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.firstpage","355"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","363"],["dc.bibliographiccitation.volume","256"],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Kallenberg, Kai"],["dc.contributor.author","Sanchez-Juan, Pascual"],["dc.contributor.author","Ramljak, Sanja"],["dc.contributor.author","Krasnianski, Anna"],["dc.contributor.author","Heinemann, U."],["dc.contributor.author","Eigenbrod, Sabina"],["dc.contributor.author","Gelpi, Elena"],["dc.contributor.author","Barsic, B."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Knauth, Michael"],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T08:32:16Z"],["dc.date.available","2018-11-07T08:32:16Z"],["dc.date.issued","2009"],["dc.description.abstract","Iatrogenic Creutzfeldt-Jakob disease (iCJD) is mainly associated with dura mater (DM) grafts and administration of human growth hormones (hGH). Data on disease course in DM-CJD are limited. We describe the clinical and diagnostic findings in this patient group with special emphasis on MRI signal alterations. Ten DM-CJD patients were studied for their clinical symptoms and diagnostic findings. The MRIs were evaluated for signal increase of the cortical and subcortical structures. DM-CJD patients had a median incubation time of 18 years and median disease duration of 7 months. The majority of patients were MM homozygous at codon 129 of the prion protein gene (PRNP) and presented with gait ataxia and psychiatric symptoms. No correlation between the graft site and the initial disease course was found. The MRI showed cortical and basal ganglia signal increase each in eight out of ten patients and thalamic hyperintensity in five out of ten cases. Of interest, patients with thalamic signal increase were homozygous for methionine. The MRI findings in DM-CJD largely resemble those seen in sporadic CJD, as the cortex and basal ganglia are mainly affected."],["dc.identifier.doi","10.1007/s00415-009-0026-z"],["dc.identifier.isi","000265732800008"],["dc.identifier.pmid","19159063"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6742"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17302"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0340-5354"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","MRI and clinical syndrome in dura materrelated Creutzfeldt-Jakob disease"],["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","2241"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Acta Neurochirurgica"],["dc.bibliographiccitation.lastpage","2250"],["dc.bibliographiccitation.volume","153"],["dc.contributor.author","Neulen, Axel"],["dc.contributor.author","Gutenberg, Angelika"],["dc.contributor.author","Takacs, Ildiko"],["dc.contributor.author","Weber, Gyoergy"],["dc.contributor.author","Wegmann, Juergen"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Giese, Alf"],["dc.date.accessioned","2018-11-07T08:50:27Z"],["dc.date.available","2018-11-07T08:50:27Z"],["dc.date.issued","2011"],["dc.description.abstract","Semisynthetic collagen matrices are promising duraplasty grafts with low risk of cerebrospinal fluid (CSF) fistulas, good tissue integration and minor foreign body reaction. The present study investigates the efficacy and biocompatibility of a novel semisynthetic bilayered collagen matrix (BCM, B. Braun Aesculap) as dural onlay graft for duraplasty. Thirty-four pigs underwent osteoclastic trepanation, excision of the dura, and placement of a cortical defect, followed by duraplasty using BCM, Suturable DuraGen (TM) (Integra Neuroscience), or periosteum. CSF tightness and intraoperative handling of the grafts were evaluated. Pigs were sacrificed after 1 and 6 months for histological analysis. BCM and DuraGen (TM) showed superior handling than periosteum with a trend for better adhesion to dura and CSF tightness for BCM. Periosteum, which was sutured unlike the synthetic grafts, had the highest intraoperative CSF tightness. Duraplasty time with periosteum was significantly higher (14.4 +/- 2.7 min) compared with BCM (2.8 +/- 0.8 min) or DuraGen (TM) (3.0 +/- 0.5 min). Tissue integration by fibroblast infiltration was observed after 1 month for all devices. More adhesions between graft and cortex were observed with DuraGen (TM) compared with BCM and periosteum. No relevant adhesions between leptomeninges and BCM were observed and all devices showed comparable lymphocytic reaction of the brain. All devices were completely integrated after 6 months. BCM and DuraGen (TM) showed a trend for an enhanced lymphocytic reaction of the brain parenchyma compared with periosteum. Implant rejection was not observed. Semisythetic collagen matrices are an attractive alternative in duraplasty due to their easy handling, lower surgical time, and high biocompatibility."],["dc.description.sponsorship","B. Braun Aesculap AG, Tuttlingen, Germany"],["dc.identifier.doi","10.1007/s00701-011-1059-5"],["dc.identifier.isi","000296083700019"],["dc.identifier.pmid","21739175"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7137"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21696"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","0001-6268"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Evaluation of efficacy and biocompatibility of a novel semisynthetic collagen matrix as a dural onlay graft in a large animal model"],["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.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","551"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Alzheimer's Disease"],["dc.bibliographiccitation.lastpage","565"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Schmitz, M."],["dc.contributor.author","Wulf, K."],["dc.contributor.author","Signore, S. C."],["dc.contributor.author","Schulz-Schaeffer, W. J."],["dc.contributor.author","Kermer, P."],["dc.contributor.author","Baehr, M."],["dc.contributor.author","Wouters, F. S."],["dc.contributor.author","Zafar, S."],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2017-09-07T11:46:57Z"],["dc.date.available","2017-09-07T11:46:57Z"],["dc.date.issued","2014"],["dc.description.abstract","Previous studies indicate an important role for the cellular prion protein (PrPC) in the development of Alzheimer's disease (AD) pathology. In the present study, we analyzed the involvement of PrPC in different pathological mechanisms underlying AD: the processing of the amyloid-beta protein precursor (A beta PP) and its interaction with A beta PP, tau, and different phosphorylated forms of the tau protein (p-tau). The effect of PrPC on tau expression was investigated in various cellular compartments using a HEK293 cell model expressing a tau mutant (3PO-tau) or wild type (WT)-tau. We could show that PrPC reduces A beta PP cleavage, leading to decreased levels of A beta(40) and sA beta PP without changing the protein expression of A beta PP, beta-secretase, or gamma-secretase. Tau and its phosphorylated forms were identified as interactions partners for PrPC, raising the question as to whether PrPC might also be involved in tau pathology. Overexpression of PrPC in PRNP and 3PO-tau transfected cells resulted in a reduction of 3PO-tau and p-tau as well as a decrease of 3PO-tau-related toxicity. In addition, we used the transgenic PrPC knockout (Prnp0/0) mouse line to study the dynamics of tau phosphorylation, an important pathological hallmark in the pathogenesis of AD in vivo. There, an effect of PrPC on tau expression could be observed under oxidative stress conditions but not during aging. In summary, we provide further evidence for interactions of PrPC with proteins that are known to be the key players in AD pathogenesis. We identified tau and its phosphorylated forms as potential PrP-interactors and report a novel protective function of PrPC in AD-like tau pathology."],["dc.identifier.doi","10.3233/JAD-130566"],["dc.identifier.gro","3142228"],["dc.identifier.isi","000327598500009"],["dc.identifier.pmid","24028865"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10657"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5954"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1875-8908"],["dc.relation.issn","1387-2877"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Impact of the Cellular Prion Protein on Amyloid-beta and 3PO-Tau Processing"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]