Schröter, Andreas

[["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","699"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","705"],["dc.bibliographiccitation.volume","249"],["dc.contributor.author","Henkel, K."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Hertel, A."],["dc.contributor.author","Gratz, K. F."],["dc.contributor.author","Schroter, A."],["dc.contributor.author","Tschampa, Henriette J."],["dc.contributor.author","Bihl, H."],["dc.contributor.author","Bull, U."],["dc.contributor.author","Grunwald, F."],["dc.contributor.author","Drzezga, A."],["dc.contributor.author","Spitz, J."],["dc.contributor.author","Poser, Sigrid"],["dc.date.accessioned","2018-11-07T10:29:01Z"],["dc.date.available","2018-11-07T10:29:01Z"],["dc.date.issued","2002"],["dc.description.abstract","The aim of this study was to explore the sites of metabolic changes with [F-18]2-fluoro-2-desoxy-D-glucose (FDG) and positron emission tomography (PET) in patients with Creutzfeldt-Jakob disease and to correlate the findings with clinical symptoms. Static [F-18]FDG-PET studies of eight patients with the diagnosis of confirmed or probable CJD were retrospectively analysed by two physicians from departments of nuclear medicine independently with a strong interrater agreement (kappa=0,98). The clinical data of the patients, based on a standardized evaluation by physicians from the German Creutzfeldt-Jakob disease surveillance study, was correlated with the PET findings. [F-18]FDG-PET shows widespread hypometabolism in CJD. All patients had a reduction of cerebral glucose metabolism in at least one temporal or parietal region. Additionally in 7 of our own 8 cases and 3 of 4 cases from the literature the occipital lobe, the cerebellum or the basal ganglia were involved. These findings differ from typical patterns of hypometabolism in Alzheimer's disease and other neurodegenerative disorders. In two thirds of the cases the distribution was markedly asymmetric. Myoclonus was present in five out of our eight own cases. Our data suggest that myoclonus might correlate with metabolic impairment of contralateral parietal and temporal lobes. In three of four patients with visual symptoms FDG uptake was reduced in the visual cortex bilaterally. Typical hyperintensities on MRI were only found in two of the eight cases at the time of PET-studies. Our results demonstrate that [F-18]FDG-PET appears to be a sensitive investigation in CJD and could be useful to differentiate CJD from other neuro degenerative disorders."],["dc.identifier.doi","10.1007/s00415-002-0695-3"],["dc.identifier.isi","000176407100008"],["dc.identifier.pmid","12111302"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43553"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0340-5354"],["dc.title","Positron emission tomography with [F-18]FDG in the diagnosis of Creutzfeldt-Jakob disease (CJD)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","91"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Der Nervenarzt"],["dc.bibliographiccitation.lastpage","95"],["dc.bibliographiccitation.volume","71"],["dc.contributor.author","Kropp, Silke"],["dc.contributor.author","Finkenstaedt, M."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Schroter, A."],["dc.contributor.author","Poser, Sigrid"],["dc.date.accessioned","2018-11-07T10:44:49Z"],["dc.date.available","2018-11-07T10:44:49Z"],["dc.date.issued","2000"],["dc.description.abstract","Today the diagnosis of Creutzfeldt-Jakob disease (UD) is proven only postmortem or by evidence of neuropathology. During the patient's lifetime EEG recordings or cerebrospinal fluid analysis may support the diagnosis. In most cases, T2-MRI scans show hyperintensities of the basal ganglia. A new imaging technique called diffusion-weighted MRI (DWI) has recently been established. The sensitivity of DWI was evaluated in five patients suspected of CJD. All five cases showed hyperintense signal changes in the basal ganglia on DWI sequences. These findings were more pronounced in DWI than in T2, FLAIR, or PD-weighted images. Thus, DWI seems to be the most sensitive sequence for detecting changes in patients with suspected UD. Moreover, its short scanning time ensures that fewer artifacts occur, especially in the case of myoclonus."],["dc.identifier.doi","10.1007/s001150070001"],["dc.identifier.isi","000085384700004"],["dc.identifier.pmid","10703009"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47357"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0028-2804"],["dc.title","Diffusion-weighted MRI in patients with Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1751"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","ARCHIVES OF NEUROLOGY"],["dc.bibliographiccitation.lastpage","1757"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Schroter, A."