Kretzschmar, Hans A.

[["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","690"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","694"],["dc.bibliographiccitation.volume","248"],["dc.contributor.author","Ratzka, Peter"],["dc.contributor.author","Schröter, Andreas"],["dc.contributor.author","Cepek, Lukas"],["dc.contributor.author","Henkel, Karsten"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Poser, S."],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2017-09-07T11:44:31Z"],["dc.date.available","2017-09-07T11:44:31Z"],["dc.date.issued","2006"],["dc.description.abstract","Creutzfeldt-Jakob disease (CJD) belongs to the group of transmissible spongiform encephalopathies. It is suspected that a pathologically altered form of the prion protein (PrPSc) is the decisive trigger of the disease. Data from animal experiments suggest an involvement of the lymphatic system in the intracorporal transport of PrPSc. However, it has not so far been possible to detect PrPSc on mononuclear cells (MNCs) either in the sporadic form of CJD or in the new variant of CJD (vCJD). In order to determine a possible alteration of MNCs in CJD, we investigated the natural and induced apoptotic behaviour of these cells.MNCs from 19 patients with sporadic CJD and from 20 patients with other neurological disorders were used. The cells were analysed by fluorescence cytometry with and without apoptosis induction by xanthine oxidase and hypoxanthine. The apoptosis rate was quantified using the stain 7-amino-actinomycin D (7-AAD). In the morphological investigation of the cells before apoptosis induction, there were no significant differences between the groups with regard to cell size and granularity of the MNCs. After apoptosis induction, the typical significant decrease in cell size and increase in granularity of the cells occurred in both groups. Significant differences between the patient populations were not found.For the first time, our investigation has demonstrated that a functional impairment of MNCs with regard to their apoptotic behaviour does not occur in sporadic CJD. It remains open to question whether this mechanism plays an important role in forms of transmissible encephalopathy other than sporadic CJD, especially after oral transmission."],["dc.identifier.doi","10.1007/pl00007834"],["dc.identifier.gro","3151691"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8510"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","chake"],["dc.relation.issn","0340-5354"],["dc.title","Unaltered apoptotic behaviour of mononuclear cells from patients with sporadic Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2485"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","2490"],["dc.bibliographiccitation.volume","73"],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Otto, M."],["dc.contributor.author","Baxter, H. C."],["dc.contributor.author","Bodemer, M."],["dc.contributor.author","Steinacker, P."],["dc.contributor.author","Bahn, E."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Kornhuber, J."],["dc.contributor.author","Kretzschmar, H. A."],["dc.contributor.author","Poser, S."],["dc.contributor.author","Rüther, E."],["dc.contributor.author","Aitken, A."],["dc.date.accessioned","2017-09-07T11:44:33Z"],["dc.date.available","2017-09-07T11:44:33Z"],["dc.date.issued","1999"],["dc.description.abstract","Two-dimensional polyacrylamide gel electrophoresis of CSF has been used in the diagnosis of Creutzfeldt-Jakob disease (CJD). One of the two diagnostic protein spots was identified as isoform(s) of the 14-3-3 family of abundant brain proteins. This has led to the development of one-dimensional 14-3-3 sodium dodecyl sulfate polyacrylamide gel electrophoresis immunoblot, which is currently used to support the diagnosis of CJD. In the present study employing western blot analysis, we have identified the panel of 14-3-3 isoforms that appear in the CSF of 10 patients with CJD compared with 10 patients with other dementias. The results clearly show that the 14-3-3 isoforms β, γ, ε, and η are present in the CSF of patients with CJD and can be used to differentiate other dementias. 