Trenkwalder, Claudia

[["dc.bibliographiccitation.firstpage","739"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","746"],["dc.bibliographiccitation.volume","119"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Trautmann, Ellen"],["dc.contributor.author","Otte, Birgit"],["dc.contributor.author","Ng, Juliana"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Lange, Peter"],["dc.contributor.author","Sixel-Doering, Friederike"],["dc.contributor.author","Hakimi, Mansoureh"],["dc.contributor.author","VonSattel, Jean-Paul"],["dc.contributor.author","Nussbaum, Robert"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Schlossmacher, Michael G."],["dc.date.accessioned","2018-11-07T09:08:50Z"],["dc.date.available","2018-11-07T09:08:50Z"],["dc.date.issued","2012"],["dc.description.abstract","The source of Parkinson disease-linked alpha-synuclein (aSyn) in human cerebrospinal fluid (CSF) remains unknown. We decided to measure the concentration of aSyn and its gradient in human CSF specimens and compared it with serum to explore its origin. We correlated aSyn concentrations in CSF versus serum (Q(aSyn)) to the albumin quotient (Q(albumin)) to evaluate its relation to blood-CSF barrier function. We also compared aSyn with several other CSF constituents of either central or peripheral sources (or both) including albumin, neuron-specific enolase, beta-trace protein and total protein content. Finally, we examined whether aSyn is present within the structures of the choroid plexus (CP). We observed that Q(aSyn) did not rise or fall with Q(albumin) values, a relative measure of blood-CSF barrier integrity. In our CSF gradient analyses, aSyn levels decreased slightly from rostral to caudal fractions, in parallel to the recorded changes for neuron-specific enolase; the opposite trend was recorded for total protein, albumin and beta-trace protein. The latter showed higher concentrations in caudal CSF fractions due to the diffusion-mediated transfer of proteins from blood and leptomeninges into CSF in the lower regions of the spine. In postmortem sections of human brain, we detected highly variable aSyn reactivity within the epithelial cell layer of CP in patients diagnosed with a range of neurological diseases; however, in sections of mice that express only human SNCA alleles (and in those without any Snca gene expression), we detected no aSyn signal in the epithelial cells of the CP. We conclude from these complementary results that despite its higher levels in peripheral blood products, neurons of the brain and spinal cord represent the principal source of aSyn in human CSF."],["dc.identifier.doi","10.1007/s00702-012-0784-0"],["dc.identifier.isi","000305525800002"],["dc.identifier.pmid","22426833"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8104"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26122"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","0300-9564"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","alpha-Synuclein in human cerebrospinal fluid is principally derived from neurons of the central nervous system"],["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","e0257372"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Bartl, Michael"],["dc.contributor.author","Dakna, Mohammed"],["dc.contributor.author","Galasko, Douglas"],["dc.contributor.author","Hutten, Samantha J."],["dc.contributor.author","Foroud, Tatiana"],["dc.contributor.author","Quan, Marian"],["dc.contributor.author","Marek, Kenneth"],["dc.contributor.author","Siderowf, Andrew"],["dc.contributor.author","Franz, Jonas"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.authorgroup","on behalf of the Parkinson’s Progression Markers Initiative"],["dc.date.accessioned","2021-12-01T09:23:14Z"],["dc.date.available","2021-12-01T09:23:14Z"],["dc.date.issued","2021"],["dc.description.abstract","Aim Several pathophysiological processes are involved in Parkinson’s disease (PD) and could inform in vivo biomarkers. We assessed an established biomarker panel, validated in Alzheimer’s Disease, in a PD cohort. Methods Longitudinal cerebrospinal fluid (CSF) samples from PPMI (252 PD, 115 healthy controls, HC) were analyzed at six timepoints (baseline, 6, 12, 24, 36, and 48 months follow-up) using Elecsys® electrochemiluminescence immunoassays to quantify neurofilament light chain (NfL), soluble TREM2 receptor (sTREM2), chitinase-3-like protein 1 (YKL40), glial fibrillary acidic protein (GFAP), interleukin-6 (IL-6), S100, and total α-synuclein (αSyn). Results αSyn was significantly lower in PD (mean 103 pg/ml vs. HC: 127 pg/ml, p<0.01; area under the curve [AUC]: 0.64), while all other biomarkers were not significantly different (AUC NfL: 0.49, sTREM2: 0.54, YKL40: 0.57, GFAP: 0.55, IL-6: 0.53, S100: 0.54, p>0.05) and none showed a significant difference longitudinally. We found significantly higher levels of all these markers between PD patients who developed cognitive decline during follow-up, except for αSyn and IL-6. Conclusion Except for αSyn, the additional biomarkers did not differentiate PD and HC, and none showed longitudinal differences, but most markers predict cognitive decline in PD during follow-up."