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Henkel, K."],["dc.contributor.author","Tschampa, Henriette J."],["dc.contributor.author","Finkenstaedt, M."],["dc.contributor.author","Poser, Sigrid"],["dc.date.accessioned","2018-11-07T09:23:41Z"],["dc.date.available","2018-11-07T09:23:41Z"],["dc.date.issued","2000"],["dc.description.abstract","Objective: To evaluate the diagnostic usefulness of magnetic resonance imaging (MRI) in the clinical diagnosis of Creutzfeldt-Jakob disease (CJD). Background: Creutzfeldt-Jakob disease is a rare neurodegenerative disease that belongs to the group of human spongiform encephalopathies and usually affects elderly people. It is clinically characterized by rapidly progressive dementia and development of neurological symptoms, such as myoclonus or ataxia. Until now, neuroradiologic investigations have only played a minor role in establishing the clinical diagnosis of CJD, and they are often performed to exclude differential diagnoses. Setting: A university hospital, base of the German National Creutzfeldt-Jakob Disease Surveillance Study. Methods and Patients: In this study, MRIs from suspected cases of CJD were examined by one investigator blinded to the diagnosis. Patients were classified according to the established clinical and neuropathological criteria. Results: Bilateral symmetric, high signal intensities on T2-weighted MRIs were present in the basal ganglia of 109 (67%) of 162 patients with CJD. In the control group, which consisted of non-CJD dementia patients, these abnormalities on T2-weighted MRIs were found in 4 (7%) of 58 patients. This corresponds to a high specificity in the differential diagnosis of CJD. Conclusion: These results indicate that MRI is a useful and valuable tool with reasonable sensitivity (67%) and high specificity (93%) and should be considered as an additional cornerstone in the clinical diagnosis of CJD."],["dc.identifier.doi","10.1001/archneur.57.12.1751"],["dc.identifier.isi","000165810400011"],["dc.identifier.pmid","11115241"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29640"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Medical Assoc"],["dc.relation.issn","0003-9942"],["dc.title","Magnetic resonance imaging in the clinical diagnosis of Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","204"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","206"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Schmidt, H."],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Niedmann, P."],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Schroter, A."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Poser, Sigrid"],["dc.date.accessioned","2018-11-07T10:52:21Z"],["dc.date.available","2018-11-07T10:52:21Z"],["dc.date.issued","2004"],["dc.description.abstract","The diagnosis of Creutzfeldt- Jakob disease (CJD) is still made by exclusion of other dementias. We now evaluated lactate dehydrogenase (LDH) in the cerebrospinal fluid (CSF) as a possible additional diagnostic tool. CSF LDH levels of patients with CJD ( n = 26) were compared with those in other dementias ( n = 28). LDH isoenzymes were determined in a subset ( n = 9). Total LDH and isoenzyme LDH-1 were significantly higher, whereas the fractions of LDH-2 and LDH-3 were significantly lower in CJD patients. We conclude that in addition to established CSF parameters, LDH and its isoenzymes might serve as a further help to discriminate between CJD and other dementias. Copyright (C) 2004 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000076357"],["dc.identifier.isi","000220084000016"],["dc.identifier.pmid","14739545"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49094"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1420-8008"],["dc.title","CSF lactate dehydrogenase activity in patients with Creutzfeldt-Jakob disease exceeds that in other dementias"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","106"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Critical Reviews in Plant Sciences"],["dc.bibliographiccitation.lastpage","119"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Baldermann, S."],["dc.contributor.author","Blagojević, L."],["dc.contributor.author","Frede, K."],["dc.contributor.author","Klopsch, R."],["dc.contributor.author","Neugart, S."],["dc.contributor.author","Neumann, A."],["dc.contributor.author","Ngwene, B."],["dc.contributor.author","Norkeweit, J."],["dc.contributor.author","Schröter, D."],["dc.contributor.author","Schröter, A."],["dc.contributor.author","Schweigert, F. J."],["dc.contributor.author","Wiesner, M."],["dc.contributor.author","Schreiner, M."],["dc.date.accessioned","2020-11-05T15:00:43Z"],["dc.date.available","2020-11-05T15:00:43Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1080/07352689.2016.1201399"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/68391"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-352.5"],["dc.relation.eissn","1549-7836"],["dc.relation.issn","0735-2689"],["dc.title","Are Neglected Plants the Food for the Future?"