Schade, Sebastian

[["dc.bibliographiccitation.artnumber","pyv102"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The International Journal of Neuropsychopharmacology"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Schade, Sebastian"],["dc.contributor.author","Paulus, Walter J."],["dc.date.accessioned","2018-11-07T10:15:46Z"],["dc.date.available","2018-11-07T10:15:46Z"],["dc.date.issued","2016"],["dc.description.abstract","D-Cycloserine, known from tuberculosis therapy, has been widely introduced to neuropsychiatric studies, since its central active mechanism as a partial NMDA-agonist has been found. In this review, we evaluate its therapeutic potential in neuropsychological disorders and discuss its pitfalls in terms of dosing and application frequency as well as its safety in low-dose therapy. Therefore, we identified 91 clinical trials by performing a Medline search. We demonstrate in part preliminary but increasing evidence that D-cycloserine may be effective in various psychiatric diseases, including schizophrenia, anxiety disorders, addiction, eating disorders, major depression, and autism as well as in neurological diseases, including dementia, Alzheimer's disease, and spinocerebellar degeneration. D-Cycloserine in low-dose therapy is safe, but there is still a need for new drugs with higher specificity to the different N-methyl-D-aspartate-receptor subunits."],["dc.identifier.doi","10.1093/ijnp/pyv102"],["dc.identifier.isi","000377111100001"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13518"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40882"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1469-5111"],["dc.relation.issn","1461-1457"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","D-Cycloserine in Neuropsychiatric Diseases: A Systematic Review"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["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.artnumber","72"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Alzheimer s Research & Therapy"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Schade, Sebastian"],["dc.contributor.author","Mollenhauer, Brit"],["dc.date.accessioned","2018-11-07T09:45:45Z"],["dc.date.available","2018-11-07T09:45:45Z"],["dc.date.issued","2014"],["dc.description.abstract","Dementia with Lewy bodies (DLB) has become the second most common neurodegenerative dementia due to demographic ageing. Differential diagnosis is still troublesome especially in early stages of the disease, since there is a great clinical and neuropathological overlap primarily with Alzheimer's disease and Parkinson's disease. Therefore, more specific biomarkers, not only for scientific reasons but also for clinical therapeutic decision-making, are urgently needed. In this review, we summarize the knowledge on fluid biomarkers for DLB, derived predominantly from cerebrospinal fluid. We discuss the value of well-defined markers (beta-amyloid, (phosphorylated) tau, alpha-synuclein) as well as some promising 'upcoming' substances, which still have to be further evaluated."],["dc.identifier.doi","10.1186/s13195-014-0072-3"],["dc.identifier.isi","000343200300014"],["dc.identifier.pmid","25478030"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12110"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34695"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1758-9193"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Biomarkers in biological fluids for dementia with Lewy bodies"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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"]]