Schneider-Gold, Christiane

[["dc.bibliographiccitation.firstpage","477"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Aktuelle Neurologie"],["dc.bibliographiccitation.lastpage","480"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Schneider-Gold, C."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Gold, R."],["dc.date.accessioned","2017-09-07T11:54:11Z"],["dc.date.available","2017-09-07T11:54:11Z"],["dc.date.issued","2005"],["dc.description.abstract","Mycophenolate mofetil (MMF) is a novel immunosuppressive drug and has been applied in myasthenia gravis, dysimmune polyneuropathies, myositis, multiple sclerosis and cerebral vasculitis. The spectrum of neurological diseases in which MMF may be effective is not finally delineated. So far, only in myasthenia gravis the efficacy and safety of MMF has been evaluated by retrospective analyses, one open-label study and one placebo-controlled double blind study. in myasthenia gravis, replacement of azathioprine or cyclosporine A by MMF seems to be useful in non-responders or in case of intolerance. Further controlled studies are necessary to evaluate short-term and long-term effects of MMF in neurological autoimmune diseases."],["dc.description.abstract","Mykophenolatmofetil (MMF) erweitert das Spektrum immunmodulatorischer Substanzen, die in der Therapie neuroimmunologischer Erkrankungen eingesetzt werden können. Bisher sind positive therapeutische Effekte bei Myasthenia gravis, Myositiden, autoimmunen Polyneuropathien, multipler Sklerose und zerebraler Vaskulitis beschrieben worden. Das Spektrum möglicher Indikationen für die Verabreichung von MMF auf neurologischem Fachgebiet ist aktuell noch nicht abschließend definiert. Die Indikation für den „Off-label”-Einsatz von MMF muss im Einzelfall sorgfältig geprüft werden. Bei Myasthenia gravis konnten sowohl retrospektive Analysen als auch eine offene Studie und eine randomisierte plazebokontrollierte Studie die Wirksamkeit und gute Verträglichkeit belegen. MMF scheint daher eine mögliche therapeutische Alternative zu Azathioprin oder Ciclosporin A bei Unverträglichkeiten oder unzureichender Wirksamkeit zu sein. Weitere kontrollierte Studien sind notwendig, um die Kurz- und Langzeiteffekte von MMF bei neuroimmunologischen Erkrankungen genauer zu evaluieren."],["dc.identifier.doi","10.1055/s-2005-866941"],["dc.identifier.gro","3143799"],["dc.identifier.isi","000232782200005"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1353"],["dc.language.iso","de"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0302-4350"],["dc.title","Mycophenolate mofetil: A new therapeutic option in neuroimmunological diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","575"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","European Journal of Neurology"],["dc.bibliographiccitation.lastpage","577"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Neusch, C."],["dc.contributor.author","Senderek, J."],["dc.contributor.author","Eggermann, T."],["dc.contributor.author","Elolff, E."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Schneider-Gold, C."],["dc.date.accessioned","2017-09-07T11:49:48Z"],["dc.date.available","2017-09-07T11:49:48Z"],["dc.date.issued","2007"],["dc.description.abstract","Charcot-Marie-Tooth disease (CMT) has been classified into two types: demyelinating forms (CMT1) and axonal forms (CMT2). Mutations in the CMT2A locus have been linked to the KIF1B and the mitofusin 2 (MFN2) genes. Here, we report a German patient with CMT2 with an underlying spontaneous mutation (c.281G -> A) in the MFN2 gene. Clinically, the patient presented with early-onset CMT that was not associated with additional central nervous system pathology. The disease course was rapidly progressive in the first years and slowed afterwards. We also suggest that single patients with early-onset axonal polyneuropathies should be screened for MFN2 mutations."],["dc.identifier.doi","10.1111/j.1468-1331.2006.01688.x"],["dc.identifier.gro","3143505"],["dc.identifier.isi","000245604500025"],["dc.identifier.pmid","17437620"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1027"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1351-5101"],["dc.title","Mitofusin 2 gene mutation (R94Q) causing severe early-onset axonal polyneuropathy (CMT2A)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","712"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Muscle & Nerve"],["dc.bibliographiccitation.lastpage","724"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Neusch, Clemens"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Schneider-Gold, Christiane"],["dc.date.accessioned","2017-09-07T11:49:47Z"],["dc.date.available","2017-09-07T11:49:47Z"],["dc.date.issued","2007"],["dc.description.abstract","In classic neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), the pathogenic concept of a cell-autonomous disease of motor neurons has been challenged increasingly in recent years. Macro- and microglial cells have come to the forefront for their role in multistep degenerative processes in ALS and respective disease models. The activation of astroglial and microglial cells occurs early in the pathogenesis of the disease and seems to greatly influence disease onset and promotion. The role of oligodendrocytes and Schwann cells remains elusive. In this review we highlight the impact of nonneuronal cells in ALS pathology. We discuss diverse glial membrane proteins that are necessary to control neuronal activity and neuronal cell survival, and summarize the contribution of these proteins to motor neuron death in ALS. We also describe recently discovered glial mechanisms that promote motor neuron degeneration using state-of-the-art genetic mouse technology. Finally, we provide an outlook on the extent to which these new pathomechanistic insights may offer novel therapeutic approaches,"],["dc.identifier.doi","10.1002/mus.20768"],["dc.identifier.gro","3143495"],["dc.identifier.isi","000246766500003"],["dc.identifier.pmid","17373702"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1016"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0148-639X"],["dc.title","Glia cells in amyotrophic lateral sclerosis: New clues to understanding an old disease?"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]