Gera, Roland Gerard

[["dc.bibliographiccitation.artnumber","mds.28738"],["dc.bibliographiccitation.firstpage","2874"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Movement Disorders"],["dc.bibliographiccitation.lastpage","2887"],["dc.bibliographiccitation.volume","36"],["dc.contributor.affiliation","Schulz, Isabel; 1\r\nParacelsus‐Elena‐Klinik\r\nKassel Germany"],["dc.contributor.affiliation","Kruse, Niels; 2\r\nDepartment of Neuropathology\r\nUniversity Medical Centre Goettingen\r\nGoettingen Germany"],["dc.contributor.affiliation","Gera, Roland G.; 3\r\nDepartment of Medical Statistics\r\nUniversity Medical Centre Goettingen\r\nGoettingen Germany"],["dc.contributor.affiliation","Kremer, Thomas; 4\r\nRoche Pharmaceutical Research and Early Development\r\nNRD Neuroscience and Rare Disease, Roche Innovation Center Basel, F. Hoffmann‐La Roche Ltd\r\nBasel Switzerland"],["dc.contributor.affiliation","Cedarbaum, Jesse; 5\r\nCoeruleus Clinical Sciences LLC\r\nWoodbidge Connecticut USA"],["dc.contributor.affiliation","Barbour, Robin; 7\r\nProthena Biosciences Inc.\r\nSan Francisco California USA"],["dc.contributor.affiliation","Zago, Wagner; 7\r\nProthena Biosciences Inc.\r\nSan Francisco California USA"],["dc.contributor.affiliation","Schade, Sebastian; 8\r\nDepartment of Neurology\r\nUniversity Medical Centre Goettingen\r\nGoettingen Germany"],["dc.contributor.affiliation","Otte, Birgit; 8\r\nDepartment of Neurology\r\nUniversity Medical Centre Goettingen\r\nGoettingen Germany"],["dc.contributor.affiliation","Bartl, Michael; 8\r\nDepartment of Neurology\r\nUniversity Medical Centre Goettingen\r\nGoettingen Germany"],["dc.contributor.affiliation","Hutten, Samantha J.; 9\r\nThe Michael J. Fox Foundation for Parkinson's Research\r\nNew York New York USA"],["dc.contributor.affiliation","Trenkwalder, Claudia; 1\r\nParacelsus‐Elena‐Klinik\r\nKassel Germany"],["dc.contributor.author","Schulz, Isabel"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Gera, Roland G."],["dc.contributor.author","Kremer, Thomas"],["dc.contributor.author","Cedarbaum, Jesse"],["dc.contributor.author","Barbour, Robin"],["dc.contributor.author","Zago, Wagner"],["dc.contributor.author","Schade, Sebastian"],["dc.contributor.author","Otte, Birgit"],["dc.contributor.author","Bartl, Michael"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Hutten, Samantha J."],["dc.contributor.author","Trenkwalder, Claudia"],["dc.date.accessioned","2021-09-01T06:42:14Z"],["dc.date.available","2021-09-01T06:42:14Z"],["dc.date.issued","2021"],["dc.date.updated","2022-03-21T11:31:27Z"],["dc.description.abstract","ABSTRACT Background Objective diagnostic biomarkers are needed to support a clinical diagnosis. Objectives To analyze markers in various neurodegenerative disorders to identify diagnostic biomarker candidates for mainly α‐synuclein (aSyn)‐related disorders (ASRD) in serum and/or cerebrospinal fluid (CSF). Methods Upon initial testing of commercially available kits or published protocols for the quantification of the candidate markers, assays for the following were selected: total and phosphorylated aSyn (pS129aSyn), neurofilament light chain (NfL), phosphorylated neurofilament heavy chain (pNfH), tau protein (tau), ubiquitin C‐terminal hydrolase L1 (UCHL‐1), glial fibrillary acidic protein (GFAP), calcium‐binding protein B (S100B), soluble triggering receptor expressed on myeloid cells 2 (sTREM‐2), and chitinase‐3‐like protein 1 (YKL‐40). The cohort comprised participants with Parkinson's disease (PD, n = 151), multiple system atrophy (MSA, n = 17), dementia with Lewy bodies (DLB, n = 45), tau protein‐related neurodegenerative disorders (n = 80, comprising patients with progressive supranuclear palsy (PSP, n = 38), corticobasal syndrome (CBS, n = 16), Alzheimer's disease (AD, n = 11), and frontotemporal degeneration/amyotrophic lateral sclerosis (FTD/ALS, n = 15), as well as healthy controls (HC, n = 20). Receiver operating curves (ROC) with area under the curves (AUC) are given for each marker. Results CSF