Trenkwalder, Claudia

[["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.firstpage","744"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","759"],["dc.bibliographiccitation.volume","142"],["dc.contributor.author","Postuma, Ronald B."],["dc.contributor.author","Iranzo, Alex"],["dc.contributor.author","Hu, Michele"],["dc.contributor.author","Högl, Birgit"],["dc.contributor.author","Boeve, Bradley F."],["dc.contributor.author","Manni, Raffaele"],["dc.contributor.author","Oertel, Wolfgang H."],["dc.contributor.author","Arnulf, Isabelle"],["dc.contributor.author","Ferini-Strambi, Luigi"],["dc.contributor.author","Puligheddu, Monica"],["dc.contributor.author","Antelmi, Elena"],["dc.contributor.author","Cochen De Cock, Valerie"],["dc.contributor.author","Arnaldi, Dario"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Videnovic, Aleksandar"],["dc.contributor.author","Sonka, Karel"],["dc.contributor.author","Jung, Ki-Young"],["dc.contributor.author","Kunz, Dieter"],["dc.contributor.author","Dauvilliers, Yves"],["dc.contributor.author","Provini, Federica"],["dc.contributor.author","Lewis, Simon J."],["dc.contributor.author","Buskova, Jitka"],["dc.contributor.author","Pavlova, Milena"],["dc.contributor.author","Heidbreder, Anna"],["dc.contributor.author","Montplaisir, Jacques Y."],["dc.contributor.author","Santamaria, Joan"],["dc.contributor.author","Barber, Thomas R."],["dc.contributor.author","Stefani, Ambra"],["dc.contributor.author","St.Louis, Erik K."],["dc.contributor.author","Terzaghi, Michele"],["dc.contributor.author","Janzen, Annette"],["dc.contributor.author","Leu-Semenescu, Smandra"],["dc.contributor.author","Plazzi, Guiseppe"],["dc.contributor.author","Nobili, Flavio"],["dc.contributor.author","Sixel-Doering, Friederike"],["dc.contributor.author","Dusek, Petr"],["dc.contributor.author","Bes, Frederik"],["dc.contributor.author","Cortelli, Pietro"],["dc.contributor.author","Ehgoetz Martens, Kaylena"],["dc.contributor.author","Gagnon, Jean-Francois"],["dc.contributor.author","Gaig, Carles"],["dc.contributor.author","Zucconi, Marco"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Gan-Or, Ziv"],["dc.contributor.author","Lo, Christine"],["dc.contributor.author","Rolinski, Michal"],["dc.contributor.author","Mahlknecht, Philip"],["dc.contributor.author","Holzknecht, Evi"],["dc.contributor.author","Boeve, Angel R."],["dc.contributor.author","Teigen, Luke N."],["dc.contributor.author","Toscano, Gianpaolo"],["dc.contributor.author","Mayer, Geert"],["dc.contributor.author","Morbelli, Silvia"],["dc.contributor.author","Dawson, Benjamin"],["dc.contributor.author","Pelletier, Amelie"],["dc.date.accessioned","2020-03-04T10:32:28Z"],["dc.date.accessioned","2021-10-27T13:22:09Z"],["dc.date.available","2020-03-04T10:32:28Z"],["dc.date.available","2021-10-27T13:22:09Z"],["dc.date.issued","2019"],["dc.description.abstract","Idiopathic REM sleep behaviour disorder (iRBD) is a powerful early sign of Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy. This provides an unprecedented opportunity to directly observe prodromal neurodegenerative states, and potentially intervene with neuroprotective therapy. For future neuroprotective trials, it is essential to accurately estimate phenoconversion rate and identify potential predictors of phenoconversion. This study assessed the neurodegenerative disease risk and predictors of neurodegeneration in a large multicentre cohort of iRBD. We combined prospective follow-up data from 24 centres of the International RBD Study Group. At baseline, patients with polysomnographically-confirmed iRBD without parkinsonism or dementia underwent sleep, motor, cognitive, autonomic and special sensory testing. Patients were then prospectively followed, during which risk of dementia and parkinsonsim were assessed. The risk of dementia and parkinsonism was estimated with Kaplan-Meier analysis. Predictors of phenoconversion were assessed with Cox proportional hazards analysis, adjusting for age, sex, and centre. Sample size estimates for disease-modifying trials were calculated using a time-to-event analysis. Overall, 1280 patients were recruited. The average age was 66.3 ± 8.4 and 82.5% were male. Average follow-up was 4.6 years (range = 1-19 years). The overall conversion rate from iRBD to an overt neurodegenerative syndrome was 6.3% per year, with 73.5% converting after 