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","14"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","npj Parkinson's Disease"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Meoni, Gaia"],["dc.contributor.author","Tenori, Leonardo"],["dc.contributor.author","Schade, Sebastian"],["dc.contributor.author","Licari, Cristina"],["dc.contributor.author","Pirazzini, Chiara"],["dc.contributor.author","Bacalini, Maria Giulia"],["dc.contributor.author","Garagnani, Paolo"],["dc.contributor.author","Turano, Paola"],["dc.contributor.author","Molin, Alessandra Dal"],["dc.contributor.author","Bartoletti-Stella, Anna"],["dc.contributor.author","Luchinat, Claudio"],["dc.contributor.authorgroup","PROPAG-AGEING Consortium"],["dc.date.accessioned","2022-04-01T10:02:38Z"],["dc.date.available","2022-04-01T10:02:38Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract Parkinson’s disease (PD) is the neurological disorder showing the greatest rise in prevalence from 1990 to 2016. Despite clinical definition criteria and a tremendous effort to develop objective biomarkers, precise diagnosis of PD is still unavailable at early stage. In recent years, an increasing number of studies have used omic methods to unveil the molecular basis of PD, providing a detailed characterization of potentially pathological alterations in various biological specimens. Metabolomics could provide useful insights to deepen our knowledge of PD aetiopathogenesis, to identify signatures that distinguish groups of patients and uncover responsive biomarkers of PD that may be significant in early detection and in tracking the disease progression and drug treatment efficacy. The present work is the first large metabolomic study based on nuclear magnetic resonance (NMR) with an independent validation cohort aiming at the serum characterization of de novo drug-naive PD patients. Here, NMR is applied to sera from large training and independent validation cohorts of German subjects. Multivariate and univariate approaches are used to infer metabolic differences that characterize the metabolite and the lipoprotein profiles of newly diagnosed de novo drug-naive PD patients also in relation to the biological sex of the subjects in the study, evidencing a more pronounced fingerprint of the pathology in male patients. The presence of a validation cohort allowed us to confirm altered levels of acetone and cholesterol in male PD patients. By comparing the metabolites and lipoproteins levels among de novo drug-naive PD patients, age- and sex-matched healthy controls, and a group of advanced PD patients, we detected several descriptors of stronger oxidative stress."],["dc.identifier.doi","10.1038/s41531-021-00274-8"],["dc.identifier.pii","274"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105969"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","2373-8057"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Metabolite and lipoprotein profiles reveal sex-related oxidative stress imbalance in de novo drug-naive Parkinson’s disease patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","755"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Movement Disorders Clinical Practice"],["dc.bibliographiccitation.lastpage","762"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Schade, Sebastian"],["dc.contributor.author","Sixel-Döring, Friederike"],["dc.contributor.author","Ebentheuer, Jens"],["dc.contributor.author","Schulz, Xenia"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Mollenhauer, Brit"],["dc.date.accessioned","2020-12-10T14:06:55Z"],["dc.date.available","2020-12-10T14:06:55Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1002/mdc3.12511"],["dc.identifier.issn","2330-1619"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70071"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Acute Levodopa Challenge Test in Patients with de novo Parkinson's Disease: Data from the DeNoPa Cohort"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","191"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Restorative Neurology and Neuroscience"],["dc.bibliographiccitation.lastpage","198"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Schade, Sebastian"],["dc.contributor.author","Moliadze, Vera"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Antal, Andrea"],["dc.date.accessioned","2018-11-07T09:15:21Z"],["dc.date.available","2018-11-07T09:15:21Z"],["dc.date.issued","2012"],["dc.description.abstract","Purpose: Transcranial direct current stimulation (tDCS) has proven to be a useful tool for fundamental brain research as well as for attempts in therapy of neurological and psychiatric diseases by modulating neuronal plasticity. Little is understood about the effects of tDCS are influenced by hemispheric dominance, even less in terms of handedness. The aim of our pilot study was to investigate whether tDCS induced neuroplastic changes may