total aSyn was decreased. NfL, pNfH, UCHL‐1, GFAP, S100B, and sTREM‐2 were increased in patients with neurodegenerative disease versus HC (P < 0.05). As expected, some of the markers were highest in AD (i.e., UCHL‐1, GFAP, S100B, sTREM‐2, YKL‐40). Within ASRD, CSF NfL levels were higher in MSA than PD and DLB (P < 0.05). Comparing PD to HC, interesting serum markers were S100B (AUC: 0.86), sTREM2 (AUC: 0.87), and NfL (AUC: 0.78). CSF S100B and serum GFAP were highest in DLB. Conclusions Levels of most marker candidates tested in serum and CSF significantly differed between disease groups and HC. In the stratification of PD versus other tau‐ or aSyn‐related conditions, CSF NfL levels best discriminated PD and MSA. CSF S100B and serum GFAP best discriminated PD and DLB. © 2021 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson Movement Disorder Society."],["dc.identifier.doi","10.1002/mds.28738"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/89011"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-455"],["dc.relation.eissn","1531-8257"],["dc.relation.issn","0885-3185"],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited."],["dc.title","Systematic Assessment of 10 Biomarker Candidates Focusing on α‐Synuclein‐Related Disorders"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1879"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Statistical Methods in Medical Research"],["dc.bibliographiccitation.lastpage","1892"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Graf, Alexandra Christine"],["dc.contributor.author","Wassmer, Gernot"],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Gera, Roland Gerard"],["dc.contributor.author","Posch, Martin"],["dc.date.accessioned","2019-07-09T11:51:55Z"],["dc.date.available","2019-07-09T11:51:55Z"],["dc.date.issued","2018"],["dc.description.abstract","With the advent of personalized medicine, clinical trials studying treatment effects in subpopulations are receiving increasing attention. The objectives of such studies are, besides demonstrating a treatment effect in the overall population, to identify subpopulations, based on biomarkers, where the treatment has a beneficial effect. Continuous biomarkers are often dichotomized using a threshold to define two subpopulations with low and high biomarker levels. If there is insufficient information on the dependence structure of the outcome on the biomarker, several thresholds may be investigated. The nested structure of such subpopulations is similar to the structure in group sequential trials. Therefore, it has been proposed to use the corresponding critical boundaries to test such nested subpopulations. We show that for biomarkers with a prognostic effect that is not adjusted for in the statistical model, the variability of the outcome may vary across subpopulations which may lead to an inflation of the family-wise type 1 error rate. Using simulations we quantify the potential inflation of testing procedures based on group sequential designs. Furthermore, alternative hypotheses tests that control the family-wise type 1 error rate under minimal assumptions are proposed. The methodological approaches are illustrated by a trial in depression."],["dc.identifier.doi","10.1177/0962280218777538"],["dc.identifier.pmid","29888651"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16230"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60042"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/602144/EU//INSPIRE"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Robustness of testing procedures for confirmatory subpopulation analyses based on a continuous biomarker"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","345"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Clinical