dc.contributor.author","Fink, Katja"],["dc.contributor.author","Freigang, Stefan"],["dc.contributor.author","Georgiev, Panco"],["dc.contributor.author","Hangartner, Lars"],["dc.contributor.author","Zellweger, Raphael"],["dc.contributor.author","Bergthaler, Andreas"],["dc.contributor.author","Hegazy, Ahmed N."],["dc.contributor.author","Eschli, Bruno"],["dc.contributor.author","Theocharides, Alexandre"],["dc.contributor.author","Jeker, Lukas T."],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Odermatt, Bernhard"],["dc.contributor.author","Hersberger, Martin"],["dc.contributor.author","Hengartner, Hans"],["dc.contributor.author","Zinkernagel, Rolf M."],["dc.date.accessioned","2018-11-07T10:57:17Z"],["dc.date.available","2018-11-07T10:57:17Z"],["dc.date.issued","2007"],["dc.description.abstract","T helper cells can support the functions of CD8(+) T cells against persistently infecting viruses such as murine lymphocytic choriomeningitis virus (LCMV), cytomegalovirus, hepatitis C virus and HIV. These viruses often resist complete elimination and remain detectable at sanctuary sites, such as the kidneys and other extralymphatic organs. The mechanisms underlying this persistence are not well understood. Here we show that mice with potent virus-specific T-cell responses have reduced levels and delayed formation of neutralizing antibodies, and these mice fail to clear LCMV from extralymphatic epithelia. Transfer of virus-specific B cells but not virus-specific T cells augmented virus clearance from persistent sites. Virus elimination from the kidneys was associated with the formation of IgG deposits in the interstitial space, presumably from kidney-infiltrating B cells. CD8(+) T cells in the kidneys of mice that did not clear virus from this site were activated but showed evidence of exhaustion. Thus, we conclude that in this model of infection, site-specific virus persistence develops as a consequence of potent immune activation coupled with reductions in virus-specific neutralizing antibodies. Our results suggest that sanctuary-site formation depends both on organ anatomy and on the induction of different adaptive immune effector mechanisms. Boosting T-cell responses alone may not reduce virus persistence."],["dc.identifier.doi","10.1038/nm1670"],["dc.identifier.isi","000250736900024"],["dc.identifier.pmid","17982463"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50207"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1078-8956"],["dc.title","Extralymphatic virus sanctuaries as a consequence of potent T-cell activation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e51"],["dc.bibliographiccitation.firstpage","0501"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","PLoS Pathogens"],["dc.bibliographiccitation.lastpage","0512"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Bergthaler, Andreas"],["dc.contributor.author","Gerber, Nicolas U."],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Horvath, Edit"],["dc.contributor.author","de la Torre, Juan Carlos"],["dc.contributor.author","Pinschewer, Daniel D."],["dc.date.accessioned","2019-07-09T11:53:46Z"],["dc.date.available","2019-07-09T11:53:46Z"],["dc.date.issued","2006-06-02"],["dc.description.abstract","Arenaviruses such as Lassa fever virus cause significant mortality in endemic areas and represent potential bioterrorist weapons. The occurrence of arenaviral hemorrhagic fevers is largely confined to Third World countries with a limited medical infrastructure, and therefore live-attenuated vaccines have long been sought as a method of choice for prevention. Yet their rational design and engineering have been thwarted by technical limitations. In addition, viral genes had not been identified that are needed to cause disease but can be deleted or substituted to generate live-attenuated vaccine strains. Lymphocytic choriomeningitis virus, the prototype arenavirus, induces cell-mediated immunity against Lassa fever virus, but its safety for humans is unclear and untested. Using this virus model, we have developed the necessary methodology to efficiently modify arenavirus genomes and have exploited these techniques to identify an arenaviral Achilles' heel suitable for targeting in vaccine design. Reverse genetic exchange of the viral glycoprotein for foreign glycoproteins created attenuated vaccine strains that remained viable although unable to cause disease in infected mice. This phenotype remained stable even after extensive propagation in immunodeficient hosts. Nevertheless, the engineered viruses induced T cell–mediated immunity protecting against overwhelming systemic infection and severe liver disease upon wild-type virus challenge. Protection was established within 3 to 7 d after immunization and lasted for approximately 300 d. The identification of an arenaviral Achilles' heel demonstrates that the reverse genetic engineering of live-attenuated arenavirus vaccines is feasible. Moreover, our findings offer lymphocytic choriomeningitis virus or other arenaviruses expressing foreign glycoproteins as promising live-attenuated arenavirus vaccine candidates."],["dc.identifier.doi","10.1371/journal.ppat.0020051"],["dc.identifier.fs","53953"],["dc.identifier.pmid","16751848"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8004"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60491"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1553-7366"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Envelope Exchange for the Generation of Live-Attenuated Arenavirus Vaccines"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","495"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Nature Medicine"],["dc.bibliographiccitation.lastpage","U135"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Nikic, Ivana"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Sorbara, Catherine"],["dc.contributor.author","Brinkoetter, Mary"],["dc.contributor.author","Kreutzfeldt, Mario"],["dc.contributor.author","Bareyre, Florence