14-3-3η also gave a baseline signal in all patients with other dementias, including six patients with Alzheimer's disease. The presence of 14-3-3η in the CSF of a patient with herpes simplex encephalitis was particularly noteworthy. This study has determined that isoform-specific 14-3-3 antibodies against β, γ, and ε should be considered for the neurochemical differentiation of CJD from other neurodegenerative diseases."],["dc.identifier.doi","10.1046/j.1471-4159.1999.0732485.x"],["dc.identifier.gro","3151688"],["dc.identifier.pmid","10582609"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8506"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0022-3042"],["dc.title","Isoform Pattern of 14-3-3 Proteins in the Cerebrospinal Fluid of Patients with Creutzfeldt-Jakob Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["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","166"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Human Genetics (Berlin)"],["dc.bibliographiccitation.lastpage","174"],["dc.bibliographiccitation.volume","118"],["dc.contributor.author","Kovács, Gábor G."],["dc.contributor.author","Puopolo, Maria"],["dc.contributor.author","Ladogana, Anna"],["dc.contributor.author","Pocchiari, Maurizio"],["dc.contributor.author","Budka, Herbert"],["dc.contributor.author","Duijn, Cornelia van"],["dc.contributor.author","Collins, Steven J."],["dc.contributor.author","Boyd, Alison"],["dc.contributor.author","Giulivi, Antonio"],["dc.contributor.author","Coulthart, Mike"],["dc.contributor.author","Delasnerie-Laupretre, Nicole"],["dc.contributor.author","Brandel, Jean Philippe"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Pedro-Cuesta, Jesus de"],["dc.contributor.author","Calero-Lara, Miguel"],["dc.contributor.author","Glatzel, Markus"],["dc.contributor.author","Aguzzi, Adriano"],["dc.contributor.author","Bishop, Matthew"],["dc.contributor.author","Knight, Richard"],["dc.contributor.author","Belay, Girma"],["dc.contributor.author","Will, Robert"],["dc.contributor.author","Mitrova, Eva"],["dc.date.accessioned","2018-11-07T10:54:39Z"],["dc.date.available","2018-11-07T10:54:39Z"],["dc.date.issued","2005"],["dc.description.abstract","A total of 10-15% of human transmissible spongiform encephalopathies (TSEs) or prion diseases are characterised by disease-specific mutations in the prion protein gene ( PRNP). We examined the phenotype, distribution, and frequency of genetic TSEs (gTSEs) in different countries/geographical regions. We collected standardised data on gTSEs between 1993 and 2002 in the framework of the EUROCJD collaborative surveillance project. Our results show that clinicopathological phenotypes include genetic Creutzfeldt-Jakob disease (gCJD), fatal familial insomnia (FFI), and Gerstmann-Straussler-Scheinker disease (GSS). Genetic TSE patients with insert mutation in the PRNP represent a separate group. Point and insertional mutations in the PRNP gene varies significantly in frequency between countries. The commonest mutation is E200K. Absence of a positive family history is noted in a significant proportion of cases in all mutation types (12-88%). FFI and GSS patients develop disease earlier than gCJD. Base pair insertions associated with the Creutzfeldt-Jakob disease (CJD) phenotype, GSS, and FFI cases have a longer duration of illness compared to cases with point mutations and gCJD. Cerebrospinal fluid 14-3-3 immunoassay, EEG, and MRI brain scan are useful in the diagnosis of CJD with point mutations, but are less sensitive in the other forms. Given the low prevalence of family history, the term \"gTSE'' is preferable to \"familial TSE''. Application of genetic screening in clinical practice has the advantage of early diagnosis and may lead to the identification of a risk of a TSE."],["dc.identifier.doi","10.1007/s00439-005-0020-1"],["dc.identifier.isi","000233996300002"],["dc.identifier.pmid","16187142"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49615"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation.issn","0340-6717"],["dc.title","Genetic prion disease: the EUROCJD experience"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["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","7951"],["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","7963"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Heber, Sol"],["dc.contributor.author","Herms, J."],["dc.contributor.author","Gajic, V."],["dc.contributor.author","Hainfellner, J."],["dc.contributor.author","Aguzzi, A."],["dc.contributor.author","Rulicke, T."