Otto, Markus

[["dc.bibliographiccitation.artnumber","e0266906"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Yousefzadeh-Nowshahr, Elham"],["dc.contributor.author","Winter, Gordon"],["dc.contributor.author","Bohn, Peter"],["dc.contributor.author","Kneer, Katharina"],["dc.contributor.author","von Arnim, Christine A. F."],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Solbach, Christoph"],["dc.contributor.author","Anderl-Straub, Sarah"],["dc.contributor.author","Polivka, Dörte"],["dc.contributor.author","Fissler, Patrick"],["dc.contributor.authorgroup","for the Alzheimer’s Disease Neuroimaging Initiative"],["dc.contributor.editor","Su, Yi"],["dc.date.accessioned","2022-05-02T08:09:28Z"],["dc.date.available","2022-05-02T08:09:28Z"],["dc.date.issued","2022"],["dc.description.abstract","Purpose The recent developments of tau-positron emission tomography (tau-PET) enable in vivo assessment of neuropathological tau aggregates. Among the tau-specific tracers, the application of 11 C-pyridinyl-butadienyl-benzothiazole 3 ( 11 C-PBB3) in PET shows high sensitivity to Alzheimer disease (AD)-related tau deposition. The current study investigates the regional tau load in patients within the AD continuum, biomarker-negative individuals (BN) and patients with suspected non-AD pathophysiology (SNAP) using 11 C-PBB3-PET. Materials and methods A total of 23 memory clinic outpatients with recent decline of episodic memory were examined using 11 C-PBB3-PET. Pittsburg compound B ( 11 C-PIB) PET was available for 17, 18 F-flurodeoxyglucose ( 18 F-FDG) PET for 16, and cerebrospinal fluid (CSF) protein levels for 11 patients. CSF biomarkers were considered abnormal based on Aβ 42 (< 600 ng/L) and t-tau (> 450 ng/L). The PET biomarkers were classified as positive or negative using statistical parametric mapping (SPM) analysis and visual assessment. Using the amyloid/tau/neurodegeneration (A/T/N) scheme, patients were grouped as within the AD continuum, SNAP, and BN based on amyloid and neurodegeneration status. The 11 C-PBB3 load detected by PET was compared among the groups using both atlas-based and voxel-wise analyses. Results Seven patients were identified as within the AD continuum, 10 SNAP and 6 BN. In voxel-wise analysis, significantly higher 11 C-PBB3 binding was observed in the AD continuum group compared to the BN patients in the cingulate gyrus, tempo-parieto-occipital junction and frontal lobe. Compared to the SNAP group, patients within the AD continuum had a considerably increased 11 C-PBB3 uptake in the posterior cingulate cortex. There was no significant difference between SNAP and BN groups. The atlas-based analysis supported the outcome of the voxel-wise quantification analysis. Conclusion Our results suggest that 11 C-PBB3-PET can effectively analyze regional tau load and has the potential to differentiate patients in the AD continuum group from the BN and SNAP group."],["dc.description.abstract","Purpose The recent developments of tau-positron emission tomography (tau-PET) enable in vivo assessment of neuropathological tau aggregates. Among the tau-specific tracers, the application of 11 C-pyridinyl-butadienyl-benzothiazole 3 ( 11 C-PBB3) in PET shows high sensitivity to Alzheimer disease (AD)-related tau deposition. The current study investigates the regional tau load in patients within the AD continuum, biomarker-negative individuals (BN) and patients with suspected non-AD pathophysiology (SNAP) using 11 C-PBB3-PET. Materials and methods A total of 23 memory clinic outpatients with recent decline of episodic memory were examined using 11 C-PBB3-PET. Pittsburg compound B ( 11 C-PIB) PET was available for 17, 18 F-flurodeoxyglucose ( 18 F-FDG) PET for 16, and cerebrospinal fluid (CSF) protein levels for 11 patients. CSF biomarkers were considered abnormal based on Aβ 42 (< 600 ng/L) and t-tau (> 450 ng/L). The PET biomarkers were classified as positive or negative using statistical parametric mapping (SPM) analysis and visual assessment. Using the amyloid/tau/neurodegeneration (A/T/N) scheme, patients were grouped as within the AD continuum, SNAP, and BN based on amyloid and neurodegeneration status. The 11 C-PBB3 load detected by PET was compared among the groups using both atlas-based and voxel-wise analyses. Results Seven patients were identified as within the AD continuum, 10 SNAP and 6 BN. In voxel-wise analysis, significantly higher 11 C-PBB3 binding was observed in the AD continuum group compared to the BN patients in the cingulate gyrus, tempo-parieto-occipital junction and frontal lobe. Compared to the SNAP group, patients within the AD continuum had a considerably increased 11 C-PBB3 uptake in the posterior cingulate cortex. There was no significant difference between SNAP and BN groups. The atlas-based analysis supported the outcome of the voxel-wise quantification analysis. Conclusion Our results suggest that 11 C-PBB3-PET can