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.1371/journal.pone.0257372"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94597"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","1932-6203"],["dc.relation.orgunit","Klinik für Neurologie"],["dc.rights","CC BY 4.0"],["dc.title","Biomarkers of neurodegeneration and glial activation validated in Alzheimer’s disease assessed in longitudinal cerebrospinal fluid samples of Parkinson’s disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","42"],["dc.bibliographiccitation.journal","BMC Neurology"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Kassubek, Jan"],["dc.contributor.author","Chaudhuri, Kallol Ray"],["dc.contributor.author","Zesiewicz, Theresa"],["dc.contributor.author","Surmann, Erwin"],["dc.contributor.author","Boroojerdi, Babak"],["dc.contributor.author","Moran, Kimberly"],["dc.contributor.author","Ghys, Liesbet"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.date.accessioned","2018-11-07T09:42:40Z"],["dc.date.available","2018-11-07T09:42:40Z"],["dc.date.issued","2014"],["dc.description.abstract","Background: Pain is a troublesome non-motor symptom of Parkinson's disease (PD). The RECOVER (Randomized Evaluation of the 24-hour Coverage: Efficacy of Rotigotine; Clintrials.gov: NCT00474058) study demonstrated significant improvements in early-morning motor function (UPDRS III) and sleep disturbances (PDSS-2) with rotigotine transdermal system. Improvements were also reported on a Likert pain scale (measuring any type of pain). This post hoc analysis of RECOVER further evaluates the effect of rotigotine on pain, and whether improvements in pain may be attributable to benefits in motor function or sleep disturbance. Methods: PD patients with unsatisfactory early-morning motor impairment were randomized to optimal-dose (up to 16 mg/24 h) rotigotine or placebo, maintained for 4 weeks. Pain was assessed in the early-morning using an 11-point Likert pain scale (rated average severity of pain (of any type) over the preceding 12 hours from 0 [no pain] to 10 [worst pain ever experienced]). Post hoc analyses for patients reporting 'any' pain (pain score = 1) at baseline, and subgroups reporting 'mild' (score 1-3), and 'moderate-to-severe' pain (score = 4) were performed. Likert pain scale change from baseline in rotigotine-treated patients was further analyzed based on a UPDRS III/PDSS-2 responder analysis (a responder defined as showing a = 30% reduction in early morning UPDRS III total score or PDSS-2 total score). As post hoc analyses, all p values presented are exploratory. Results: Of 267 patients with Likert pain data (178 rotigotine, 89 placebo), 187 (70%) reported 'any' pain; of these 87 (33%) reported 'mild', and 100 (37%) 'moderate-to-severe' pain. Change from baseline pain scores decreased with rotigotine compared with placebo in patients with 'any' pain (-0.88 [95% CI: -1.56, -0.19], p = 0.013), and in the subgroup with 'moderate-to-severe' pain (-1.38 [-2.44, -0.31], p = 0.012). UPDRS III or PDSS-2 responders showed greater improvement in pain than non-responders. Conclusions: The results from this post hoc analysis of the RECOVER study suggest that pain was improved in patients with PD treated with rotigotine; this may be partly attributable to benefits in motor function and sleep disturbances. Prospective studies are warranted to investigate this potential benefit and the clinical relevance of these findings."],["dc.description.sponsorship","UCB Pharma, Brussels, Belgium"],["dc.identifier.doi","10.1186/1471-2377-14-42"],["dc.identifier.fs","611732"],["dc.identifier.isi","000332639900002"],["dc.identifier.pmid","24602411"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11924"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34008"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2377"],["dc.rights.access","openAccess"],["dc.subject.mesh","Administration, Cutaneous"],["dc.subject.mesh","Adult"],["dc.subject.mesh","Aged"],["dc.subject.mesh","Aged, 