Schneider-Gold, Christiane

[["dc.bibliographiccitation.firstpage","1236"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","1237"],["dc.bibliographiccitation.volume","253"],["dc.contributor.author","Schneider-Gold, Christiane"],["dc.contributor.author","Wessig, Carsten"],["dc.contributor.author","Hoepker, Martin"],["dc.contributor.author","Erdlenbruch, Bernhard"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Toyka, Klaus V."],["dc.date.accessioned","2018-11-07T09:21:23Z"],["dc.date.available","2018-11-07T09:21:23Z"],["dc.date.issued","2006"],["dc.identifier.doi","10.1007/s00415-006-0150-y"],["dc.identifier.isi","000241113100021"],["dc.identifier.pmid","16598612"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29091"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0340-5354"],["dc.title","Pregnancy and delivery of a healthy baby in autoimmune Lambert-Eaton myasthenic syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1904"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","1909"],["dc.bibliographiccitation.volume","255"],["dc.contributor.author","Minnerop, Martina"],["dc.contributor.author","Luders, Eileen"],["dc.contributor.author","Specht, Karsten"],["dc.contributor.author","Ruhlmann, Juergen"],["dc.contributor.author","Schneider-Gold, Christiane"],["dc.contributor.author","Schroeder, Rolf"],["dc.contributor.author","Thompson, Paul M."],["dc.contributor.author","Toga, Arthur W."],["dc.contributor.author","Klockgether, Thomas"],["dc.contributor.author","Kornblum, Cornelia"],["dc.date.accessioned","2018-11-07T11:08:40Z"],["dc.date.available","2018-11-07T11:08:40Z"],["dc.date.issued","2008"],["dc.description.abstract","Myotonic dystrophy type 2 (DM2) is an autosomal dominantly inherited multisystemic disorder and a common cause of muscular dystrophy in adults. Although neuromuscular symptoms predominate, there is clinical and imaging evidence of cerebral involvement. We used voxel-based morphometry (VBM) based on T1-weighted magnetic resonance images to investigate brain morphology in 13 DM2 patients in comparison to 13 sex- and age-matched controls. Further, we employed novel computational surface-based methods that specifically assess callosal thickness. We found grey and white matter loss along cerebral midline structures in our patient group. Grey matter reductions were present in brain-stem and adjacent hypothalamic and thalamic regions, while white matter was mainly reduced in corpus callosum. The reduced callosal size was highly significant and independently confirmed by different methods. Our data provide first evidence for grey and white matter loss along brain midline structures in DM2 patients. The reduced size of the corpus callosum further extends the spectrum of white matter changes in DM2 and may represent the morphological substrate of neuropsychological abnormalities previously described in this disorder."],["dc.identifier.doi","10.1007/s00415-008-0997-1"],["dc.identifier.isi","000263221100007"],["dc.identifier.pmid","19224318"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52838"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0340-5354"],["dc.title","Grey and white matter loss along cerebral midline structures in myotonic dystrophy type 2"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","500"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","502"],["dc.bibliographiccitation.volume","60"],["dc.contributor.author","Schneider-Gold, C."],["dc.contributor.author","Beck, M."],["dc.contributor.author","Wessig, C."],["dc.contributor.author","George, A."],["dc.contributor.author","Kele, H."],["dc.contributor.author","Reiners, Kerstin"],["dc.contributor.author","Toyka, Klaus V."],["dc.date.accessioned","2018-11-07T10:40:56Z"],["dc.date.available","2018-11-07T10:40:56Z"],["dc.date.issued","2003"],["dc.description.abstract","The efficacy and safety of creatine monohydrate (Cr) in patients with myotonic dystrophy type 2/proximal myotonic myopathy were studied in a small placebo-controlled double-blind trial. Twenty patients received either Cr or placebo for 3 months. After 3 months, there were no significant differences of muscle strength as assessed by hand-held dynamometry, testing of maximum grip strength, Medical Research Council scoring, and the Neuromuscular Symptom Score between the two groups. Some measures indicated trends toward mild improvement with Cr. Myalgia improved in two patients."],["dc.identifier.isi","000181014500027"],["dc.identifier.pmid","12578937"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46421"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0028-3878"],["dc.title","Creatine monohydrate in DM2/PROMM - A double-blind placebo-controlled clinical study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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","579"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","580"],["dc.bibliographiccitation.volume","66"],["dc.contributor.author","Rudnik-Schoneborn, S."],["dc.contributor.author","Schneider-Gold, C."],["dc.contributor.author","Raabe, U."],["dc.contributor.author","Kress, W."],["dc.contributor.author","Zerres, K."],["dc.contributor.author","Schoser, BGH"],["dc.date.accessioned","2018-11-07T10:17:26Z"],["dc.date.available","2018-11-07T10:17:26Z"],["dc.date.issued","2006"],["dc.description.abstract","The authors reviewed