Neuroradiology"],["dc.bibliographiccitation.lastpage","353"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Behme, D."],["dc.contributor.author","Gera, R. G."],["dc.contributor.author","Tsogkas, I."],["dc.contributor.author","Colla, R."],["dc.contributor.author","Liman, J."],["dc.contributor.author","Maier, I. L."],["dc.contributor.author","Liebeskind, D. S."],["dc.contributor.author","Psychogios, M. N."],["dc.date.accessioned","2021-04-14T08:26:15Z"],["dc.date.available","2021-04-14T08:26:15Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1007/s00062-019-00786-0"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81878"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1869-1447"],["dc.relation.issn","1869-1439"],["dc.title","Impact of Time on Thrombolysis in Cerebral Infarction Score Results"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0210334"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","PLOS ONE"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Behme, Daniel"],["dc.contributor.author","Tsogkas, Ioannis"],["dc.contributor.author","Colla, Ruben"],["dc.contributor.author","Gera, Roland G."],["dc.contributor.author","Schregel, Katharina"],["dc.contributor.author","Hesse, Amélie C."],["dc.contributor.author","Maier, Ilko L."],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Liebeskind, David S."],["dc.contributor.author","Psychogios, Marios-Nikos"],["dc.date.accessioned","2019-07-09T11:50:09Z"],["dc.date.available","2019-07-09T11:50:09Z"],["dc.date.issued","2019"],["dc.description.abstract","BACKGROUND: A thrombolysis in cerebral infarction (TICI) score of 2b is defined as a good recanalization result although the reperfusion may only cover 50% of the affected territory. An additional mTICI2c category was introduced to further differentiate between mTICI scores. Despite the new mTICI2c category, mTICI2b still covers a range of 50-90% reperfusion which might be too imprecise to predict neurological improvement after therapy. AIM: To compare the 7-point \"expanded TICI\" (eTICI) scale with the traditional mTICI in regard to predict functional independence at 90 days. METHODS: Retrospective review of 225 patients with large artery occlusion. Angiograms were graded by 2 readers according the 7-point eTICI score (0% = eTICI0; reduced clot = eTICI1; 1-49% = eTICI2a, 50-66% = eTICI2b50; 67-89% = eTICI2b67, 90-99% = eTICI2c and complete reperfusion = eTICI3) and the conventional mTICI score. The ability of e- and mTICI to predict favorable outcome at 90days was compared. RESULTS: Given the ROC analysis eTICI was the better predictor of favorable outcome (p-value 0.047). Additionally, eTICI scores 2b50, 2b67 and 2c (former mTICI2b) were significantly superior at predicting the probability of a favorable outcome at 90 days after endovascular therapy with a p-value of 0.033 (probabilities of 17% for mTICI2b50, 24% for mTICI2b67 and 54% for mTICI2c vs. 36% for mTICI2b). CONCLUSIONS: The 7-point eTICI allows for a more accurate outcome prediction compared to the mTICI score because it refines the broad range of former mTICI2b results."],["dc.identifier.doi","10.1371/journal.pone.0210334"],["dc.identifier.pmid","30629664"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15873"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59714"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Validation of the extended thrombolysis in cerebral infarction score in a real world cohort"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1999"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Movement Disorders"],["dc.bibliographiccitation.lastpage","2008"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Dakna, Mohammed"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Galasko, Douglas"],["dc.contributor.author","Foroud, Tatiana"],["dc.contributor.author","Zetterberg, Henrik"],["dc.contributor.author","Schade, Sebastian"],["dc.contributor.author","Gera, Roland G."],["dc.contributor.author","Wang, Wenting"],["dc.contributor.author","Gao, Feng"],["dc.contributor.author","Frasier, Mark"],["dc.contributor.author","Chahine, Lana M."],["dc.contributor.author","Coffey, Christopher S."],["dc.contributor.author","Singleton, Andrew B."],["dc.contributor.author","Simuni, Tanya"],["dc.contributor.author","Weintraub, Daniel"],["dc.contributor.author","Seibyl, John"],["dc.contributor.author","Toga, Arthur