80 and over"],["dc.subject.mesh","Dopamine Agonists"],["dc.subject.mesh","Female"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Male"],["dc.subject.mesh","Middle Aged"],["dc.subject.mesh","Pain"],["dc.subject.mesh","Pain Measurement"],["dc.subject.mesh","Parkinson Disease"],["dc.subject.mesh","Prospective Studies"],["dc.subject.mesh","Tetrahydronaphthalenes"],["dc.subject.mesh","Thiophenes"],["dc.title","Rotigotine transdermal system and evaluation of pain in patients with Parkinson's disease: a post hoc analysis of the RECOVER study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","79"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Basal Ganglia"],["dc.bibliographiccitation.lastpage","85"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Trenkwalder, C."],["dc.contributor.author","Kies, B."],["dc.contributor.author","Dioszeghy, P."],["dc.contributor.author","Hill, D."],["dc.contributor.author","Surmann, E."],["dc.contributor.author","Boroojerdi, B."],["dc.contributor.author","Whitesides, J."],["dc.contributor.author","Chaudhuri, K.R."],["dc.date.accessioned","2019-07-09T11:42:28Z"],["dc.date.available","2019-07-09T11:42:28Z"],["dc.date.issued","2012"],["dc.description.abstract","In RECOVER, a multinational, double-blind, placebo-controlled trial, continuous 24-h transdermal delivery of rotigotine resulted in significant improvements in early-morning motor function and nocturnal sleep disturbances in subjects with idiopathic Parkinson’s disease (PD). On completion of RECOVER, subjects were eligible to enter a 1-year, open-label extension in which they received rotigotine (2–16 mg/24 h) for a 10-month maintenance period. Safety and tolerability were assessed by monitoring adverse events, changes in vital signs, physical and neurological findings, ECGs, and clinical laboratory values. The primary efficacy measure was the Unified Parkinson’s Disease Rating Scale (UPDRS) Part III (Motor Examination) with the modified Parkinson’s Disease Sleep Scale (PDSS-2) as a co-primary measure. Of 84 subjects from RECOVER who enrolled, 79% completed 1 year of open-label treatment. Rotigotine was well tolerated; the most common adverse events (AEs; open-label phase) were application site reactions (ASRs; 24%); somnolence and hallucinations (13% each); nausea and fall (12% each); and dizziness and dyskinesia (11% each). Most were mild or moderate in intensity and had resolved at the end of the trial. Twelve subjects (14%) discontinued due to AEs, most commonly ASRs (5 subjects) and peripheral edema (2 subjects). At end of maintenance, the mean UPDRS Part III score was improved by 5.8 (±9.4) points relative to open-label baseline and 10.9 (±10.7) points relative to double-blind baseline and the mean PDSS-2 score by 5.8 (±7.8) points relative to double-blind baseline. Hence, the beneficial effects of rotigotine transdermal system on motor function and sleep disturbances were sustained for up to 1 year."],["dc.identifier.doi","10.1016/j.baga.2012.05.009"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13526"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58678"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2210-5336"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","Rotigotine transdermal system for the management of motor function and sleep disturbances in Parkinson’s disease: Results from a 1-year, open-label extension of the RECOVER study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","373"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","NEUROREHABILITATION AND NEURAL REPAIR"],["dc.bibliographiccitation.lastpage","381"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Rothkegel, Holger"],["dc.contributor.author","Sommer, Martin"],["dc.contributor.author","Rammsayer, Thomas H."],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Paulus, Walter J."],["dc.date.accessioned","2018-11-07T08:30:31Z"],["dc.date.available","2018-11-07T08:30:31Z"],["dc.date.issued","2009"],["dc.description.abstract","Background. Focal single-session repetitive transcranial magnetic stimulation (rTMS) of the primary motor cortex has been claimed to be capable of improving motor function in Parkinson's disease. Objective. The authors sought to determine which type of rTMS protocol holds the highest potential for future therapeutic application. Methods. Twenty-two patients with Parkinson's disease received 5 different rTMS protocols on 5 consecutive days in a pseudorandomized and counterbalanced order either in the defined OFF condition or with their usual