the obstetric histories of 42 women of 37 families with myotonic dystrophy type 2 (DM2). Nine women (21%) had the first symptoms during pregnancy and worsening in subsequent pregnancies. Of 96 pregnancies, 13% ended as early and 4% as late miscarriages. Preterm labor occurred in 50% of pregnancies resulting in 27% preterm deliveries in women with overt DM2 in pregnancy. There was no evidence of a congenital DM2."],["dc.identifier.doi","10.1212/01.wnl.0000198227.91131.1e"],["dc.identifier.isi","000235645200029"],["dc.identifier.pmid","16505316"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41224"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0028-3878"],["dc.title","Outcome and effect of pregnancy in myotonic dystrophy type 2"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","145"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Movement Disorders"],["dc.bibliographiccitation.lastpage","147"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Hiller, Anja"],["dc.contributor.author","Hagenah, Johann M."],["dc.contributor.author","Djarmati, Ana"],["dc.contributor.author","Hedrich, Katja"],["dc.contributor.author","Reetz, Kathrin"],["dc.contributor.author","Schneider-Gold, Christiane"],["dc.contributor.author","Kress, Wolfgang"],["dc.contributor.author","Muenchau, Alexander"],["dc.contributor.author","Klein, Christine"],["dc.date.accessioned","2018-11-07T11:07:05Z"],["dc.date.available","2018-11-07T11:07:05Z"],["dc.date.issued","2007"],["dc.description.abstract","The phenotypic spectrum of PINK1-associated Parkinsonism was studied in a family with homozygous (n = 4) or heterozygous (n = 3) PINK1 mutations. All homozygous mutation carriers were definitely affected; the heterozygous carriers were asymptomatic but displayed unequivocal signs of probable or possible Parkinsonism. This finding suggests a role not only of homozygous but also of heterozygous PINK1 mutations in the development of parkinsonian signs and underlines the necessity to carefully investigate family members of affected mutation carriers. (C) 2006 Movement Disorder Society."],["dc.identifier.doi","10.1002/mds.21059"],["dc.identifier.isi","000244073400026"],["dc.identifier.pmid","17013904"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52473"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0885-3185"],["dc.title","Phenotypic spectrum of PINK1-associated parkinsonism in 15 mutation carriers from 1 family"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","235604"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","Journal of Physics Condensed Matter"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Peyker, L."],["dc.contributor.author","Gold, C."],["dc.contributor.author","Scheidt, E-W"],["dc.contributor.author","Scherer, Wolfgang"],["dc.contributor.author","Donath, J. G."],["dc.contributor.author","Gegenwart, Philipp"],["dc.contributor.author","Mayr, F."],["dc.contributor.author","Unruh, T."],["dc.contributor.author","Eyert, V."],["dc.contributor.author","Bauer, E."],["dc.contributor.author","Michor, H."],["dc.date.accessioned","2018-11-07T08:28:46Z"],["dc.date.available","2018-11-07T08:28:46Z"],["dc.date.issued","2009"],["dc.description.abstract","Crystal structure, specific heat, thermal expansion, magnetic susceptibility and electrical resistivity studies of the heavy fermion system CeNi9-xCuxGe4 (0 <= x <= 1) reveal a continuous tuning of the ground state by Ni/Cu substitution from an effectively fourfold-degenerate non-magnetic Kondo ground state of CeNi9Ge4 (with pronounced non-Fermi-liquid features) towards a magnetically ordered, effectively twofold-degenerate ground state in CeNi8CuGe4 with T-N = 175 +/- 5 mK. Quantum critical behavior, C/T proportional to chi proportional to - ln T, is observed for x congruent to 0.4. Hitherto, CeNi9-xCuxGe4 represents the first system where a substitution-driven quantum phase transition is connected not only with changes of the relative strength of the Kondo effect and RKKY interaction, but also with a reduction of the effective crystal field ground state degeneracy."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft (DFG) [SCHE487/7-1]; European Union"],["dc.identifier.doi","10.1088/0953-8984/21/23/235604"],["dc.identifier.isi","000266581200017"],["dc.identifier.pmid","21825591"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16499"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Iop Publishing Ltd"],["dc.relation.issn","0953-8984"],["dc.title","Evolution of quantum criticality in CeNi9-xCuxGe4"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","833"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","ARCHIVES OF NEUROLOGY"],["dc.bibliographiccitation.lastpage","838"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Hedrich, K."],["dc.contributor.author","Hagenah, Johann M."],["dc.contributor.author","Djarmati, A."],["dc.contributor.author","Hiller, A."],["dc.contributor.author","Lohnau, T."],["dc.contributor.author","Lasek, K."],["dc.contributor.author","Grunewald, A."],["dc.contributor.author","Hilker, Ruediger"],["dc.contributor.author","Steinlechner, S."],["dc.contributor.author","Boston, H."],["dc.contributor.author","Kock, N."],["dc.contributor.author","Schneider-Gold, C."],["dc.contributor.author","Kress, W."],["dc.contributor.author","Siebner, Hartwig