be different in right-and left-handed individuals due to existing differences in hemispheric lateralisation. Methods: We measured changes in motor evoked potentials (MEPs) after application of tDCS in 8 right-handers, 8 left-handers and 8 mixed-handers according to the Edinburgh Handedness Inventory (EHI). In double-blind sessions, we applied either anodal or cathodal tDCS for 5 minutes for each hemisphere. Results: While motor thresholds (MT) seem to be not influenced by handedness significantly, in right-handed subjects we reproduced the well-known effects of tDCS: anodal stimulation increased while cathodal stimulation decreased MEP amplitudes. However, left-and mixed-handed subjects differed from right-handed subjects. After anodal stimulation of the left hemisphere the increase of the MEP amplitudes was stronger in right handed subjects than in left and mixed handed subjects. Interestingly, after cathodal stimulation of the left hemisphere this difference was less marked. The stimulation of the right hemisphere showed the same tendency, but results were not significant. Conclusions: For the first time, we are able to demonstrate that the modulating effects of tDCS on corticospinal excitability differ moderately in the left-and mixed-handed population compared to right-handed subjects. The shown differences according to handedness should be taken into account in further studies."],["dc.identifier.doi","10.3233/RNN-2012-110175"],["dc.identifier.isi","000304474600002"],["dc.identifier.pmid","22377833"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27664"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ios Press"],["dc.relation.issn","0922-6028"],["dc.title","Modulating neuronal excitability in the motor cortex with tDCS shows moderate hemispheric asymmetry due to subjects' handedness: A pilot study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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.firstpage","1"],["dc.bibliographiccitation.journal","Journal of Parkinson's Disease"],["dc.bibliographiccitation.lastpage","16"],["dc.contributor.author","Bartl, Michael"],["dc.contributor.author","Dakna, Mohammed"],["dc.contributor.author","Schade, Sebastian"],["dc.contributor.author","Wicke, Tamara"],["dc.contributor.author","Lang, Elisabeth"],["dc.contributor.author","Ebentheuer, Jens"],["dc.contributor.author","Weber, Sandrina"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Mollenhauer, Brit"],["dc.date.accessioned","2021-12-01T09:23:00Z"],["dc.date.available","2021-12-01T09:23:00Z"],["dc.date.issued","2021"],["dc.description.abstract","Background: The MDS-Unified Parkinson’s disease (PD) Rating Scale (MDS-UPDRS) is the most used scale in clinical trials. Little is known about the predictive potential of its single items. Objective: To systematically dissect MDS-UPDRS to predict PD progression. Methods: 574 de novo PD patients and 305 healthy controls were investigated at baseline (BL) in the single-center DeNoPa (6-year follow-up) and multi-center PPMI (8-year follow-up) cohorts. We calculated cumulative link mixed models of single MDS-UPDRS items for odds ratios (OR) for class change within the scale. Models were adjusted for age, sex, time, and levodopa equivalent daily dose. Annual change and progression of the square roots of the MDS-UDPRS subscores and Total Score were estimated by linear mixed modeling. Results: Baseline demographics revealed more common tremor dominant subtype in DeNoPa and postural instability and gait disorders-subtype and multiethnicity in PPMI. Subscore progression estimates were higher in PPMI but showed similar slopes and progression in both cohorts. Increased ORs for faster progression were found from BL subscores I and II (activities of daily living; ADL) most marked for subscore III (rigidity of neck/lower extremities, agility of the legs, gait, hands, and global spontaneity of movements). Tremor items showed low ORs/negative values. Conclusion: Higher scores at baseline for ADL, freezing, and rigidity were predictors of faster deterioration in both cohorts. Precision and predictability of the MDS-UPDRS were higher in the single-center setting, indicating the need for rigorous training and/or video documentation to improve its use in multi-center cohorts, for example, clinical trials."],["dc.description.abstract","Background: The MDS-Unified Parkinson’s disease (PD) Rating Scale (MDS-UPDRS) is the most used scale in clinical trials. Little is known about the predictive potential of its single items. Objective: To systematically dissect MDS-UPDRS to predict PD progression. Methods: 574 de novo PD patients and 305 healthy controls were investigated at baseline (BL) in the single-center DeNoPa (6-year follow-up) and multi-center PPMI (8-year follow-up) cohorts. We calculated cumulative link mixed models of single MDS-UPDRS items for odds ratios (OR) for class change