Martine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Bishop, Derron"],["dc.contributor.author","Misgeld, Thomas"],["dc.contributor.author","Kerschensteiner, Martin"],["dc.date.accessioned","2018-11-07T08:57:32Z"],["dc.date.available","2018-11-07T08:57:32Z"],["dc.date.issued","2011"],["dc.description.abstract","In multiple sclerosis, a common inflammatory disease of the central nervous system, immune-mediated axon damage is responsible for permanent neurological deficits(1,2). How axon damage is initiated is not known. Here we use in vivo imaging to identify a previously undescribed variant of axon damage in a mouse model of multiple sclerosis. This process, termed 'focal axonal degeneration' (FAD), is characterized by sequential stages, beginning with focal swellings and progressing to axon fragmentation. Notably, most swollen axons persist unchanged for several days, and some recover spontaneously. Early stages of FAD can be observed in axons with intact myelin sheaths. Thus, contrary to the classical view(2-6), demyelination-a hallmark of multiple sclerosis-is not a prerequisite for axon damage. Instead, focal intra-axonal mitochondrial pathology is the earliest ultrastructural sign of damage, and it precedes changes in axon morphology. Molecular imaging and pharmacological experiments show that macrophage-derived reactive oxygen and nitrogen species (ROS and RNS) can trigger mitochondrial pathology and initiate FAD. Indeed, neutralization of ROS and RNS rescues axons that have already entered the degenerative process. Finally, axonal changes consistent with FAD can be detected in acute human multiple sclerosis lesions. In summary, our data suggest that inflammatory axon damage might be spontaneously reversible and thus a potential target for therapy."],["dc.identifier.doi","10.1038/nm.2324"],["dc.identifier.isi","000289245100041"],["dc.identifier.pmid","21441916"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23423"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1078-8956"],["dc.title","A reversible form of axon damage in experimental autoimmune encephalomyelitis and multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","356"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","364"],["dc.bibliographiccitation.volume","128"],["dc.contributor.author","Buss, A."],["dc.contributor.author","Pech, K."],["dc.contributor.author","Merkler, D."],["dc.contributor.author","Kakulas, B. A."],["dc.contributor.author","Martin, D."],["dc.contributor.author","Schoenen, J."],["dc.contributor.author","Noth, J."],["dc.contributor.author","Schwab, M. E."],["dc.contributor.author","Brook, G. A."],["dc.date.accessioned","2018-11-07T11:24:59Z"],["dc.date.available","2018-11-07T11:24:59Z"],["dc.date.issued","2005"],["dc.description.abstract","Axons undergo Wallerian degeneration (WD) distal to a point of injury. In the lesioned PNS, WD may be followed by successful axonal regeneration and functional recovery. However, in the lesioned mammalian CNS, there is no significant axonal regeneration. Myelin-associated proteins (MAPs) have been shown to play significant roles in preventing axonal regeneration in the CNS. Since relatively little is known about such events in human CNS pathologies, we performed an immunohistochemical investigation on the temporal changes of four MAPs during WD in post-mortem spinal cords of 22 patients who died 2 days to 30 years after either cerebral infarction or traumatic spinal cord injury. In contrast to experimental studies in rats, the loss of myelin sheaths is greatly delayed in humans and continues slowly over a number of years. However, in agreement with animal data, a sequential loss of myelin proteins was found which was dependent on their location within the myelin sheath. Myelin proteins situated on the peri-axonal membrane were the first to be lost, the time course correlating with the loss of axonal markers. Proteins located within compact myelin or on the outer myelin membrane were still detectable 3 years after injury in degenerating fibre tracts, long after the disappearance of the corresponding axons. The persistence of axon growth-inhibitory proteins such as NOGO-A in degenerating nerve fibre tracts may contribute to the maintenance of an environment that is hostile to axon regeneration, long after the initial injury. The present data highlight the importance of correlating the well documented, lesion-induced changes that take place in controlled laboratory investigations with those that take place in the clinical domain."],["dc.identifier.doi","10.1093/brain/awh355"],["dc.identifier.isi","000226605800015"],["dc.identifier.pmid","15634734"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56537"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0006-8950"],["dc.title","Sequential loss of myelin proteins during Wallerian degeneration in the human spinal cord"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Juergens, T."],["dc.contributor.author","Glaser, Raoul"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Brinkmann, Bastian G."],["dc.contributor.author","Sereda, Michael W."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Liebetanz, David"],["dc.date.accessioned","2018-11-07T11:25:14Z"],["dc.date.available","2018-11-07T11:25:14Z"],["dc.date.issued","2009"],["dc.format.extent","S180"],["dc.identifier.isi","000269652500538"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56580"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","25th Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis"],["dc.relation.eventlocation","Dusseldorf, GERMANY"],["dc.relation.issn","1352-4585"],["dc.title","Propagation of cortical spreading depression inversely correlates with cortical myelin content"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]