Roman"],["dc.contributor.author","Binkofski, F."],["dc.contributor.author","Lencer, R."],["dc.contributor.author","Munchau, A."],["dc.contributor.author","Klein, C."],["dc.date.accessioned","2018-11-07T09:42:59Z"],["dc.date.available","2018-11-07T09:42:59Z"],["dc.date.issued","2006"],["dc.description.abstract","Background: Although homozygous mutations in the PTEN-induced putative kinase 1 (PINK1) gene have been unequivocally associated with early-onset Parkinson disease (PD), the role of single heterozygous PINK1 mutations is less clear. Objective: To investigate the role of homozygous and heterozygous PINK1 mutations in a large German pedigree (family W). Design: Mutation analysis of PINK1 and results of standardized neurological and motor examination by 3 independent movement disorder specialists, including blinded video rating. Settings: University of Lubeck. Participants: Twenty family members. Main Outcome Measures: The PINK1 genotype and PD status of all family members. Results: The index patient of family W carried a homozygous nonsense mutation (c.1366C > T; p.Q456X) and presented with a phenotype closely resembling idiopathic PD but with an onset at 39 years of age. The family included a total of 4 affected homozygous members (age, 60-71 years; age at onset, 39-61 years), 6 members with slight or mild signs of PD (affected) and a heterozygous mutation (age, 31-49 years), and 5 unaffected heterozygous mutation carriers (age, 34-44 years). Although none of the heterozygous affected family members was aware of their signs (asymptomatic), the clinical findings were unequivocal and predominantly or exclusively present on their dominant right-hand side, eg, unilaterally reduced or absent arm swing and unilateral rigidity. The heterozygous members were all considerably younger than the affected homozygous mutation carriers. Conclusions: Heterozygous PINK1 mutations may predispose to PD, as was previously suggested by the presence of dopamine hypometabolism in asymptomatic mutation carriers. Long-term follow-up of our large family W provides an excellent opportunity to further evaluate the role of single heterozygous PINK1 mutations later in life, which will have major implications on genetic counseling."],["dc.identifier.doi","10.1001/archneur.63.6.833"],["dc.identifier.isi","000238197600006"],["dc.identifier.pmid","16769864"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34080"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Medical Assoc"],["dc.relation.issn","0003-9942"],["dc.title","Clinical spectrum of homozygous and heterozygous PINK1 mutations in a large German family with Parkinson disease Role of a single hit?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2266"],["dc.bibliographiccitation.issue","11-12"],["dc.bibliographiccitation.journal","Experimental Cell Research"],["dc.bibliographiccitation.lastpage","2278"],["dc.bibliographiccitation.volume","314"],["dc.contributor.author","Salisbury, Elizabeth"],["dc.contributor.author","Sakai, Keiko"],["dc.contributor.author","Schoser, Benedikt"],["dc.contributor.author","Huichalaf, Claudia"],["dc.contributor.author","Schneider-Gold, Christiane"],["dc.contributor.author","Nguyen, Heather"],["dc.contributor.author","Wang, G."],["dc.contributor.author","Albrecht, Jeffrey H."],["dc.contributor.author","Timchenko, Lubou T."],["dc.date.accessioned","2018-11-07T11:13:25Z"],["dc.date.available","2018-11-07T11:13:25Z"],["dc.date.issued","2008"],["dc.description.abstract","Differentiation of myocytes is impaired in patients with myotonic dystrophy type 1, DM1, CUG repeat binding protein, CUGBP1, is a key regulator of translation of proteins that are involved in muscle development and differentiation. In this paper, we present evidence that RNA-binding activity of CUGBP1 and its interactions with initiation translation complex eIF2 are differentially regulated during myogenesis by specific phosphorylation and that this regulation is altered in DM1. In normal myoblasts, Akt kinase phosphorylates CUGBP1 at Ser28 and increases interactions of CUGBP1 with cyclin D1 mRNA. During differentiation, CUGBP1 is phosphorylated by cyclinD3-cdk4/6 at Ser302, which increases CUGBP1 binding with p21 and C/EB beta mRNAs. While cyclin D3 and cdk4 are elevated in normal myotubes; DM1 differentiating cells do not increase these proteins. In normal myotubes, CUGBP1 interacts with cyclin D3/cdk4/6 and eIF2; however, interactions of CUGBP1 with eIF2 are reduced in DM1 differentiating cells and correlate with impaired muscle differentiation in DM1. Ectopic expression of cyclin D3 in DM1 cells increases the CUGBP1-eIF2 complex, corrects expression of differentiation markers, myogenin and desmin, and enhances fusion of DM1 myoblasts. Thus, normalization of cyclin D3 might be a therapeutic approach to correct differentiation of skeletal muscle in DM1 patients. (C) 2008 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.yexcr.2008.04.018"],["dc.identifier.isi","000257199500011"],["dc.identifier.pmid","18570922"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53887"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Inc"],["dc.relation.issn","0014-4827"],["dc.title","Ectopic expression of cyclin D3 corrects differentiation of DM1 myoblasts through activation of RNA CUG-binding protein, CUGBP1"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]