within the scale. Models were adjusted for age, sex, time, and levodopa equivalent daily dose. Annual change and progression of the square roots of the MDS-UDPRS subscores and Total Score were estimated by linear mixed modeling. Results: Baseline demographics revealed more common tremor dominant subtype in DeNoPa and postural instability and gait disorders-subtype and multiethnicity in PPMI. Subscore progression estimates were higher in PPMI but showed similar slopes and progression in both cohorts. Increased ORs for faster progression were found from BL subscores I and II (activities of daily living; ADL) most marked for subscore III (rigidity of neck/lower extremities, agility of the legs, gait, hands, and global spontaneity of movements). Tremor items showed low ORs/negative values. Conclusion: Higher scores at baseline for ADL, freezing, and rigidity were predictors of faster deterioration in both cohorts. Precision and predictability of the MDS-UPDRS were higher in the single-center setting, indicating the need for rigorous training and/or video documentation to improve its use in multi-center cohorts, for example, clinical trials."],["dc.identifier.doi","10.3233/JPD-212860"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94538"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","1877-718X"],["dc.relation.issn","1877-7171"],["dc.title","Longitudinal Change and Progression Indicators Using the Movement Disorder Society-Unified Parkinson’s Disease Rating Scale in Two Independent Cohorts with Early Parkinson’s Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","343"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Movement Disorders Clinical Practice"],["dc.bibliographiccitation.lastpage","345"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Schade, Sebastian"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.date.accessioned","2020-12-10T14:06:55Z"],["dc.date.available","2020-12-10T14:06:55Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1002/mdc3.v7.3"],["dc.identifier.eissn","2330-1619"],["dc.identifier.issn","2330-1619"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70073"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Levodopa Equivalent Dose Conversion Factors: An Updated Proposal Including Opicapone and Safinamide"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","78"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","npj Parkinson's Disease"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Baldelli, Luca"],["dc.contributor.author","Schade, Sebastian"],["dc.contributor.author","Jesús, Silvia"],["dc.contributor.author","Schreglmann, Sebastian R."],["dc.contributor.author","Sambati, Luisa"],["dc.contributor.author","Gómez-Garre, Pilar"],["dc.contributor.author","Halsband, Claire"],["dc.contributor.author","Calandra-Buonaura, Giovanna"],["dc.contributor.author","Adarmes-Gómez, Astrid Daniela"],["dc.contributor.author","Sixel-Döring, Friederike"],["dc.contributor.author","Provini, Federica"],["dc.contributor.authorgroup","PROPAG-AGEING consortium"],["dc.date.accessioned","2021-10-01T09:57:43Z"],["dc.date.available","2021-10-01T09:57:43Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract A prodromal phase of Parkinson’s disease (PD) may precede motor manifestations by decades. PD patients’ siblings are at higher risk for PD, but the prevalence and distribution of prodromal symptoms are unknown. The study objectives were (1) to assess motor and non-motor features estimating prodromal PD probability in PD siblings recruited within the European PROPAG-AGEING project; (2) to compare motor and non-motor symptoms to the well-established DeNoPa cohort. 340 PD siblings from three sites (Bologna, Seville, Kassel/Goettingen) underwent clinical and neurological evaluations of PD markers. The German part of the cohort was compared with German de novo PD patients (dnPDs) and healthy controls (CTRs) from DeNoPa. Fifteen (4.4%) siblings presented with subtle signs of motor impairment, with MDS-UPDRS-III scores not clinically different from CTRs. Symptoms of orthostatic hypotension were present in 47 siblings (13.8%), no different to CTRs ( p  = 0.072). No differences were found for olfaction and overall cognition; German-siblings performed worse than CTRs in visuospatial-executive and language tasks. 3/147 siblings had video-polysomnography-confirmed REM sleep behavior disorder (RBD), none was positive on the RBD Screening Questionnaire. 