Schulz-Schaeffer, Walter Joachim

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Prion"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Wemheuer, Wiebke M."],["dc.contributor.author","Benestad, Sylvie L."],["dc.contributor.author","Wrede, Arne"],["dc.contributor.author","Wemheuer, Wilhelm E."],["dc.contributor.author","Pfander, Tatjana"],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.date.accessioned","2018-11-07T08:41:59Z"],["dc.date.available","2018-11-07T08:41:59Z"],["dc.date.issued","2010"],["dc.format.extent","126"],["dc.identifier.isi","000285872300045"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19596"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.publisher.place","Austin"],["dc.relation.issn","1933-6896"],["dc.title","Types or Strains: What Classifies Prion Diseases?"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2288"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","2296"],["dc.bibliographiccitation.volume","129"],["dc.contributor.author","Krasnianski, Anna"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Kallenberg, Kai"],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Collie, Donald A."],["dc.contributor.author","Roeber, Sigrun"],["dc.contributor.author","Bartl, Mario"],["dc.contributor.author","Heinemann, Uta"],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:17:31Z"],["dc.date.available","2018-11-07T09:17:31Z"],["dc.date.issued","2006"],["dc.description.abstract","A typical clinical course and low sensitivity of established diagnostic tests are the main diagnostic problems in the MV2 subtype of sporadic Creutzfeldt-Jakob disease (sCJD). Clinical symptoms and signs, MRI, EEG and biochemical CSF markers were studied in 26 patients. Histological findings were semiquantitatively evaluated. Compared with typical sCJD, the disease duration was prolonged (median 12 months). Dementia, ataxia and psychiatric symptoms were present in all patients. Extrapyramidal signs were observed in 88%. T2-weighted MRI showed basal ganglia hyperintensities in 90%. Increased thalamic signal intensity was detected in 88% on diffusion-weighted MRI. Increased CSF tau-protein was found in 83%, and the 14-3-3 test was positive in 76%. The EEG revealed periodic sharp wave complexes in only two patients. Kuru plaques, severe thalamic and basal ganglia gliosis and spongiform changes, and neuronal loss in the pulvinar were the prominent histological features. At least one of the three diagnostic tests (MRI, tau- and 14-3-3 protein) supported the clinical diagnosis in all patients. MRI was the most sensitive of the diagnostic tests applied. Thalamic hyperintensities were observed unusually frequently. Prolonged disease duration, early and prominent psychiatric symptoms, absence of typical EEG, thalamic hyperintensities on MRI and relatively low 14-3-3 protein sensitivity may be suspicious for variant CJD. However, distinct sensory symptoms and young age at onset, which are often found in the latter, are not common in the MV2 subtype, and the pulvinar sign was observed in only one case."],["dc.identifier.doi","10.1093/brain/awl123"],["dc.identifier.isi","000240679700006"],["dc.identifier.pmid","16720682"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28191"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.title","Clinical findings and diagnostic tests in the MV2 subtype of sporadic CJD"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","937"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurology Neurosurgery & Psychiatry"],["dc.bibliographiccitation.lastpage","938"],["dc.bibliographiccitation.volume","75"],["dc.contributor.author","Hellenbroich, Y."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Nitschke, M. F."],["dc.contributor.author","Kohnke, J."],["dc.contributor.author","Handler, G."],["dc.contributor.author","Burk, K."],["dc.contributor.author","Schwinger, E."],["dc.contributor.author","Zuhlke, C."],["dc.date.accessioned","2018-11-07T10:48:37Z"],["dc.date.available","2018-11-07T10:48:37Z"],["dc.date.issued","2004"],["dc.identifier.doi","10.1136/jnnp.2003.028381"],["dc.identifier.isi","000221675700035"],["dc.identifier.pmid","15146023"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48237"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","B M J Publishing Group"],["dc.relation.issn","0022-3050"],["dc.title","Coincidence of a large SCA12 repeat allele with a case of Creutzfeld-Jacob disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","198"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Nuclear Medicine"],["dc.bibliographiccitation.lastpage","203"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Rullmann, Michael"],["dc.contributor.author","Dukart, Juergen"],["dc.contributor.author","Hoffmann, Karl-Titus"],["dc.contributor.author","Luthardt, Julia"],["dc.contributor.author","Tiepolt, Solveig"],["dc.contributor.author","Patt, Marianne"],["dc.contributor.author","Gertz, Hermann-Josef"],["dc.contributor.author","Schroeter, Matthias