12-year follow-up. The rate of phenoconversion was significantly increased with abnormal quantitative motor testing [hazard ratio (HR) = 3.16], objective motor examination (HR = 3.03), olfactory deficit (HR = 2.62), mild cognitive impairment (HR = 1.91-2.37), erectile dysfunction (HR = 2.13), motor symptoms (HR = 2.11), an abnormal DAT scan (HR = 1.98), colour vision abnormalities (HR = 1.69), constipation (HR = 1.67), REM atonia loss (HR = 1.54), and age (HR = 1.54). There was no significant predictive value of sex, daytime somnolence, insomnia, restless legs syndrome, sleep apnoea, urinary dysfunction, orthostatic symptoms, depression, anxiety, or hyperechogenicity on substantia nigra ultrasound. Among predictive markers, only cognitive variables were different at baseline between those converting to primary dementia versus parkinsonism. Sample size estimates for definitive neuroprotective trials ranged from 142 to 366 patients per arm. This large multicentre study documents the high phenoconversion rate from iRBD to an overt neurodegenerative syndrome. Our findings provide estimates of the relative predictive value of prodromal markers, which can be used to stratify patients for neuroprotective trials."],["dc.identifier.doi","10.1093/brain/awz030"],["dc.identifier.pmid","30789229"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17196"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92072"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","1460-2156"],["dc.relation.issn","1460-2156"],["dc.relation.issn","0006-8950"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.subject.ddc","610"],["dc.title","Risk and predictors of dementia and parkinsonism in idiopathic REM sleep behaviour disorder: a multicentre study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0241752"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.lastpage","11"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Malinova, Vesna"],["dc.contributor.author","Pinter, Anabel"],["dc.contributor.author","Dragaescu, Cristina"],["dc.contributor.author","Rohde, Veit"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Sixel-Döring, Friederike"],["dc.contributor.author","Eckardstein, Kajetan L. von"],["dc.date.accessioned","2020-12-04T13:28:18Z"],["dc.date.accessioned","2021-10-27T13:22:23Z"],["dc.date.available","2020-12-04T13:28:18Z"],["dc.date.available","2021-10-27T13:22:23Z"],["dc.date.issued","2020"],["dc.description.abstract","Objective Intraoperative microelectrode recording (MER) and test-stimulation are regarded as the gold standard for proper placement of subthalamic (STN) deep brain stimulation (DBS) electrodes in Parkinson’s disease (PD), requiring the patient to be awake during the procedure. In accordance with good clinical practice, most attending neurologists will request the clinically most efficacious trajectory for definite lead placement. However, the necessity of microelectrode-test-stimulation is disputed, as it may limit the access to DBS therapy, excluding those not willing or incapable of undergoing awake surgery. Methods We retrospectively analyzed the MERs and microelectrode-test-stimulation results with regard to the decision on definite lead placement and clinical outcome in a cohort of 67 PD-patients with STN-DBS. All patients received bilateral quadripolar ring electrodes. To ascertain overall procedural efficacy, we calculated the surgical index (SI) by comparing preoperative motor improvement induced by levodopa to that induced by stimulation 7 to 18 months after surgery, measured as the relative difference between ON and OFF-states on the Unified Parkinson’s Disease Rating Scale motor part (UPDRS-3). Additionally, a side-specific surgical index (SSSI) was calculated using the unilateral assessable items of the UPDRS-3. The SSSI where microelectrode-test-stimulation overruled MER were compared to those where the result of microelectrode-test-stimulation was congruent to MER results. Results A total of 134 electrodes were analyzed. For final lead placement, the central trajectory was chosen in 54% of patient hemispheres. The mean SI was 0.99 (± 0.24). SSSI averaged 1.04 (± 0.45). In 37 lead placements, microelectrode-test-stimulation overruled MER in the final trajectory selection, in 27 of these lead placements adverse effects during microelectrode-test-stimulation were decisive. Neither the number of test electrodes used nor the STN-signal length had an impact on the SSSI. The SSSI did not differ between lead placements with MER/microelectrode-test-stimulation congruency and those where the results of microelectrode-test-stimulation initiated lead placement in a trajectory with shorter STN signal. Conclusion Intraoperative testing is mandatory to ensure an optimal motor outcome of STN DBS in PD-patients when using quadripolar ring electrodes. However, we also demonstrated that neither the length of the STN-signal on MER nor the number of test electrodes influenced the motor outcome."