173/300 siblings had <1% probability of having prodromal PD; 100 between 1 and 10%, 26 siblings between 10 and 80%, one fulfilled the criteria for prodromal PD. According to the current analysis, we cannot confirm the increased risk of PD siblings for prodromal PD. Siblings showed a heterogeneous distribution of prodromal PD markers and probability. Additional parameters, including strong disease markers, should be investigated to verify if these results depend on validity and sensitivity of prodromal PD criteria, or if siblings’ risk is not elevated."],["dc.description.abstract","Abstract A prodromal phase of Parkinson’s disease (PD) may precede motor manifestations by decades. PD patients’ siblings are at higher risk for PD, but the prevalence and distribution of prodromal symptoms are unknown. The study objectives were (1) to assess motor and non-motor features estimating prodromal PD probability in PD siblings recruited within the European PROPAG-AGEING project; (2) to compare motor and non-motor symptoms to the well-established DeNoPa cohort. 340 PD siblings from three sites (Bologna, Seville, Kassel/Goettingen) underwent clinical and neurological evaluations of PD markers. The German part of the cohort was compared with German de novo PD patients (dnPDs) and healthy controls (CTRs) from DeNoPa. Fifteen (4.4%) siblings presented with subtle signs of motor impairment, with MDS-UPDRS-III scores not clinically different from CTRs. Symptoms of orthostatic hypotension were present in 47 siblings (13.8%), no different to CTRs ( p  = 0.072). No differences were found for olfaction and overall cognition; German-siblings performed worse than CTRs in visuospatial-executive and language tasks. 3/147 siblings had video-polysomnography-confirmed REM sleep behavior disorder (RBD), none was positive on the RBD Screening Questionnaire. 173/300 siblings had <1% probability of having prodromal PD; 100 between 1 and 10%, 26 siblings between 10 and 80%, one fulfilled the criteria for prodromal PD. According to the current analysis, we cannot confirm the increased risk of PD siblings for prodromal PD. Siblings showed a heterogeneous distribution of prodromal PD markers and probability. Additional parameters, including strong disease markers, should be investigated to verify if these results depend on validity and sensitivity of prodromal PD criteria, or if siblings’ risk is not elevated."],["dc.identifier.doi","10.1038/s41531-021-00219-1"],["dc.identifier.pii","219"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/89902"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-469"],["dc.relation.eissn","2373-8057"],["dc.title","Heterogeneity of prodromal Parkinson symptoms in siblings of Parkinson disease patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","321"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","AKTUELLE NEUROLOGIE"],["dc.bibliographiccitation.lastpage","326"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Csoti, Ilona"],["dc.contributor.author","Fogel, W."],["dc.contributor.author","Schade, Sebastian"],["dc.contributor.author","Schnitzler, Alfons"],["dc.contributor.author","Suedmeyer, M."],["dc.contributor.author","Winkler, Christian"],["dc.contributor.author","Winkler, J."],["dc.date.accessioned","2018-11-07T09:21:48Z"],["dc.date.available","2018-11-07T09:21:48Z"],["dc.date.issued","2013"],["dc.description.abstract","Pain and discomfort in Parkinson's disease (MP) are counted as non-motor symptoms and disease have significant impact on the well-being and health satisfaction and the quality of life of PD patients. Although they occur very often, they are still too often not adequately perceived and treated. The reasons for this are, among other things, the diversity of pain and in the challenging differential diagnosis. The disease together under the umbrella term Parkinson's disease pain of various kinds analogous to chronic pain syndrome can, however, distinguish three major subgroups: the neuropathic, nociceptive and mixed pain. The pathophysiology of pain in Parkinson's disease is very complex and still unclear in many respects. New scientific findings indicate a dysfunction of the basal ganglia in the development, transfer and processing of pain. Pain may occur already in the pre-symptomatic phase of the disease and motor symptoms precede, or they occur in analogy to the motor symptoms after diagnosis. There is pain that can be alleviated by optimizing the dopaminergic medication, but also pain, show no response to Levodopa. Pain, which occur associated with motor symptoms and off phases, indicate a necessary optimization of dopaminergic medication. Botulinum toxin has proven effective in the treatment of focal dystonias. Casuistic reports on improvement of pain and dysesthesia after deep brain stimulation. Not Levodopa responsive pain should be fed a multimodal pain therapy, which should in particular take on possible interactions with Parkinson's medications consideration."],["dc.identifier.doi","10.1055/s-0033-1343339"],["dc.identifier.isi","000323110200005"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29195"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","0302-4350"],["dc.title","Pain in Parkinson's Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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"]]