L."],["dc.contributor.author","Seiby, John"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Sabri, Osama"],["dc.contributor.author","Barthel, Henryk"],["dc.date.accessioned","2018-11-07T10:18:50Z"],["dc.date.available","2018-11-07T10:18:50Z"],["dc.date.issued","2016"],["dc.description.abstract","Neocortical atrophy reduces PET signal intensity, potentially affecting the diagnostic efficacy of beta-amyloid (AR) brain PET imaging. This study investigated whether partial-volume effect correction (PVEC), adjusting for this atrophy bias, improves the accuracy of F-18-florbetaben A beta PET. Methods: We analyzed F-18-florbetaben PET and MRI data obtained from 3 cohorts. The first was 10 patients with probable Alzheimer disease (AD) and 10 age-matched healthy controls (HCs), the second was 31 subjects who underwent in vivo imaging and postmortem histopathology for A beta plaques, and the third was 5 subjects who underwent PET and MRI at baseline and 1 y later. The imaging data were coregistered and segmented. PVEC was performed using the voxel-based modified Muller-Gartner method (PVELab, SPM8). From the PET data, regional and composite SUV ratios (SUVRs) with and without PVEC were obtained. In the MRI data, mesial temporal lobe atrophy was determined by the Scheltens mesial temporal atrophy scale and gray matter volumes by voxel-based morphometry. Results: In cohort 1, PVEC increased the effect on AD-versus-HO discrimination from a Cohen d value of 1.68 to 2.0 for composite SUVRs and from 0.04 to 1.04 for mesial temporal cortex SUVRs. The PVEC-related increase in mesial temporal cortex SUVR correlated with the Scheltens score (r = 0.84, P < 0.001), and that of composite SUVR correlated with the composite gray matter volume (r = -0.75, P < 0.001). In cohort 2, PVEC increased the correlation coefficient between mesial temporal cortex SUVR and histopathology score for A beta plaque load from 0.28 (P = 0.09) to 0.37 (P = 0.03). In cohort 3, PVEC did not affect the composite SUVR dynamics over time for the A beta-negative subject. This finding was in contrast to the 4 A beta-positive subjects, in 2 of whom PVEC changed the composite SUVR dynamics. Conclusion: The influence of PVEC on F-18-florbetaben PET data is associated with the degree of brain atrophy. Thus, PVEC increases the ability of F-18-florbetaben PET to discriminate between AD patients and HCs, to detect An plaques in the atrophic mesial temporal cortex, and potentially to evaluate changes in brain Ap load over time. As such, the use of PVEC should be considered for quantitative F-18-florbetaben PET scans, especially in assessing patients with brain atrophy."],["dc.identifier.doi","10.2967/jnumed.115.161893"],["dc.identifier.isi","000369354500033"],["dc.identifier.pmid","26541776"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41530"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Soc Nuclear Medicine Inc"],["dc.relation.issn","1535-5667"],["dc.relation.issn","0161-5505"],["dc.title","Partial-Volume Effect Correction Improves Quantitative Analysis of F-18-Florbetaben beta-Amyloid PET Scans"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","420"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Comparative Pathology"],["dc.bibliographiccitation.lastpage","424"],["dc.bibliographiccitation.volume","151"],["dc.contributor.author","Benneter, S. S."],["dc.contributor.author","Siunmers, B. A."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Haertig, Wolfgang"],["dc.contributor.author","Mollidor, J."],["dc.contributor.author","Schoeniger, S."],["dc.date.accessioned","2018-11-07T09:32:47Z"],["dc.date.available","2018-11-07T09:32:47Z"],["dc.date.issued","2014"],["dc.description.abstract","This report describes an oligoastrocytoma in the brain of a 3.5-year-old female pet African hedgehog (Atelerix albiventris) that showed progressive central nervous system signs for 6 months. Microscopical examination of the brain revealed a widely infiltrative, deep-seated glioma within the white matter of the cerebral hemispheres, basal nuclei, hippocampus, thalamus, midbrain, pons and the medulla of the cerebellum with extension of neoplastic cells into the cerebral cortex and overlying leptomeninges. Morphological features of the neoplastic cells, together with variable immunohistochemical expression of glial fibrillary acidic protein, Olig-2 and Nogo-A, indicated the presence of intermingled astrocytic and oligodendroglial tumour cells with an astrocytic component of approximately 40% consistent with an oligoastrocytoma. The distribution of the tumour is consistent with gliomatosis cerebri. (C) 2014 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.jcpa.2014.07.002"],["dc.identifier.isi","000347662200017"],["dc.identifier.pmid","25172052"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31820"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ltd"],["dc.relation.issn","1532-3129"],["dc.relation.issn","0021-9975"],["dc.title","Mixed Glioma (Oligoastrocytoma) in the Brain of an African Hedgehog (Atelerix albiventris)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","715"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","724"],["dc.bibliographiccitation.volume","251"],["dc.contributor.author","Harder, A."],["dc.contributor.author","Gregor, A."],["dc.contributor.author","Wirth, T."],["dc.contributor.author","Kreuz, F."