Schröter, Andreas

[["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","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","1099"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","1102"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Esselmann, Herrmann"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Neumann, M."],["dc.contributor.author","Schroter, A."],["dc.contributor.author","Ratzka, P."],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Wiltfang, J."],["dc.date.accessioned","2018-11-07T08:45:04Z"],["dc.date.available","2018-11-07T08:45:04Z"],["dc.date.issued","2000"],["dc.description.abstract","Objectives: Decreased levels of A beta(1-42) are found in CSF of patients with AD. Because early stages of Creutzfeldt-Jakob disease (CJD) and AD share several clinical features, we investigated A beta(1-42) levels in CSF of these groups, inferring that this might give additional help in differentiating patients with CJD from AD patients. Methods: We investigated 27 patients with CJD, 14 patients with AD, 19 patients with other dementias, and 20 nondemented controls (NDC) for A beta(1-42) in CSF. Twenty-four of the 27 CJD patients were neuropathologically verified. All the neuropathologically verified patients presented with a type 1 prion protein pattern. CJD patients were all homozygous for methionine at codon 129. Except in five CJD patients, no beta-amyloid plaques were seen. Additionally, APOE status was determined in patients with CJD. Results: Levels of A beta(1-42) in CSF were decreased in patients with AD as well as in CJD. Levels of A beta(1-42) in CSF of patients with CJD and AD were significantly different from the other dementia and NDC groups. There was no substantial difference between the CJD and AD groups (p = 0.66). Decreased levels of A beta(1-42) did not correlate with the APOE epsilon 4 load in patients with CJD. Conclusion: Low levels of A beta(1-42) in CSF do not exclude a diagnosis of CJD. Decreased levels of A beta(1-42) in CSF can occur without p-amyloid plaque formation in the brain. However, the underlying mechanism of this phenomenon must be elucidated."],["dc.identifier.isi","000085785700017"],["dc.identifier.pmid","10720281"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20346"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0028-3878"],["dc.title","Decreased beta-amyloid(1-42) in cerebrospinal fluid of 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","323"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","329"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Giese, A."],["dc.contributor.author","Bodemer, Monika"],["dc.contributor.author","Schroter, A."],["dc.contributor.author","Henkel, K."],["dc.contributor.author","Tschampa, Henriette J."],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Pfahlberg, Annette"],["dc.contributor.author","Steinhoff, B. J."],["dc.contributor.author","Gefeller, Olaf"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Poser, Sigrid"],["dc.date.accessioned","2018-11-07T10:23:19Z"],["dc.date.available","2018-11-07T10:23:19Z"],["dc.date.issued","2000"],["dc.description.abstract","According to the recently established molecular basis for phenotypic heterogeneity of sporadic Creutzfeldt-Jakob disease (CJD), six different phenotypes are characterized by the size of the protease-resistant fragment of the pathological prion protein (types 1 and 2) and homozygosity or heterozygosity for methionine or valine at codon 129 of the prion protein gene (designated by MM1, MM2, MV1, MV2, VV1, and VV2). In the present investigation, we analyzed the value of commonly used clinical tests (electroencephalogram [EEG], detection of 14-3-3 protein in cerebrospinal fluid [CSF], and hyperintensity of the basal ganglia in magnetic resonance imaging) for the clinical diagnosis in each CJD phenotype. The detection of periodic sharp and slow wave complexes in the EEG is reliable in the clinical diagnosis of MM1 and MV1 patients only. The CSF analysis for 14-3-3 protein showed high sensitivity in all analyzed subgroups with the exception of MV2 patients. Valine-homozygous patients had a negative EEG, but most had detectable levels of neuronal proteins in the CSF. The sensitivity of the magnetic resonance imaging was 70%, irrespective of the subgroup, but was particularly reliable in the clinical diagnosis of MV2 patients. The widening spectrum of diagnostic techniques in CJD is not only useful in the increased accuracy of the clinical diagnosis but should also lead to the identification of more atypical cases of sporadic CJD."],["dc.identifier.doi","10.1002/1531-8249(200009)48:3<323::AID-ANA6>3.0.CO;2-5"],["dc.identifier.isi","000089024600006"],["dc.identifier.pmid","10976638"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42437"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0364-5134"],["dc.title","Current