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","450"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","456"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Kohler, K."],["dc.contributor.author","Kortner, K."],["dc.contributor.author","Bartl, Mario"],["dc.contributor.author","Jastrow, U."],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Schroter, A."],["dc.contributor.author","Finkenstaedt, M."],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T10:46:27Z"],["dc.date.available","2018-11-07T10:46:27Z"],["dc.date.issued","2004"],["dc.description.abstract","Objective: To assess if clinical features, prion protein codon 129, and molecular subtype correlate with MRI basal ganglia hyperintensity in sporadic Creutzfeldt-Jakob disease (CJD). Methods: The authors studied 219 patients including 153 confirmed CJD cases for their neurologic symptoms and MRI findings. The MRI was assessed by a blinded investigator for the presence of high signal intensity on T2-weighted images in the basal ganglia. Results: Patients with basal ganglia high signal on T2-weighted images were more likely to present with rapid progressive dementia in an early stage and shorter disease duration (median 6.7 months and 8.6 months). Surprisingly, among the CJD cases, patients without signal increase of the basal ganglia were shown to have a higher frequency of extrapyramidal disturbances (82% vs 70%). More striking differences were found for symptoms such as depression and sensory disturbances, which were more frequent among cases without signal increase. MRI was more likely to be diagnostic in patients with MV2 molecular subtype. Conclusions: Selected clinical and pathologic features correlate with the presence of basal ganglia high signal on T2-weighted MRI in patients with definite or probable CJD."],["dc.identifier.isi","000223229100009"],["dc.identifier.pmid","15314808"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47747"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0028-3878"],["dc.title","Sporadic Creutzfeldt-Jakob disease - Magnetic resonance imaging and clinical findings"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","33"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neurology Neurosurgery & Psychiatry"],["dc.bibliographiccitation.lastpage","39"],["dc.bibliographiccitation.volume","71"],["dc.contributor.author","Tschampa, Henriette J."],["dc.contributor.author","Neumann, M."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Henkel, K."],["dc.contributor.author","Schroter, A."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Steinhoff, B. J."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Poser, Sigrid"],["dc.date.accessioned","2018-11-07T08:56:13Z"],["dc.date.available","2018-11-07T08:56:13Z"],["dc.date.issued","2001"],["dc.description.abstract","Objectives-To describe the clinical presentation of patients with Alzheimer's disease (AD) or dementia with Lewy bodies (DLB) who were suspected of having Creutzfeldt-Jakob disease (CJD) and to investigate whether current clinical diagnostic criteria cover these atypical forms of AD and DLB. Methods-Brains from necropsy were examined for the diagnosis of CJD at the German reference centre for spongiform encephalopathies. Symptoms and signs in patients with suspected CJD in whom necropsy showed AD (n=19) or DLB (n=12) were analysed. Their data were compared with a group of patients with CJD (n=25) to determine overlapping and discriminating clinical features. All patients were classified according to clinical diagnostic criteria for CJD, AD, and DLB. Results-Demented patients were suspected of having CJD if disease was rapidly progressing and/or focal neurological signs appeared and/or an EEG showed sharp wave complexes. Myoclonus and limb rigidity were the most common neurological signs in all three dementias. DLB was not suspected in any patient, although patients with DLB showed parkinsonism (58%) and fluctuations (58%). Periodic sharp wave complexes (PSWCs) in EEG typical of CJD were found in five patients with AD and one patient with DLB. 14-3-3 Protein in CSF was detected in 20 patients with CJD, in two patients with AD, but not in any patient with DLB. Although most patients with DLB or AD met the clinical criteria for their respective diagnosis (74% and 90%), they also fulfilled criteria for CJD (42% and 58%). Conclusions-in patients with rapidly progressive dementia and focal neurological signs, CJD should be the first line diagnosis. Facing the triad