Windl, Otto

[["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","8866"],["dc.bibliographiccitation.issue","20"],["dc.bibliographiccitation.journal","The Journal of neuroscience"],["dc.bibliographiccitation.lastpage","8875"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Herms, J."],["dc.contributor.author","Tings, T"],["dc.contributor.author","Gall, S."],["dc.contributor.author","Madlung, A."],["dc.contributor.author","Giese, Armin"],["dc.contributor.author","Siebert, H."],["dc.contributor.author","Schurmann, P."],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Kretzschmar, Hans"],["dc.date.accessioned","2017-09-07T11:47:27Z"],["dc.date.available","2017-09-07T11:47:27Z"],["dc.date.issued","1999"],["dc.description.abstract","The prion protein (PrPC) is a copper-binding protein of unknown function that plays an important role in the etiology of transmissible spongiform encephalopathies. Using morphological techniques and synaptosomal fractionation methods, we show that PrPC is predominantly localized to synaptic membranes. Atomic absorption spectroscopy was used to identify PrPC-related changes in the synaptosomal copper concentration in transgenic mouse lines. The synaptic transmission in the presence of H2O2, which is known to be decomposed to highly reactive hydroxyl radicals in the presence of iron or copper and to alter synaptic activity, was studied in these animals. The response of synaptic activity to H2O2 was found to correlate with the amount of PrPC expression in the presynaptic neuron in cerebellar slice preparations from wild-type, Prnp(0/0), and PrP gene-reconstituted transgenic mice. Thus, our data gives strong evidence for the predominantly synaptic location of PrPC, its involvement in the regulation of the presynaptic copper concentration, and synaptic activity in defined conditions."],["dc.identifier.doi","10.1523/JNEUROSCI.19-20-08866.1999"],["dc.identifier.gro","3144439"],["dc.identifier.isi","000083072500020"],["dc.identifier.pmid","10516306"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2063"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0270-6474"],["dc.title","Evidence of presynaptic location and function of the prion protein"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","249"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Neurogenetics"],["dc.bibliographiccitation.lastpage","250"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Grasbon-Frodl, Eva-Maria"],["dc.contributor.author","Schmalzbauer, R."],["dc.contributor.author","Weber, P."],["dc.contributor.author","Krebs, B."],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.date.accessioned","2018-11-07T10:43:34Z"],["dc.date.available","2018-11-07T10:43:34Z"],["dc.date.issued","2004"],["dc.identifier.doi","10.1007/s10048-004-0196-x"],["dc.identifier.isi","000226285100008"],["dc.identifier.pmid","15480878"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47087"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1364-6745"],["dc.title","A novel three extra-repeat insertion in the prion protein gene (PRNP) in a patient with Creutzfeldt-Jakob 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","75"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Biochemical and Biophysical Research Communications"],["dc.bibliographiccitation.lastpage","82"],["dc.bibliographiccitation.volume","332"],["dc.contributor.author","Vassallo, N."],["dc.contributor.author","Herms, Jochen W."],["dc.contributor.author","Behrens, C."],["dc.contributor.author","Krebs, B."],["dc.contributor.author","Saeki, K."],["dc.contributor.author","Onodera, T."],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.date.accessioned","2018-11-07T09:50:26Z"],["dc.date.available","2018-11-07T09:50:26Z"],["dc.date.issued","2005"],["dc.description.abstract","The cellular prion protein (PrPC) is thought to be involved in protection against cell death, however the exact Cellular mechanisms involved are still controversial. Herein we present data that strongly indicate a functional link between PrPC-expression and phosphatidylinositol 3-kinase (Pl 3-kinase) activation, a protein kinase that plays a pivotal role in cell survival. Both Mouse neuroblastoma N2a cells and immortalized murine hippocampal neuronal cell lines expressing wild-type PrPC had significantly higher Pl 3-kinase activity levels than their respective controls. Moreover, PI 3-kinase activity was found to be elevated in brain lysates from wild-type mice as compared to prion protein-knockout mice. Recruitment of Pl 3-kinase by PrPC was shown to contribute to cellular survival toward oxidative stress by using 3-morpholinosydnonimine (SIN-1) and Serum deprivation. Moreover, both PI 3-kinase activation and cytoprotection by PrPC appeared to rely oil copper binding to the N-terminal octapeptide of PrPC. Thus, we propose a model in which the interaction of copper(II) with the N-terminal domain of PrPC enables transduction of a signal to PI 3-kinase: the latter. in turn, mediates downstream regulation Of Cell Survival. (c) 2005 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.bbrc.2005.04.099"],["dc.identifier.isi","000229355200012"],["dc.identifier.pmid","15896301"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35712"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0006-291X"],["dc.title","Activation of phosphatidylinositol in 3-kinase by cellular prion protein and its role cell survival"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","97"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neurogenetics"],["dc.bibliographiccitation.lastpage","100"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Krebs, B."],["dc.contributor.author","Lederer, R. M."],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Grasbon-Frodl, Eva-Maria"],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.date.accessioned","2018-11-07T11:05:33Z"],["dc.date.available","2018-11-07T11:05:33Z"],["dc.date.issued","2005"],["dc.identifier.doi","10.1007/s10048-004-0208-x"],["dc.identifier.isi","000229107200007"],["dc.identifier.pmid","15776279"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52093"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1364-6745"],["dc.title","Creutzfeldt-Jakob disease associated with an R148H mutation of the prion protein gene"],["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","14971"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","Journal of Virology"],["dc.bibliographiccitation.lastpage","14975"],["dc.bibliographiccitation.volume","79"],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Buchholz, M."],["dc.contributor.author","Neubauer, A."