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2020"],["dc.identifier.doi","10.1371/journal.pone.0241752"],["dc.identifier.doi","10.1371/journal.pone.0241752.g001"],["dc.identifier.doi","10.1371/journal.pone.0241752.g002"],["dc.identifier.doi","10.1371/journal.pone.0241752.g003"],["dc.identifier.doi","10.1371/journal.pone.0241752.g004"],["dc.identifier.doi","10.1371/journal.pone.0241752.g005"],["dc.identifier.doi","10.1371/journal.pone.0241752.s001"],["dc.identifier.doi","10.1371/journal.pone.0241752.r001"],["dc.identifier.doi","10.1371/journal.pone.0241752.r002"],["dc.identifier.doi","10.1371/journal.pone.0241752.r003"],["dc.identifier.doi","10.1371/journal.pone.0241752.r004"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17684"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92090"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","1932-6203"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","The role of intraoperative microelectrode recording and stimulation in subthalamic lead placement for Parkinson’s disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Movement Disorders Clinical Practice"],["dc.bibliographiccitation.lastpage","4"],["dc.bibliographiccitation.volume","Early View Status"],["dc.contributor.author","Halsband, Claire"],["dc.contributor.author","Zapf, Antonia"],["dc.contributor.author","Sixel-Döring, Friederike"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Mollenhauer, Brit"],["dc.date.accessioned","2019-07-09T11:45:02Z"],["dc.date.available","2019-07-09T11:45:02Z"],["dc.date.issued","2018"],["dc.description.abstract","Background: Rapid eye movement (REM) sleep behavior disorder (RBD) is one of the most specific prodromal indicators for Parkinson's disease (PD). Objectives: To test the validity of the RBD-Screening Questionnaire (RBDSQ) in assessing RBD in early PD. Methods: The RBDSQ was completed before video-supported polysomnography (vPSG) by 134 de novo PD patients, 109 matched controls without neurological disorder (CTR) and 30 subjects with idiopathic RBD (iRBD) without clinical signs of PD; results were compared with vPSG-confirmed RBD diagnosis. Results and Conclusions: Sensitivity/specificity of the RBDSQ for the PD cohort were 0.44/0.84 at the previously published cut-off score of 6 for PD patients, and the area under the curve (AUC) 0.68 (95% CI, 0.56–0.79). By contrast, in the iRBD/CTR cohort the RBDSQ (cut-off = 5) had a sensitivity/specificity of 0.97/0.84 and an AUC of 0.95 (95% CI, 0.90–1.00). Subanalysis of question 6 only (4 subitems asking for dream enactment) at a cut-off score of 1 revealed a sensitivity of 0.74 and a specificity of 0.70 for the de novo PD cohort, AUC was 0.74 (95% CI, 0.63–0.84). RBDSQ is an insufficient screening tool for RBD in de novo PD. New screening tools for RBD assessment need to be developed."],["dc.identifier.doi","10.1002/mdc3.12591"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15012"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59145"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/H2020/634821/EU//PROPAG-AGEING"],["dc.relation.issn","2330-1619"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","The REM Sleep Behavior Disorder Screening Questionnaire is not Valid in De Novo Parkinson's Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","184"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","193"],["dc.bibliographiccitation.volume","87"],["dc.contributor.author","Tilch, Erik"],["dc.contributor.author","Schormair, Barbara"],["dc.contributor.author","Zhao, Chen"],["dc.contributor.author","Salminen, Aaro V."],["dc.contributor.author","Antic Nikolic, Ana"],["dc.contributor.author","Holzknecht, Evi"],["dc.contributor.author","Högl, Birgit"],["dc.contributor.author","Poewe, Werner"],["dc.contributor.author","Bachmann, Cornelius