medication. The protocols tested in the present study included 2 conventional rTMS protocols (0.5 and 10 Hz) as well as the recently introduced theta burst stimulation (cTBS, iTBS) and a sham condition. Cortical excitability, motor performance (pointing movement, pronation-supination, Purdue Pegboard Test, walking), and mood were assessed before and after each session. Results. The authors observed motor training from days 1 to 4, particularly in the group on dopaminergic medication. None of the rTMS paradigms excelled placebo stimulation. The only exception was the Purdue Pegboard Test, in which all active stimulation paradigms yielded slightly stronger effects than sham stimulation. Conclusions. Within a single session, no clinically relevant difference in the rTMS protocols could be detected. Training effects outweigh and may have masked rTMS effects, particularly in the group on dopaminergic mediation."],["dc.identifier.doi","10.1177/1545968308322842"],["dc.identifier.isi","000264876100009"],["dc.identifier.pmid","18978029"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13103"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16906"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Inc"],["dc.relation.issn","1545-9683"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Training Effects Outweigh Effects of Single-Session Conventional rTMS and Theta Burst Stimulation in PD Patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","822"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","ANNALS OF CLINICAL AND TRANSLATIONAL NEUROLOGY"],["dc.bibliographiccitation.lastpage","832"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Doss, Sarah"],["dc.contributor.author","Wandinger, Klaus-Peter"],["dc.contributor.author","Hyman, Bradley T."],["dc.contributor.author","Panzer, Jessica A."],["dc.contributor.author","Synofzik, Matthis"],["dc.contributor.author","Dickerson, Bradford"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Scherzer, Clemens R."],["dc.contributor.author","Ivinson, Adrian J."],["dc.contributor.author","Finke, Carsten"],["dc.contributor.author","Schoels, Ludger"],["dc.contributor.author","vom Hagen, Jennifer Muller"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Jahn, Holger"],["dc.contributor.author","Hoeltje, Markus"],["dc.contributor.author","Biswal, Bharat B."],["dc.contributor.author","Harms, Lutz"],["dc.contributor.author","Ruprecht, Klemens"],["dc.contributor.author","Buchert, Ralph"],["dc.contributor.author","Hoeglinger, Guenther U."],["dc.contributor.author","Oertel, Wolfgang Hermann"],["dc.contributor.author","Unger, Marcus Michael"],["dc.contributor.author","Koertvelyessy, Peter"],["dc.contributor.author","Bittner, Daniel"],["dc.contributor.author","Priller, Josef"],["dc.contributor.author","Spruth, Eike J."],["dc.contributor.author","Paul, Friedemann"],["dc.contributor.author","Meisel, Andreas"],["dc.contributor.author","Lynch, David R."],["dc.contributor.author","Dirnagl, Ulrich"],["dc.contributor.author","Endres, Matthias"],["dc.contributor.author","Teegen, Bianca"],["dc.contributor.author","Probst, Christian"],["dc.contributor.author","Komorowski, Lars"],["dc.contributor.author","Stoecker, Winfried"],["dc.contributor.author","Dalmau, Josep"],["dc.contributor.author","Pruess, Harald"],["dc.date.accessioned","2018-11-07T09:34:55Z"],["dc.date.available","2018-11-07T09:34:55Z"],["dc.date.issued","2014"],["dc.description.abstract","Objective: To retrospectively determine the frequency of N-Methyl-D-Aspartate (NMDA) receptor (NMDAR) autoantibodies in patients with different forms of dementia. Methods: Clinical characterization of 660 patients with dementia, neurodegenerative disease without dementia, other neurological disorders and age-matched healthy controls combined with retrospective analysis of serum or cerebrospinal fluid (CSF) for the presence of NMDAR antibodies. Antibody binding to receptor mutants and the effect of immunotherapy were determined in a subgroup of patients. Results: Serum NMDAR antibodies of IgM, IgA, or IgG subtypes were detected in 16.1% of 286 dementia patients (9.5% IgM, 4.9% IgA, and 1.7% IgG) and in 2.8% of 217 cognitively healthy controls (1.9% IgM and 0.9% IgA). Antibodies were rarely found in CSF. The highest prevalence of serum antibodies was detected in patients with \"unclassified dementia\" followed by progressive supranuclear palsy, corticobasal syndrome, Parkinson's disease-related dementia, and primary progressive aphasia. Among the unclassified dementia group, 60% of 20 patients had NMDAR antibodies, accompanied by higher