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Groschup, M."],["dc.contributor.author","Walter, S."],["dc.contributor.author","Arendt, S."],["dc.contributor.author","Neumann, M."],["dc.contributor.author","Voss, A. K."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.date.accessioned","2018-11-07T10:53:58Z"],["dc.date.available","2018-11-07T10:53:58Z"],["dc.date.issued","2005"],["dc.description.abstract","Transmissible mink encephalopathy (TME) is a rare disease of the North American mink, which has never been successfully transmitted to laboratory mice. We generated transgenic mice expressing the mink prion protein (PrP) and inoculated them with TME or the mouse-adapted scrapie strain 79A. TME infected mink PrP-transgenic mice on a murine PrP knockout background. The absolute species barrier between the infectious agent of TME and mice was therefore broken. Following TME and 79A infection of mice carrying both mink and murine PrPC, only proteinase-resistant PrP homologous to the incoming agent was detectable. The presence of the murine PrPC prolonged the incubation time of TME substantially."],["dc.identifier.doi","10.1128/JVI.79.23.14971-14975.2005"],["dc.identifier.isi","000233279300052"],["dc.identifier.pmid","16282497"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49462"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","0022-538X"],["dc.title","Breaking an absolute species barrier: Transgenic mice expressing the mink PrP gene are susceptible to transmissible mink encephalopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","533"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","543"],["dc.bibliographiccitation.volume","58"],["dc.contributor.author","Boesenberg, C."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Kallenberg, Kai"],["dc.contributor.author","Bartl, Mario"],["dc.contributor.author","Heinemann, U."],["dc.contributor.author","Krasnianski, Anna"],["dc.contributor.author","Stoeck, Katharina"],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T10:55:04Z"],["dc.date.available","2018-11-07T10:55:04Z"],["dc.date.issued","2005"],["dc.description.abstract","Sporadic Creutzfeldt-jakob disease (sCJD) is a rare neurodegenerative disease with the greatest incidence occurring in patients between 60 and 70 years old. Younger patients may also be affected. In this study, we used all case material available from 52 patients with sCJD aged 50 years of younger at disease onset, who were identified between 1993 and 2003 in Germany. The objective of this study was to describe the psychiatric and neurological features of these young patients with emphasis on the different codon 129 genotypes and PrP types, and to compare them with elder patients with sCJD and patients with variant CJD. We also gave particular attention to electroencephalogram, magnetic resonance imaging, and 14-3-3 results, as well as to the neuropathological lesion profile. The clinical syndrome in young patients differs from elder patients with CJD with respect to clinical signs, disease duration, technical investigations, and neuropathological lesion profile. The psychiatric symptoms in young patients with sCJD are similar to the psychiatric symptoms expressed by patients with variant CJD; however, in contrast with the variant cases, young patients with sCJD experience development of prominent dementia early in the disease course."],["dc.identifier.doi","10.1002/ana.20568"],["dc.identifier.isi","000232309900006"],["dc.identifier.pmid","16037975"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49703"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1531-8249"],["dc.relation.issn","0364-5134"],["dc.title","Clinical course in young 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"]]

[["dc.bibliographiccitation.artnumber","e2147"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Roeber, Sigrun"],["dc.contributor.author","Grasbon-Frodl, Eva-Maria"],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Krebs, Bjarne"],["dc.contributor.author","Xiang, Wei"],["dc.contributor.author","Vollmert, Caren"],["dc.contributor.author","Illig, Thomas"],["dc.contributor.author","Schroeter, Andreas"],["dc.contributor.author","Arzberger, Thomas"],["dc.contributor.author","Weber, Petra"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.date.accessioned","2018-11-07T11:15:06Z"],["dc.date.available","2018-11-07T11:15:06Z"],["dc.date.issued","2008"],["dc.description.abstract","Clinical and pathological changes in familial Creutzfeldt-Jakob disease (CJD) cases may be similar or indistinguishable from sporadic CJD. Therefore determination of novel mutations in PRNP remains of major importance. We identified two different rare mutations in codon 188 of the prion protein gene (PRNP) in four patients suffering from a disease clinically very similar to the major subtype of sporadic CJD. Both mutations result in an exchange of the amino acid residue threonine for a highly basic residue, either arginine (T188R) or lysine (T188K). The T188R mutation was found in one patient and the T188K mutation in three patients. The prevalence of mutations at codon 188 of PRNP was tested in 593 sporadic CJD cases and 735 healthy individuals. Neither mutation was