G."],["dc.contributor.author","Paulus, Walter"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Oertel, Wolfgang H."],["dc.contributor.author","Hornyak, Magdolna"],["dc.contributor.author","Fietze, Ingo"],["dc.contributor.author","Berger, Klaus"],["dc.contributor.author","Lichtner, Peter"],["dc.contributor.author","Gieger, Christian"],["dc.contributor.author","Peters, Annette"],["dc.contributor.author","Müller‐Myhsok, Bertram"],["dc.contributor.author","Hoischen, Alexander"],["dc.contributor.author","Winkelmann, Juliane"],["dc.contributor.author","Oexle, Konrad"],["dc.date.accessioned","2020-01-14T08:34:05Z"],["dc.date.accessioned","2021-10-27T13:22:02Z"],["dc.date.available","2020-01-14T08:34:05Z"],["dc.date.available","2021-10-27T13:22:02Z"],["dc.date.issued","2019"],["dc.description.abstract","OBJECTIVE: Restless legs syndrome is a frequent neurological disorder with substantial burden on individual well-being and public health. Genetic risk loci have been identified, but the causatives genes at these loci are largely unknown, so that functional investigation and clinical translation of molecular research data are still inhibited. To identify putatively causative genes, we searched for highly significant mutational burden in candidate genes. METHODS: We analyzed 84 candidate genes in 4,649 patients and 4,982 controls by next generation sequencing using molecular inversion probes that targeted mainly coding regions. The burden of low-frequency and rare variants was assessed, and in addition, an algorithm (binomial performance deviation analysis) was established to estimate independently the sequence variation in the probe binding regions from the variation in sequencing depth. RESULTS: Highly significant results (considering the number of genes in the genome) of the conventional burden test and the binomial performance deviation analysis overlapped significantly. Fourteen genes were highly significant by one method and confirmed with Bonferroni-corrected significance by the other to show a differential burden of low-frequency and rare variants in restless legs syndrome. Nine of them (AAGAB, ATP2C1, CNTN4, COL6A6, CRBN, GLO1, NTNG1, STEAP4, VAV3) resided in the vicinity of known restless legs syndrome loci, whereas 5 (BBS7, CADM1, CREB5, NRG3, SUN1) have not previously been associated with restless legs syndrome. Burden test and binomial performance deviation analysis also converged significantly in fine-mapping potentially causative domains within these genes. INTERPRETATION: Differential burden with intragenic low-frequency variants reveals putatively causative genes in restless legs syndrome. ANN NEUROL 2019."],["dc.identifier.doi","10.1002/ana.25658"],["dc.identifier.eissn","1531-8249"],["dc.identifier.isbn","31788832"],["dc.identifier.issn","0364-5134"],["dc.identifier.pmid","31788832"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17073"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92063"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","1531-8249"],["dc.relation.issn","1531-8249"],["dc.relation.issn","0364-5134"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.subject.ddc","610"],["dc.title","Identification of Restless Legs Syndrome Genes by Mutational Load Analysis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","870"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Gröschel, Carina"],["dc.contributor.author","Hübscher, Daniela"],["dc.contributor.author","Nolte, Jessica"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Sasse, André"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Paulus, Walter"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Polić, Bojan"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2019-07-09T11:43:35Z"],["dc.date.available","2019-07-09T11:43:35Z"],["dc.date.issued","2017"],["dc.description.abstract","Natural killer (NK) cells play an important role as cytotoxic effector cells, which scan the organism for infected or tumorigenic cells. Conflicting data have been published whether NK cells can also kill allogeneic or even autologous pluripotent stem cells (PSCs) and which receptors are involved. A clarification of this question is relevant since an activity of NK cells against PSCs could reduce the risk of teratoma growth after transplantation of