effectively analyze regional tau load and has the potential to differentiate patients in the AD continuum group from the BN and SNAP group."],["dc.identifier.doi","10.1371/journal.pone.0266906"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107385"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-561"],["dc.relation.eissn","1932-6203"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Quantitative analysis of regional distribution of tau pathology with 11C-PBB3-PET in a clinical setting"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","919"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","927"],["dc.bibliographiccitation.volume","114"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Esselmann, Herrmann"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T11:06:56Z"],["dc.date.available","2018-11-07T11:06:56Z"],["dc.date.issued","2007"],["dc.description.abstract","To evaluate variations in amyloid beta (A beta) peptide pattern in cerebrospinal fluid (CSF) in neurodegenerative disorders. A recently estabfished quantitative urea-based A beta-sodium-dodecylsulfate-polyacrylamide-gel-electrophoresis with western immunoblot (AP-SDS-PAGE/immunoblot) revealed a highly conserved A beta peptide (A beta 1-37, 1-38, 1-39, 1-40, 1-42) pattern in CSF. We asked whether the variation might be useful to further elucidate the overlap between or distinctions among neurodegenerative diseases in A beta-processing. We used the A beta-SDS-PAGE/immunoblot to investigate CSF for diseasespecific A beta peptide patterns. CSF samples from 96 patients with mainly clinically diagnosed Alzheimer's disease (n = 15), progressive supranuclear palsy (n = 20), corticobasal degeneration (n =: 12), Parkinson's disease (n = 11), multiple systems atrophy (n = 18), and dementia with Lewy-bodies (n = 20) were analysed as well a comparison group (n = 19). The A beta peptide patterns varied between tauopathies and synucleinopathies and between all diseases and the comparison group, possibly due to the influence of tau and a-synuctein on Ap-processing."],["dc.identifier.doi","10.1007/s00702-007-0629-4"],["dc.identifier.isi","000248001800007"],["dc.identifier.pmid","17318305"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52433"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","0300-9564"],["dc.title","Tauopathies and synucleinopathies: Do cerebrospinal fluid beta-amyloid peptides reflect disease-specific pathogenesis?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","355"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","ELECTROPHORESIS"],["dc.bibliographiccitation.lastpage","362"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Halbgebauer, Steffen"],["dc.contributor.author","Haußmann, Ute"],["dc.contributor.author","Klafki, Hans"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2017-09-07T11:44:42Z"],["dc.date.available","2017-09-07T11:44:42Z"],["dc.date.issued","2014"],["dc.description.abstract","The detection of oligoclonal bands (OCBs) in cerebrospinal fluid is an indicator of intrathecal synthesis of immunoglobulins which is a neurochemical sign of chronic inflammatory brain diseases. Intrathecally synthesized IgGs are typically observed in patients with multiple sclerosis. The current standard protocol for the detection of OCBs is IEF on agarose or polyacrylamide gels followed by immunoblotting or silver staining. These methods are time consuming, show substantial interlaboratory variation and cannot be used in a high throughput-approach. We have developed a new nanoscale method for the detection of OCBs based on automated capillary IEF followed by immunological detection. Evidence for intrathecal IgG synthesis was found in all tested patients (n = 27) with multiple sclerosis, even in two subjects who did not have oligoclonal bands according to standard methods. The test specificity was at 97.5% (n = 19). Our findings indicate that the novel OCB-CIEF-immunoassay is suitable for the rapid and highly sensitive detection of OCBs in clinical samples. Furthermore, the method allows for a higher sample throughput than the current standard methods."],["dc.identifier.doi","10.1002/elps.201400339"],["dc.identifier.gro","3151730"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8550"],["dc.language.iso","en"],["dc.notes.status","public"],["dc.notes.submitter","chake"],["dc.relation.issn","0173-0835"],["dc.title","Capillary isoelectric focusing immunoassay as a new nanoscale approach for the detection of oligoclonal bands"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","alz.12794"],["dc.bibliographiccitation.journal","Alzheimer's & Dementia"],["dc.contributor.author","Schaeverbeke, Jolien"],["dc.contributor.author","Tomé, Sandra O."],["dc.contributor.author","Ronisz, Alicja"],["dc.contributor.author","Ospitalieri, Simona"],["dc.contributor.author","von Arnim, Christine A. F."],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Vandenberghe, Rik"],["dc.contributor.author","Thal, Dietmar