dementia, myoclonus, and rigidity, AD should be considered if the disease course is longer and DLB is the differential diagnosis if parkinsonism or fluctuations are present. Findings on EEG or CSF typical of CJD do not exclude AD or DLB."],["dc.identifier.doi","10.1136/jnnp.71.1.33"],["dc.identifier.isi","000169436500009"],["dc.identifier.pmid","11413259"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23085"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","British Med Journal Publ Group"],["dc.relation.issn","0022-3050"],["dc.title","Patients with Alzheimer's disease and dementia with Lewy bodies mistaken for Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","150"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neurobiology of Disease"],["dc.bibliographiccitation.lastpage","156"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Arlt, Soenke"],["dc.contributor.author","Kontush, A."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Buhmann, Carsten"],["dc.contributor.author","Jacobi, C."],["dc.contributor.author","Schroter, A."],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Beisiegel, U."],["dc.date.accessioned","2018-11-07T10:23:28Z"],["dc.date.available","2018-11-07T10:23:28Z"],["dc.date.issued","2002"],["dc.description.abstract","Oxidative pathomechanisms play an important role in neurodegenerative diseases like Alzheimer's disease (AD). It has been shown that lipid peroxidation in cerebrospinal fluid (CSF) and plasma is increased in AD. To assess the role of oxidative stress in Creutzfeldt-Jakob disease (CJD), we investigated the oxidizability of lipids, the lipid composition and the levels of the antioxidants ascorbate and alpha-tocopherol in CSF and plasma of 15 CJD patients and 12 neurologically healthy controls. CSF and plasma lipid peroxidation was increased in CJD patients and polyunsaturated fatty acids were reduced in CSF of these patients. Ascorbate levels were lower in CSF and plasma of CJD patients, while alpha-tocopherol was found to be decreased in CSF but not in plasma. These results support the hypothesis that oxidative mechanisms are involved in the pathogenesis of CJD and provide a rationale for the use of antioxidants in the therapy of this disease. (C) 2002 Elsevier Science (USA)."],["dc.identifier.doi","10.1006/nbdi.2002.0496"],["dc.identifier.isi","000177049700008"],["dc.identifier.pmid","12127153"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42460"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","0969-9961"],["dc.title","Increased lipid peroxidation in cerebrospinal fluid and plasma from patients with Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","29"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","32"],["dc.bibliographiccitation.volume","343"],["dc.contributor.author","Ratzka, Peter"],["dc.contributor.author","Döhlinger, Susanne"],["dc.contributor.author","Cepek, Lukas"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Arlt, Sönke"],["dc.contributor.author","Jacobi, Christian"],["dc.contributor.author","Schröter, Andreas"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Poser, Sigrid"],["dc.date.accessioned","2021-06-01T10:50:14Z"],["dc.date.available","2021-06-01T10:50:14Z"],["dc.date.issued","2003"],["dc.description.abstract","In Creutzfeldt-Jakob disease (CJD), progressive neuronal cell death probably occurs as a result of a change in conformation of the physiological prion protein (PrPC). There is evidence of participation of the lymphatic system and in particular of lymphocytes in the intracorporeal transportation of the pathological prion protein (PrPSc) in new variant CJD and scrapie. Using fluorescence cytometry, we investigated a possible alteration of PrPC on lymphocytes of patients with sporadic CJD. We demonstrated a significantly lower binding pattern of antibodies (3F4) against physiological prion protein to lymphocytes of patients with sporadic CJD (n = 16) compared with control patients. In contrast this difference was not found on platelets (n = 23). For the first time we were able to present a measurable difference of antibody binding on lymphocytes of patients with CID. One interpretation of this finding is that lymphocytes patrolling the brain bind and transport PrPSc which has a lower binding affinity for the antibodies directed against physiological PrP. (C) 2003 Elsevier Science Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/S0304-3940(03)00315-X"],["dc.identifier.isi","000183128900008"],["dc.identifier.pmid","12749990"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86584"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","Different binding pattern of antibodies to prion protein on lymphocytes from patients with sporadic Creutzfeldt–Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]