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Plotkin, M."],["dc.contributor.author","Amthauer, H."],["dc.contributor.author","Neukirch, K."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Kuhlmann, T."],["dc.contributor.author","Braas, R."],["dc.contributor.author","Hahne, H. H."],["dc.contributor.author","Jendroska, K."],["dc.date.accessioned","2018-11-07T10:48:36Z"],["dc.date.available","2018-11-07T10:48:36Z"],["dc.date.issued","2004"],["dc.description.abstract","Fatal familial insomnia (FFI) is a prion disease exhibiting the PRNP D178N/129M genotype. Features of this autosomal dominant illness are progressive insomnia, dysautonomia, myoclonus, cognitive decline and motor signs associated with thalamic nerve cell loss and gliosis. In contrast to the new variant of Creutzfeldt-Jakob disease (vCJD) the onset of FFI is in middle to late adulthood. We report two male patients who belong to a large German FFI kindred. They were examined clinically, and postmortem neuropathological examination was carried out in collaboration with the German reference centre for prion disease. Additionally, the prion protein gene (PRNP) was analysed. To identify further patients with disease onset under 30 years of age a comprehensive literature review was carried out. Two male patients presented with typical symptoms of FFI at the age of 23 and 24 years. In their kindred, the age of onset has never before been under 44 years of age. Our literature review identified five additional early onset cases who died at age 21 to 25 years. In all 22 reviewed FFI families the median manifestation age was 49.5 years. Although phenotypic variability of FFI is common, age of onset under 30 years has been considered to be a hallmark of vCJD with a mean manifestation at 27 years of age. Our findings underline that in addition to vCJD, FFI must be considered in cases of young-onset prion disease. This has considerable impact on clinical management and genetic counselling."],["dc.identifier.doi","10.1007/s00415-004-0409-0"],["dc.identifier.isi","000222251000011"],["dc.identifier.pmid","15311348"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48236"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0340-5354"],["dc.title","Early age of onset in fatal familial insomnia - Two novel cases and review of the literature"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Brain Pathology"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","McBride, P. A."],["dc.contributor.author","Beekes, M."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.date.accessioned","2018-11-07T10:29:42Z"],["dc.date.available","2018-11-07T10:29:42Z"],["dc.date.issued","2000"],["dc.format.extent","663"],["dc.identifier.isi","000088213000364"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43695"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Int Soc Neuropathology"],["dc.publisher.place","Pittsburgh"],["dc.relation.issn","1015-6305"],["dc.title","Spread of PrPSc in orally infected animals during the incubation time of prion disease"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","985"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","EMERGING INFECTIOUS DISEASES"],["dc.bibliographiccitation.lastpage","988"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Krasemann, Susanne"],["dc.contributor.author","Mearini, Giulia"],["dc.contributor.author","Kraemer, Elisabeth"],["dc.contributor.author","Wagenfuehr, Katja"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Neumann, Melanie"],["dc.contributor.author","Bodemer, Walter"],["dc.contributor.author","Kaup, Franz-Josef"],["dc.contributor.author","Beekes, Michael"],["dc.contributor.author","Carrier, Lucie"],["dc.contributor.author","Aguzzi, Adriano"],["dc.contributor.author","Glatzel, Markus"],["dc.date.accessioned","2018-11-07T09:23:46Z"],["dc.date.available","2018-11-07T09:23:46Z"],["dc.date.issued","2013"],["dc.description.abstract","Prion amyloidosis occurred in the heart of 1 of 3 macaques intraperitoneally inoculated with bovine spongiform encephalopathy prions. This macaque had a remarkably long duration of disease and signs of cardiac distress. Variant Creutzfeldt-Jakob disease, caused by transmission of bovine spongiform encephalopathy to humans, may manifest with cardiac symptoms from prion-amyloid