Rudolf"],["dc.date.accessioned","2022-10-04T10:21:57Z"],["dc.date.available","2022-10-04T10:21:57Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1002/alz.12794"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114547"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-600"],["dc.relation.eissn","1552-5279"],["dc.relation.issn","1552-5260"],["dc.title","Neuronal loss of the nucleus basalis of Meynert in primary progressive aphasia is associated with Alzheimer's disease neuropathological changes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","690"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","694"],["dc.bibliographiccitation.volume","248"],["dc.contributor.author","Ratzka, Peter"],["dc.contributor.author","Schröter, Andreas"],["dc.contributor.author","Cepek, Lukas"],["dc.contributor.author","Henkel, Karsten"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Poser, S."],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2017-09-07T11:44:31Z"],["dc.date.available","2017-09-07T11:44:31Z"],["dc.date.issued","2006"],["dc.description.abstract","Creutzfeldt-Jakob disease (CJD) belongs to the group of transmissible spongiform encephalopathies. It is suspected that a pathologically altered form of the prion protein (PrPSc) is the decisive trigger of the disease. Data from animal experiments suggest an involvement of the lymphatic system in the intracorporal transport of PrPSc. However, it has not so far been possible to detect PrPSc on mononuclear cells (MNCs) either in the sporadic form of CJD or in the new variant of CJD (vCJD). In order to determine a possible alteration of MNCs in CJD, we investigated the natural and induced apoptotic behaviour of these cells.MNCs from 19 patients with sporadic CJD and from 20 patients with other neurological disorders were used. The cells were analysed by fluorescence cytometry with and without apoptosis induction by xanthine oxidase and hypoxanthine. The apoptosis rate was quantified using the stain 7-amino-actinomycin D (7-AAD). In the morphological investigation of the cells before apoptosis induction, there were no significant differences between the groups with regard to cell size and granularity of the MNCs. After apoptosis induction, the typical significant decrease in cell size and increase in granularity of the cells occurred in both groups. Significant differences between the patient populations were not found.For the first time, our investigation has demonstrated that a functional impairment of MNCs with regard to their apoptotic behaviour does not occur in sporadic CJD. It remains open to question whether this mechanism plays an important role in forms of transmissible encephalopathy other than sporadic CJD, especially after oral transmission."],["dc.identifier.doi","10.1007/pl00007834"],["dc.identifier.gro","3151691"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8510"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","chake"],["dc.relation.issn","0340-5354"],["dc.title","Unaltered apoptotic behaviour of mononuclear cells from patients with sporadic Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2485"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","2490"],["dc.bibliographiccitation.volume","73"],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Otto, M."],["dc.contributor.author","Baxter, H. C."],["dc.contributor.author","Bodemer, M."],["dc.contributor.author","Steinacker, P."],["dc.contributor.author","Bahn, E."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Kornhuber, J."],["dc.contributor.author","Kretzschmar, H. A."],["dc.contributor.author","Poser, S."],["dc.contributor.author","Rüther, E."],["dc.contributor.author","Aitken, A."],["dc.date.accessioned","2017-09-07T11:44:33Z"],["dc.date.available","2017-09-07T11:44:33Z"],["dc.date.issued","1999"],["dc.description.abstract","Two-dimensional polyacrylamide gel electrophoresis of CSF has been used in the diagnosis of Creutzfeldt-Jakob disease (CJD). One of the two diagnostic protein spots was identified as isoform(s) of the 14-3-3 family of abundant brain proteins. This has led to the development of one-dimensional 14-3-3 sodium dodecyl sulfate polyacrylamide gel electrophoresis immunoblot, which is currently used to support the diagnosis of CJD. In the present study employing western blot analysis, we have identified the panel of 14-3-3 isoforms that appear in the CSF of 10 patients with CJD compared with 10 patients with other dementias. The results clearly show that the 14-3-3 isoforms β, γ, ε, and η are present in the CSF of patients with CJD and can be used to differentiate other dementias. 