PSC-derived grafts. Therefore, the hypothesis has been tested that the activity of NK cells against PSCs depends on cytokine activation and specifically on the activating NK receptor NKG2D. It is shown that a subcutaneous injection of autologous iPSCs failed to activate NK cells against these iPSCs and can give rise to teratomas. In agreement with this result, several PSC lines, including two iPSC, two embryonic stem cell (ESC), and two so-called multipotent adult germline stem cell (maGSC) lines, were largely resistant against resting NK cells although differences in killing were found at low level. All PSC lines were killed by interleukin (IL)-2-activated NK cells, and maGSCs were better killed than the other PSC types. The PSCs expressed ligands of the activating NK receptor NKG2D and NKG2D-deficient NK cells from Klrk1−/− mice were impaired in their cytotoxic activity against PSCs. The low-cytotoxic activity of resting NK cells was almost completely dependent on NKG2D. The cytotoxic activity of IL-2-activated NKG2D-deficient NK cells against PSCs was reduced, indicating that also other activating receptors on cytokine-activated NK cells must be engaged by ligands on PSCs. Thus, NKG2D is an important activating receptor involved in killing of murine PSCs. However, NK cells need to be activated by cytokines before they efficiently target PSCs and then also other NK receptors become relevant. These features of NK cells might be relevant for transplantation of PSC-derived grafts since NK cells have the capability to kill undifferentiated cells, which might be present in grafts in trace amounts."],["dc.identifier.doi","10.3389/fimmu.2017.00870"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14587"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58923"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/297"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C05: Bedeutung von zellulären Immunreaktionen für das kardiale Remodeling und die Therapie der Herzinsuffizienz durch Stammzelltransplantation"],["dc.relation.eissn","1664-3224"],["dc.relation.issn","1664-3224"],["dc.relation.workinggroup","RG Dressel"],["dc.relation.workinggroup","RG Guan (Application of patient-specific induced pluripotent stem cells in disease modelling)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Efficient Killing of Murine Pluripotent Stem Cells by Natural Killer (NK) Cells Requires Activation by Cytokines and Partly Depends on the Activating NK Receptor NKG2D"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","International journal of Alzheimer's disease"],["dc.bibliographiccitation.volume","2010"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Mollenhauer, Brit"],["dc.date.accessioned","2019-07-09T11:53:09Z"],["dc.date.available","2019-07-09T11:53:09Z"],["dc.date.issued","2010"],["dc.description.abstract","We studied the diagnostic value of CSF Aβ42/tau versus low Aβ1-42% and high Aβ1-40(ox)% levels for differential diagnosis of Alzheimer's disease (AD) and dementia with Lewy bodies (DLB), respectively. CSF of 45 patients with AD, 15 with DLB, 21 with Parkinson's disease dementia (PDD), and 40 nondemented disease controls (NDC) was analyzed by Aβ-SDS-PAGE/immunoblot and ELISAs (Aβ42 and tau). Aβ42/tau lacked specificity in discriminating AD from DLB and PDD. Best discriminating biomarkers were Aβ1-42% and Aβ1-40(ox)% for AD and DLB, respectively. AD and DLB could be differentiated by both Aβ1-42% and Aβ1-40(ox)% with an accuracy of 80% at minimum. Thus, we consider Aβ1-42% and Aβ1-40(ox)% to be useful biomarkers for AD and DLB, respectively. We propose further studies on the integration of Aβ1-42% and Aβ1-40(ox)% into conventional assay formats. Moreover, future studies should investigate the combination of Aβ1-40(ox)% and CSF alpha-synuclein for the diagnosis of DLB."],["dc.identifier.doi","10.4061/2010/761571"],["dc.identifier.fs","575758"],["dc.identifier.pmid","20862375"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6918"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60350"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2090-0252"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Combined Analysis of CSF Tau, Aβ42, Aβ1-42% and Aβ1-40% in Alzheimer's Disease, Dementia with Lewy Bodies and Parkinson's Disease Dementia."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]