clinical diagnosis in Creutzfeldt-Jakob disease: Identification of uncommon variants"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1099"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","1102"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Schulz-Schaeffer, W."],["dc.contributor.author","Neumann, Manuela"],["dc.contributor.author","Schröter, A."],["dc.contributor.author","Ratzka, P."],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Windl, O."],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2017-09-07T11:44:28Z"],["dc.date.available","2017-09-07T11:44:28Z"],["dc.date.issued","2012"],["dc.description.abstract","bjectives: Decreased levels of Aβ1-42 are found in CSF of patients with AD. Because early stages of Creutzfeldt-Jakob disease (CJD) and AD share several clinical features, we investigated Aβ1-42 levels in CSF of these groups, inferring that this might give additional help in differentiating patients with CJD from AD patients.Methods: We investigated 27 patients with CJD, 14 patients with AD, 19 patients with other dementias, and 20 nondemented controls (NDC) for Aβ1-42 in CSF. Twenty-four of the 27 CJD patients were neuropathologically verified. All the neuropathologically verified patients presented with a type 1 prion protein pattern. CJD patients were all homozygous for methionine at codon 129. Except in five CJD patients, no β-amyloid plaques were seen. Additionally, APOE status was determined in patients with CJD.Results: Levels of Aβ1-42 in CSF were decreased in patients with AD as well as in CJD. Levels of Aβ1-42 in CSF of patients with CJD and AD were significantly different from the other dementia and NDC groups. There was no substantial difference between the CJD and AD groups (p = 0.66). Decreased levels of Aβ1-42 did not correlate with the APOE ε4 load in patients with CJD.Conclusion: Low levels of Aβ1-42 in CSF do not exclude a diagnosis of CJD. Decreased levels of Aβ1-42 in CSF can occur without β-amyloid plaque formation in the brain. However, the underlying mechanism of this phenomenon must be elucidated."],["dc.identifier.doi","10.1212/wnl.54.5.1099"],["dc.identifier.gro","3151662"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8479"],["dc.language.iso","en"],["dc.notes.status","public"],["dc.notes.submitter","chake"],["dc.relation.issn","0028-3878"],["dc.title","Decreased  β-amyloid1-42 in cerebrospinal fluid of patients with Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","248"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Psychiatrische Praxis"],["dc.bibliographiccitation.lastpage","251"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Kropp, Silke"],["dc.contributor.author","Riedemann, C."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Schroter, A."],["dc.contributor.author","Poser, Sigrid"],["dc.date.accessioned","2018-11-07T10:42:45Z"],["dc.date.available","2018-11-07T10:42:45Z"],["dc.date.issued","2000"],["dc.description.abstract","To assess the attitude of Creutzfeldt-Jakob patients relatives and of relatives of cognitively unimpaired individuals towards dementia research by a questionnaire survey. Methods: 42 relatives of cases and 41 controls who were interviewed within the german part of the European Union collaborative study of CJD were asked to answer structured questions concerning their personal attitude towards three hypothetical projects: a diagnostic research project without personal benefit, a project with possible therapeutic option and a study of hereditary dementia. Results: 31 relatives of cases and 26 relatives of the controls were willing to participate in this survey. In both groups the willingness to participate in dementia research is high. Research without approval of patients or relatives is rejected in most cases. Relatives want to decide to which extent genetic results are used for scientific of personal purposes. Conclusions: Although research with (and for) demented patients is restricted by the law in many countries to certain limits, relatives are willing to participate in these efforts to a greater extend than expected. As long as the responsible physicians will respect their demented patients as severely ill human beings, the view towards research is this field might be as positive as shown in this sample."],["dc.identifier.isi","000088241700014"],["dc.identifier.pmid","10941776"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46881"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag"],["dc.relation.issn","0303-4259"],["dc.title","Attitude of Creutzfeldt-Jakob disease relatives towards dementia research"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]