cardiomyopathy."],["dc.identifier.doi","10.3201/eid1906.120906"],["dc.identifier.isi","000328173500020"],["dc.identifier.pmid","23735198"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29660"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Centers Disease Control"],["dc.relation.issn","1080-6059"],["dc.relation.issn","1080-6040"],["dc.title","BSE-associated Prion-Amyloid Cardiomyopathy in Primates"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1544"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","1550"],["dc.bibliographiccitation.volume","65"],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Westner, I. M."],["dc.contributor.author","Kallenberg, Kai"],["dc.contributor.author","Krasnianski, Anna"],["dc.contributor.author","Bartl, Mario"],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Bosenberg, C."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Knauth, Michael"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T10:54:10Z"],["dc.date.available","2018-11-07T10:54:10Z"],["dc.date.issued","2005"],["dc.description.abstract","Background: Recently, six molecular subtypes of sporadic CJD ( sCJD) have been identified showing differences regarding the disease course, neuropathologic lesion patterns, and sensitivity to diagnostic tools. Only isolated cases of the rare VV1 type have been reported so far. Objective: To describe the clinical characteristics and neuropathologic lesion profiles in nine cases. Methods: In the years 1993 until late 2003, 571 definite neuropathologically confirmed cases of sporadic CJD were identified in Germany. Of these, nine were homozygous for valine and displayed type 1 of the pathologic PrPSc in the brain ( VV1 type). Results: The authors describe eight men and one woman belonging to the VV1 type. All patients were relatively young at disease onset ( median 44 years vs 65 years in all sCJD) with prolonged disease duration ( median 21 months vs 6 months in all sCJD). During the initial stages, their main clinical signs were personality changes and slowly progressive dementia as well as focal neurologic deficits. None of the nine VV1 patients had periodic sharp- wave complexes ( PSWCs) in the EEG. Only two out of seven displayed the typical signal increase of the basal ganglia on MRI, whereas signal increase of the cortex was seen in all patients. The 14- 3- 3 protein levels were elevated in CSF in all cases tested. Conclusions: The clinical diagnosis of the VV1 type of sCJD can be best supported by the 14- 3- 3 test and cortical signal increase on MRI. Because of the young age at onset vCJD is sometimes suspected as a differential diagnosis. MRI plays an important role in differentiating these two disease types and should be performed early during the disease course."],["dc.identifier.doi","10.1212/01.wnl.0000184674.32924.c9"],["dc.identifier.isi","000233428100008"],["dc.identifier.pmid","16221949"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49508"],["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 - Clinical and diagnostic characteristics of the rare VV1 type"],["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 Pathologe"],["dc.bibliographiccitation.lastpage","97"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Koch, S."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Kramer, Anneke"],["dc.date.accessioned","2018-11-07T10:40:48Z"],["dc.date.available","2018-11-07T10:40:48Z"],["dc.date.issued","2003"],["dc.description.abstract","In former times autopsies were the main task of a pathologist and therefore the most frequent source of infection but nowadays cytological and biopsy investigations dominate the pathologist's work. Usually the time interval between the extraction of a specimen, its transport into the laboratory and return of the report is no longer than a few hours. Consequently the staff must often handle unfixed or insufficiently fixed material. This and the occurrence of new infectious diseases, e.g. AIDS and TSE (transmissible spongiform encephalopathies), makes it necessary to analyse and perhaps even change the work in respect to hygiene risks and demands for permanent protection against infection. First of all the risks of infection and the common measures of protection from infections for the staff in biopsy and autopsy departments will be described. Subsequently suggestions to reduce infectious risks in special activities will be presented. The examination of frozen sections or intraoperative biopsy material and the handling of specimens possibly contaminated by HIV and TSE will be considered separately."],["dc.identifier.doi","10.1007/s00292-002-0590-9"],["dc.identifier.isi","000182145900002"],["dc.identifier.pmid","12673496"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46387"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0172-8113"],["dc.title","Hygienic requirements for biopsy and autopsy diagnostics"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]