W."],["dc.contributor.author","Tanner, Caroline M."],["dc.contributor.author","Kieburtz, Karl"],["dc.contributor.author","Marek, Kenneth"],["dc.contributor.author","Siderowf, Andrew"],["dc.contributor.author","Cedarbaum, Jesse M."],["dc.contributor.author","Hutten, Samantha J."],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Graham, Danielle"],["dc.date.accessioned","2021-04-14T08:24:53Z"],["dc.date.available","2021-04-14T08:24:53Z"],["dc.date.issued","2020"],["dc.description.abstract","Abstract Background The objective of this study was to assess neurofilament light chain as a Parkinson's disease biomarker. Methods We quantified neurofilament light chain in 2 independent cohorts: (1) longitudinal cerebrospinal fluid samples from the longitudinal de novo Parkinson's disease cohort and (2) a large longitudinal cohort with serum samples from Parkinson's disease, other cognate/neurodegenerative disorders, healthy controls, prodromal conditions, and mutation carriers. Results In the Parkinson's Progression Marker Initiative cohort, mean baseline serum neurofilament light chain was higher in Parkinson's disease patients (13 ± 7.2 pg/mL) than in controls (12 ± 6.7 pg/mL), P = 0.0336. Serum neurofilament light chain increased longitudinally in Parkinson's disease patients versus controls (P \\u0026lt; 0.01). Motor scores were positively associated with neurofilament light chain, whereas some cognitive scores showed a negative association. Conclusions Neurofilament light chain in serum samples is increased in Parkinson's disease patients versus healthy controls, increases over time and with age, and correlates with clinical measures of Parkinson's disease severity. Although the specificity of neurofilament light chain for Parkinson's disease is low, it is the first blood‐based biomarker candidate that could support disease stratification of Parkinson's disease versus other cognate/neurodegenerative disorders, track clinical progression, and possibly assess responsiveness to neuroprotective treatments. However, use of neurofilament light chain as a biomarker of response to neuroprotective interventions remains to be assessed. © 2020 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society."],["dc.description.sponsorship","AbbVie http://dx.doi.org/10.13039/100006483"],["dc.description.sponsorship","Avid Radiopharmaceuticals http://dx.doi.org/10.13039/100014392"],["dc.description.sponsorship","Biogen Idec http://dx.doi.org/10.13039/100006314"],["dc.description.sponsorship","Bristol‐Myers Squibb http://dx.doi.org/10.13039/100002491"],["dc.description.sponsorship","Covance"],["dc.description.sponsorship","Eli Lilly \\u0026 Co"],["dc.description.sponsorship","F. Hoffman‐La Roche, Ltd"],["dc.description.sponsorship","GE Healthcare http://dx.doi.org/10.13039/100006775"],["dc.description.sponsorship","Genentech http://dx.doi.org/10.13039/100004328"],["dc.description.sponsorship","GlaxoSmithKline http://dx.doi.org/10.13039/100004330"],["dc.description.sponsorship","Lundbeck http://dx.doi.org/10.13039/501100013327"],["dc.description.sponsorship","Merck http://dx.doi.org/10.13039/100004334"],["dc.description.sponsorship","MesoScale"],["dc.description.sponsorship","Michael J. Fox Foundation for Parkinson's Research http://dx.doi.org/10.13039/100000864"],["dc.description.sponsorship","Pfizer http://dx.doi.org/10.13039/100004319"],["dc.description.sponsorship","Piramal"],["dc.description.sponsorship","UCB http://dx.doi.org/10.13039/100011110"],["dc.identifier.doi","10.1002/mds.28206"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81454"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.publisher","John Wiley \\u0026 Sons, Inc."],["dc.relation.eissn","1531-8257"],["dc.relation.issn","0885-3185"],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited."],["dc.title","Validation of Serum Neurofilament Light Chain as a Biomarker of Parkinson's Disease Progression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]