frequency of CSF abnormalities, and subacute or fluctuating disease progression. Immunotherapy in selected prospective cases resulted in clinical stabilization, loss of antibodies, and improvement of functional imaging parameters. Epitope mapping showed varied determinants in patients with NMDAR IgA-associated cognitive decline. Interpretation: Serum IgA/IgM NMDAR antibodies occur in a significant number of patients with dementia. Whether these antibodies result from or contribute to the neurodegenerative disorder remains unknown, but our findings reveal a subgroup of patients with high antibody levels who can potentially benefit from immunotherapy."],["dc.description.sponsorship","NINDS NIH HHS [U01 NS082157, K12 NS049453, R01 NS077851, U01 NS082080]"],["dc.identifier.doi","10.1002/acn3.120"],["dc.identifier.isi","000209815600008"],["dc.identifier.pmid","25493273"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11774"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32281"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","2328-9503"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","High prevalence of NMDA receptor IgA/IgM antibodies in different dementia types"],["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","230"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","237"],["dc.bibliographiccitation.volume","257"],["dc.contributor.author","Hoegl, Birgit"],["dc.contributor.author","Garcia-Borreguero, Diego"],["dc.contributor.author","Kohnen, Ralf"],["dc.contributor.author","Ferini-Strambi, Luigi"],["dc.contributor.author","Hadjigeorgiou, Georgios M."],["dc.contributor.author","Hornyak, Magdolna"],["dc.contributor.author","de Weerd, A. L."],["dc.contributor.author","Happe, Svenja"],["dc.contributor.author","Stiasny-Kolster, Karin"],["dc.contributor.author","Gschliesser, Viola"],["dc.contributor.author","Egatz, Renata"],["dc.contributor.author","Frauscher, Birgit"],["dc.contributor.author","Benes, Heike"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Hening, Wayne A."],["dc.contributor.author","Allen, Richard P."],["dc.date.accessioned","2018-11-07T08:46:22Z"],["dc.date.available","2018-11-07T08:46:22Z"],["dc.date.issued","2010"],["dc.description.abstract","The European Restless Legs Syndrome (RLS) Study Group performed the first multi-center, long-term study systematically evaluating RLS augmentation under levodopa treatment. This prospective, open-label 6-month study was conducted in six European countries and included 65 patients (85% treatment naive) with idiopathic RLS. Levodopa was flexibly up-titrated to a maximum dose of 600 mg/day. Presence of augmentation was diagnosed independently by two international experts using established criteria. In addition to the augmentation severity rating scale (ASRS), changes in RLS severity (International RLS severity rating scale (IRLS), clinical global impression (CGI)) were analyzed. Sixty patients provided evaluable data, 35 completed the trial and 25 dropped out. Augmentation occurred in 60% (36/60) of patients, causing 11.7% (7/60) to drop out. Median time to occurrence of augmentation was 71 days. The mean maximum dose of levodopa was 311 mg/day (SD: 105). Patients with augmentation compared to those without were significantly more likely to be on higher doses of levodopa (a parts per thousand yen300 mg, 83 vs. 54%, P = 0.03) and to show less improvement of symptom severity (IRLS, P = 0.039). Augmentation was common with levodopa, but could be tolerated by most patients during this 6-month trial. Patients should be followed over longer periods to determine if dropout rates increase with time."],["dc.description.sponsorship","Pharmacia (now Pfizer) USA"],["dc.identifier.doi","10.1007/s00415-009-5299-8"],["dc.identifier.isi","000274251700011"],["dc.identifier.pmid","19756826"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6747"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20677"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0340-5354"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Progressive development of augmentation during long-term treatment with levodopa in restless legs syndrome: results of a prospective multi-center study"],["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.artnumber","11"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Translational Neurodegeneration"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Hopfner, Franziska"],["dc.contributor.author","Müller, Stefanie