14-3-3η also gave a baseline signal in all patients with other dementias, including six patients with Alzheimer's disease. The presence of 14-3-3η in the CSF of a patient with herpes simplex encephalitis was particularly noteworthy. This study has determined that isoform-specific 14-3-3 antibodies against β, γ, and ε should be considered for the neurochemical differentiation of CJD from other neurodegenerative diseases."],["dc.identifier.doi","10.1046/j.1471-4159.1999.0732485.x"],["dc.identifier.gro","3151688"],["dc.identifier.pmid","10582609"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8506"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0022-3042"],["dc.title","Isoform Pattern of 14-3-3 Proteins in the Cerebrospinal Fluid of Patients with Creutzfeldt-Jakob Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Alzheimer's Research & Therapy"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Halbgebauer, Steffen"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Riedel, Daniel"],["dc.contributor.author","Oeckl, Patrick"],["dc.contributor.author","Anderl-Straub, Sarah"],["dc.contributor.author","Lombardi, Jolina"],["dc.contributor.author","von Arnim, Christine A. F."],["dc.contributor.author","Nagl, Magdalena"],["dc.contributor.author","Giese, Armin"],["dc.contributor.author","Ludolph, Albert C."],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2022-12-01T08:31:24Z"],["dc.date.available","2022-12-01T08:31:24Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract\n \n Background\n Visinin-like protein 1 (VILIP-1) belongs to the group of emerging biomarkers with the potential to support the early diagnosis of Alzheimer’s disease (AD). However, studies investigating the differential diagnostic potential in cerebrospinal fluid (CSF) are rare and are not available for blood.\n \n \n Methods\n We set up a novel, sensitive single molecule array (Simoa) assay for the detection of VILIP-1 in CSF and serum. In total, paired CSF and serum samples from 234 patients were investigated: 73 AD, 18 behavioral variant frontotemporal dementia (bvFTD), 26 parkinsonian syndromes, 20 amyotrophic lateral sclerosis (ALS), 22 Creutzfeldt-Jakob disease (CJD), and 75 non-neurodegenerative control (Con) patients. The differential diagnostic potential of CSF and serum VILIP-1 was assessed using the receiver operating characteristic curve analysis and findings were compared to core AD biomarkers.\n \n \n Results\n \n CSF and serum VILIP-1 levels correlated weakly (\n r\n =0.32 (CI: 0.20–0.43),\n p\n <0.0001). VILIP-1 concentrations in CSF and serum were elevated in AD compared to Con (\n p\n <0.0001 and\n p\n <0.01) and CJD (\n p\n <0.0001 for CSF and serum), and an increase in CSF was observed already in early AD stages (\n p\n <0.0001). In the discrimination of AD versus Con, we could demonstrate a strong diagnostic potential for CSF VILIP-1 alone (area under the curve (AUC): 0.87), CSF VILIP-1/CSF Abeta 1-42 (AUC: 0.98), and serum VILIP-1/CSF Abeta 1-42 ratio (AUC: 0.89).\n \n \n \n Conclusions\n We here report on the successful establishment of a novel Simoa assay for VILIP-1 and illustrate the potential of CSF and serum VILIP-1 in the differential diagnosis of AD with highest levels in CJD."],["dc.description.sponsorship","Intramural funding University of Ulm"],["dc.description.sponsorship","EU Joint Programme-Neurodegenerative Diseases networks Genfi-Prox"],["dc.description.sponsorship","German Federal Ministry of Education and Research"],["dc.description.sponsorship","EU (Moodmarker) program"],["dc.description.sponsorship","German Research Foundation/DFG"],["dc.description.sponsorship","Foundation of the state Baden-Württemberg"],["dc.description.sponsorship","Boehringer Ingelheim Ulm University BioCenter"],["dc.description.sponsorship","Thierry Latran Foundation"],["dc.description.sponsorship","Martin-Luther-Universität Halle-Wittenberg"],["dc.identifier.doi","10.1186/s13195-022-01122-4"],["dc.identifier.pii","1122"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118163"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-621"],["dc.relation.eissn","1758-9193"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Visinin-like protein 1 levels in blood and CSF as emerging markers for Alzheimer’s and other neurodegenerative diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","34"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","41"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Guerchet, Maelenn"],["dc.contributor.author","Houinato, Dismand"],["dc.contributor.author","Paraiso, Moussiliou Noel"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Nubukpo, Philippe"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Clement, Jean-Pierre"],["dc.contributor.author","Preux, Pierre-Marie"],["dc.contributor.author","Dartigues, Jean-Francos"],["dc.date.accessioned","2018-11-07T08:34:21Z"],["dc.date.available","2018-11-07T08:34:21Z"],["dc.date.issued","2009"],["dc.description.abstract","Background/Aims: Dementia is increasing as a priority public health problem because of the ageing of the world population. Our goal was to estimate dementia and cognitive impairment prevalence in an elderly population