found. The data presented here argue in favor of T188K being a pathogenic mutation causing genetic CJD. Since one individual with this mutation, who is the father of a clinically affected patient with T188K mutation, is now 79 years old and shows no signs of disease, this mutation is likely associated with a penetrance under 100%. Further observations will have to show whether T188R is a pathogenic mutation."],["dc.identifier.doi","10.1371/journal.pone.0002147"],["dc.identifier.isi","000262172800012"],["dc.identifier.pmid","18478114"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8256"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54294"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Evidence for a Pathogenic Role of Different Mutations at Codon 188 of PRNP"],["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","1871"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","1879"],["dc.bibliographiccitation.volume","260"],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Wemheuer, Wiebke M."],["dc.contributor.author","Damman, Insa"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Cramm, Maria"],["dc.contributor.author","Kallenberg, Kai"],["dc.contributor.author","Shirneshan, Katayoon"],["dc.contributor.author","Elkenani, Manar"],["dc.contributor.author","Markwort, Susanne"],["dc.contributor.author","Faist, Michael"],["dc.contributor.author","Kohlhase, Juergen"],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:23:06Z"],["dc.date.available","2018-11-07T09:23:06Z"],["dc.date.issued","2013"],["dc.description.abstract","We discuss relevant aspects in two siblings with a neurodegenerative process of unclear aetiology who developed progressive dementia with global aphasia and hyperoral behaviour at the ages of 39 and 46 years and who died 6 and 5 years after disease onset. The cases were reported to the National Reference Center for TSE Surveillance in Gottingen, Germany. Detailed clinical examinations, CSF, blood samples, and copies of the important diagnostic tests (magnetic resonance imaging, electroencephalogram, laboratory tests) were obtained. Further neuropathological and genetic analyses were performed. Cerebral magnetic resonance imaging of both siblings showed prominent changes in signal intensity, especially in the left medial temporal cortex, but also the hippocampal formation. Neuropathological examination revealed spongiform changes, neuronal loss, and astrocytic gliosis, which are typical in Creutzfeldt-Jakob disease. However, no prion protein deposits were detectable by immunohistochemical analysis, Western blot, or PET blot, though abundant tau protein deposits were observed. A mutation in the coding region of the prion protein genes of both siblings was excluded. A detailed search of the literature revealed no other cases with a similar clinical and neuropathological appearance. While the disease aetiology remains unclear, the findings point to a neurodegenerative process and most likely a genetic disease."],["dc.identifier.doi","10.1007/s00415-013-6897-z"],["dc.identifier.isi","000321610500025"],["dc.identifier.pmid","23546304"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29501"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0340-5354"],["dc.title","Spongiform encephalopathy in siblings with no evidence of protease-resistant prion protein or a mutation in the prion protein gene"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2558"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","2566"],["dc.bibliographiccitation.volume","125"],["dc.contributor.author","Tschampa, Henriette J."],["dc.contributor.author","Herms, J. W."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Maruschak, B."],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Jastrow, U."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Steinhoff, B. J."],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.date.accessioned","2018-11-07T09:51:28Z"],["dc.date.available","2018-11-07T09:51:28Z"],["dc.date.issued","2002"],["dc.description.abstract","The pathogenesis underlying the typical findings in Creutzfeldt-Jakob disease (CJD) such as periodic EEG changes or myoclonus is not fully understood. The thalamus possesses a high density of inhibitory neurones and serves as a crucial pacemaker of rhythmic EEG activity. As inhibitory neurones expressing parvalbumin (PV) are reduced in the cerebral cortex and hippocampus in sporadic CJD (sCJD), we studied the distribution and number of PV-immunoreactive neurones in sCJD thalami in order to determine whether damage to them could account for certain clinical findings. Immuno histochemical analysis was performed on the thalami from 21 sCJD patients and five controls. The number of PV+ neurones was counted in the thalamic nuclei and compared with clinical and molecular findings. In sCJD patients, PV+ neurones were significantly reduced in the ventrolateral posterior (VLp), ventrolateral anterior (VLa), anteroventral (AV), lateral dorsal (LD), mediodorsal (MD) and reticular (Re) thalamic nuclei (P < 0.05). The VLp was especially damaged in sCJD patients with homozygosity for methionine at codon 129 and scrapie prion protein (PrPSc) type 1. Patients with typical EEG changes [periodic sharp wave complexes (PSWCs)] and myoclonus had a predominant loss of PV+ cells in the reticular thalamic nucleus. In conclusion, our data support the hypothesis that the damage to PV-immunoreactive neurones determines the generation of certain typical clinical features of CJD, i.e. PSWCs associated with myoclonus."],["dc.identifier.doi","10.1093/brain/awf253"],["dc.identifier.isi","000178834400016"],["dc.identifier.pmid","12390980"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35920"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.title","Clinical findings in sporadic Creutzfeldt-Jakob disease correlate with thalamic pathology"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]