H."],["dc.contributor.author","Steppat, Dagmar"],["dc.contributor.author","Miller, Joanna"],["dc.contributor.author","Schmidt, Nele"],["dc.contributor.author","Wandinger, Klaus-Peter"],["dc.contributor.author","Leypoldt, Frank"],["dc.contributor.author","Berg, Daniela"],["dc.contributor.author","Franke, Andre"],["dc.contributor.author","Lieb, Wolfgang"],["dc.contributor.author","Tittmann, Lukas"],["dc.contributor.author","Balzer-Geldsetzer, Monika"],["dc.contributor.author","Baudrexel, Simon"],["dc.contributor.author","Dodel, Richard"],["dc.contributor.author","Hilker-Roggendorf, Ruediger"],["dc.contributor.author","Kalbe, Elke"],["dc.contributor.author","Kassubek, Jan"],["dc.contributor.author","Klockgether, Thomas"],["dc.contributor.author","Liepelt-Scarfone, Inga"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Neuser, Petra"],["dc.contributor.author","Reetz, Kathrin"],["dc.contributor.author","Riedel, Oliver"],["dc.contributor.author","Schulte, Claudia"],["dc.contributor.author","Schulz, Jörg B."],["dc.contributor.author","Spottke, Annika"],["dc.contributor.author","Storch, Alexander"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Wittchen, Hans-Ulrich"],["dc.contributor.author","Witt, Karsten"],["dc.contributor.author","Wüllner, Ullrich"],["dc.contributor.author","Deuschl, Günther"],["dc.contributor.author","Kuhlenbäumer, Gregor"],["dc.date.accessioned","2019-07-09T11:51:41Z"],["dc.date.available","2019-07-09T11:51:41Z"],["dc.date.issued","2019"],["dc.description.abstract","Background: IgG-class autoantibodies to N-Methyl-D-Aspartate (NMDA)-type glutamate receptors define a novel entity of autoimmune encephalitis. Studies examining the prevalence of NMDA IgA/IgM antibodies in patients with Parkinson disease with/without dementia produced conflicting results. We measured NMDA antibodies in a large, well phenotyped sample of Parkinson patients without and with cognitive impairment (n = 296) and controls (n = 295) free of neuropsychiatric disease. Detailed phenotyping and large numbers allowed statistically meaningful correlation of antibody status with diagnostic subgroups as well as quantitative indicators of disease severity and cognitive impairment. Methods: NMDA antibodies were analysed in the serum of patients and controls using well established validated assays. We used anti-NMDA antibody positivity as the main independent variable and correlated it with disease status and phenotypic characteristics. Results: The frequency of NMDA IgA/IgM antibodies was lower in Parkinson patients (13%) than in controls (22%) and higher than in previous studies in both groups. NMDA IgA/IgM antibodies were neither significantly associated with diagnostic subclasses of Parkinson disease according to cognitive impairment, nor with quantitative indicators of disease severity and cognitive impairment. A positive NMDA antibody status was positively correlated with age in controls but not in Parkinson patients. Conclusion: It is unlikely albeit not impossible that NMDA antibodies play a significant role in the pathogenesis or progression of Parkinson disease e.g. to Parkinson disease with dementia, while NMDA IgG antibodies define a separate disease of its own."],["dc.identifier.doi","10.1186/s40035-019-0153-0"],["dc.identifier.pmid","30984390"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16171"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59990"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","No association between Parkinson disease and autoantibodies against NMDA-type glutamate receptors"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e2622"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Schindehuette, Jan"],["dc.contributor.author","Kuhlmann, Tanja"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Novota, Peter"],["dc.contributor.author","Baier, Paul Christian"],["dc.contributor.author","Schillert, Arne"],["dc.contributor.author","Bickeboeller, Heike"],["dc.contributor.author","Herrmann, Thomas R."],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Mansouri, Ahmed"],["dc.date.accessioned","2018-11-07T11:13:02Z"],["dc.date.available","2018-11-07T11:13:02Z"],["dc.date.issued","2008"],["dc.description.abstract","Embryonic stem (ES) cells have the potential to differentiate into all cell types and are considered as a valuable source of cells for transplantation therapies. A critical issue, however, is the risk of teratoma formation after transplantation. The effect of the immune response on the tumorigenicity of transplanted cells is poorly understood. We have systematically compared the tumorigenicity of mouse ES cells and in vitro differentiated neuronal cells in various