of rural Benin. Methods: In a door-to-door survey, elderly people aged 65 years and above were screened using the Community Screening Interview for Dementia and the Five-Word Test. Results: The prevalence of cognitive impairment was 10.4% and that of dementia was 2.6%. Age, current depressive disorder and absence of the APOE epsilon 2 allele were significantly associated with cognitive impairment. Conclusion: Prevalence of dementia and cognitive impairment appears to be lower in this study than in developed countries. Copyright (c) 2009 S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000188661"],["dc.identifier.isi","000262899200005"],["dc.identifier.pmid","19136831"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9316"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17790"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1420-8008"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Cognitive Impairment and Dementia in Elderly People Living in Rural Benin, West Africa"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","200"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","208"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Brechlin, Peter"],["dc.contributor.author","Schindehuette, Jan"],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T10:33:04Z"],["dc.date.available","2018-11-07T10:33:04Z"],["dc.date.issued","2006"],["dc.description.abstract","Measurement of tau-protein and beta-amyloid(1-42) (A beta 42) in cerebrospinal fluid (CSF) has gained increasing acceptance in the differential diagnosis of Alzheimer's disease. We investigated CSF tau-protein and A beta 42 concentrations in 73 patients with advanced idiopathic Parkinson's disease with dementia (PDD) and 23 patients with idiopathic Parkinson's disease without dementia (PD) and in a comparison group of 41 non-demented neurological patients (CG) using commercially available enzyme-linked-immunoabsorbant- assay ( ELISA). tau-Protein levels were statistically significantly higher and A beta 42 lower in the PDD patients compared to PD patients and the CG. This observation was most marked ( p < 0.05) in a subgroup of patients with PDD carrying the apolipoprotein genotype epsilon 3/epsilon 3. The distribution of the apolipoprotein genotypes in PDD and PD patients was similar to that of the CG. Although a significant difference in tau-protein values was observed between PDD and CG, no diagnostic cut-off value was established. These findings suggest that such protein CSF changes may help to support the clinical diagnosis of cognitive decline in PD and that there may be apolipoprotein-E-isoform- specific differences in CSF protein regulation in advanced PDD. Copyright (C) 2006 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000094871"],["dc.identifier.isi","000242167100003"],["dc.identifier.pmid","16899997"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44513"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1420-8008"],["dc.title","Beta-amlyoid 1-42 and tau-protein in cerebrospinal fluid of patients with Parkinson's disease dementia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","387"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Biochemical Society Transactions"],["dc.bibliographiccitation.lastpage","391"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Baxter, H. C."],["dc.contributor.author","Fraser, J. R."],["dc.contributor.author","Liu, W.-G."],["dc.contributor.author","Forster, J. L."],["dc.contributor.author","Clokie, S."],["dc.contributor.author","Steinacker, P."],["dc.contributor.author","Otto, M."],["dc.contributor.author","Bahn, E."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Aitken, A."],["dc.date.accessioned","2017-09-07T11:44:41Z"],["dc.date.available","2017-09-07T11:44:41Z"],["dc.date.issued","2002"],["dc.description.abstract","14-3-3 proteins are involved in signalling processes in neuronal cells. Using isoform-specific antibodies we have examined the variation in 14-3-3 isoform neurolocation in normal and scrapie-infected murine brain and show that in defined areas of the brain there are significant changes associated with the pathology of the disease process. The appearance of 14-3-3 proteins in the cerebrospinal fluid (CSF) is a consequence of neuronal disease and the detection of specific isoforms of the 14-3-3 proteins in the CSF is characteristic of some neurodegenerative diseases. In this study, monitoring specifically for theγ 14-3-3 isoform in the CSF by both Western-blot analysis and ELISA we can show a level of correlation between the assays."],["dc.identifier.doi","10.1042/bst0300387"],["dc.identifier.gro","3151722"],["dc.identifier.pmid","12196100"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8543"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0300-5127"],["dc.title","Specific 14-3-3 isoform detection and immunolocalization in prion diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]