recipients. Subcutaneous injection of 1 x 10(6) ES or differentiated cells into syngeneic or allogeneic immunodeficient mice resulted in teratomas in about 95% of the recipients. Both cell types did not give rise to tumors in immunocompetent allogeneic mice or xenogeneic rats. However, in 61% of cyclosporine A-treated rats teratomas developed after injection of differentiated cells. Undifferentiated ES cells did not give rise to tumors in these rats. ES cells turned out to be highly susceptible to killing by rat natural killer (NK) cells due to the expression of ligands of the activating NK receptor NKG2D on ES cells. These ligands were downregulated on differentiated cells. The activity of NK cells which is not suppressed by cyclosporine A might contribute to the prevention of teratomas after injection of ES cells but not after inoculation of differentiated cells. These findings clearly point to the importance of the immune response in this process. Interestingly, the differentiated cells must contain a tumorigenic cell population that is not present among ES cells and which might be resistant to NK cell-mediated killing."],["dc.identifier.doi","10.1371/journal.pone.0002622"],["dc.identifier.isi","000264065800024"],["dc.identifier.pmid","18612432"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8264"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53801"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","The Tumorigenicity of Mouse Embryonic Stem Cells and In Vitro Differentiated Neuronal Cells Is Controlled by the Recipients' Immune Response"],["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","140"],["dc.bibliographiccitation.issue","3-4"],["dc.bibliographiccitation.journal","European Neurology"],["dc.bibliographiccitation.lastpage","147"],["dc.bibliographiccitation.volume","71"],["dc.contributor.author","Swick, Todd J."],["dc.contributor.author","Friedman, Joseph H."],["dc.contributor.author","Chaudhuri, Kallol Ray"],["dc.contributor.author","Surmann, Erwin"],["dc.contributor.author","Boroojerdi, Babak"],["dc.contributor.author","Moran, Kimberly"],["dc.contributor.author","Ghys, Liesbet"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.date.accessioned","2018-11-07T09:46:20Z"],["dc.date.available","2018-11-07T09:46:20Z"],["dc.date.issued","2014"],["dc.description.abstract","Background: RECOVER (NCT00474058), a double-blind, placebo-controlled trial in patients with Parkinson's disease (PD) and unsatisfactory early-morning motor symptom control, demonstrated significant improvements with rotigotine in early-morning motor function (Unified Parkinson's Disease Rating Scale [UPDRS] III), and nocturnal sleep disturbances (modified Parkinson's Disease Sleep Scale [PDSS-2]), and improvements in nonmotor symptoms (NMS; Non-Motor Symptom Scale [NMSS]). Methods: Post hoc analyses investigated the correlation between motor symptom and NMS severity in PD by evaluating associations between UPDRS Ill and both NMSS and PDSS-2 scores. Categories were defined for UPDRS Ill, NMSS, and PDSS-2 total scores; analyses were conducted for the full analysis set (n = 267). Results: There was a trend toward increasing PDSS-2 and NMSS total and domain scores with increasing UPDRS Ill category at baseline and end of maintenance (EoM). Pearson correlation coefficients between UPDRS III and both NMSS and PDSS-2 total and domain scores were r=0.12-0.44 (r(2)=0.01-0.19) at baseline, r = 0.05-0.38 (r(2) = 0.00-0.14) at EoM, and r = -0.02-0.36 (r(2) = 0.00-0.13) for change from baseline to EoM. Conclusion: There was only a small correlation between severity of early-morning motor symptoms and overall burden of NMS and nocturnal sleep disturbances in RECOVER, suggesting that motor symptoms and NMS originate, at least partly, from distinct pathophysiological pathways. (C) 2014 S. Karger AG, Basel"],["dc.description.sponsorship","UCB Pharma, Smyrna, Ga., USA"],["dc.identifier.doi","10.1159/000355019"],["dc.identifier.isi","000333866400007"],["dc.identifier.pmid","24457253"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34848"],["dc.language.iso","en"],["dc.notes.intern","DeepGreen Import"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","S. Karger AG"],["dc.relation.eissn","1421-9913"],["dc.relation.issn","1421-9913"],["dc.relation.issn","0014-3022"],["dc.rights","https://www.karger.com/Services/SiteLicenses"],["dc.title","Associations between Severity of Motor Function and Nonmotor Symptoms in Parkinson's Disease: A Post Hoc Analysis of the RECOVER Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]