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","von Koch, C."],["dc.contributor.author","Sisodia, S."],["dc.contributor.author","Tremml, P."],["dc.contributor.author","Lipp, H. P."],["dc.contributor.author","Wolfer, D. P."],["dc.contributor.author","Mueller, U."],["dc.date.accessioned","2018-11-07T08:31:10Z"],["dc.date.available","2018-11-07T08:31:10Z"],["dc.date.issued","2000"],["dc.description.abstract","The amyloid precursor protein (APP) involved in Alzheimer's disease is a member of a larger gene family including amyloid precursor-like proteins APLP1 and APLP2. We generated and examined the phenotypes of mice lacking individual or all possible combinations of APP family members to assess potential functional redundancies within the gene family. Mice deficient for the nervous system-specific APLP1 protein showed a postnatal growth deficit as the only obvious abnormality. In contrast to this minor phenotype, APLP2(-/-) /APLP1(-/-) and APLP2(-/-) / APP(-/-) mice proved lethal early postnatally. Surprisingly, APLP1(-/-) /APP(-/-) mice were viable, apparently normal, and showed no compensatory upregulation of APLP2 expression. These data indicate redundancy between APLP2 and both other family members and corroborate a key physiological role for APLP2. This view gains further support by the observation that APLP1(-/-) /APP(-/-) /APLP2(+/-) mice display postnatal lethality. In addition, they provide genetic evidence for at least some distinct physiological roles of APP and APLP2 by demonstrating that combinations of single knock-outs with the APLP1 mutation resulted in double mutants of clearly different phenotypes, being either lethal, or viable. None of the lethal double mutants displayed, however, obvious histopathological abnormalities in the brain or any other organ examined. Moreover, cortical neurons from single or combined mutant mice showed unaltered survival rates under basal culture conditions and unaltered susceptibility to glutamate excitotoxicity in vitro."],["dc.identifier.isi","000090003600013"],["dc.identifier.pmid","11050115"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17060"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Soc Neuroscience"],["dc.relation.issn","0270-6474"],["dc.title","Mice with combined gene knock-outs reveal essential and partially redundant functions of amyloid precursor protein family members"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","395"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","International Journal of Cancer"],["dc.bibliographiccitation.lastpage","402"],["dc.bibliographiccitation.volume","89"],["dc.contributor.author","Herms, J."],["dc.contributor.author","Neidt, I."],["dc.contributor.author","Luscher, B."],["dc.contributor.author","Sommer, A."],["dc.contributor.author","Schurmann, P."],["dc.contributor.author","Schroder, T."],["dc.contributor.author","Bergmann, M."],["dc.contributor.author","Wilken, Barbara"],["dc.contributor.author","Probst-Cousin, S."],["dc.contributor.author","Hernaiz-Driever, P."],["dc.contributor.author","Behnke, J."],["dc.contributor.author","Hanefeld, Folker"],["dc.contributor.author","Pietsch, Torsten"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.date.accessioned","2018-11-07T10:07:05Z"],["dc.date.available","2018-11-07T10:07:05Z"],["dc.date.issued","2000"],["dc.description.abstract","To identify prognostic factors in medulloblastoma, a common malignant brain tumor of childhood, expression of the oncogene c-myc was examined at the mRNA level by in situ hybridization. c-myc mRNA expression was observed in 30 of 72 tumors (42%), The c-myc gene copy number was determined by quantitative PCR from genomic DNA of paraffin-embedded tumors. c-myc gene amplification was present in 5 of 62 cases (8.3%), Therefore, c-myc amplification was obviously not the cause of c-myc mRNA expression in most samples, Kaplan-Meier estimation revealed a significant correlation between c-myc mRNA expression and survival (total mean follow-up 4.6 +/- 3.6 years, log-rank p = 0.02), Multivariate logistic regression analysis including sex, age, histological type, degree of surgical resection and expression of synaptophysin, GFAP and c-myc, was carried out on 54 patients who received both radiotherapy and chemotherapy. The analysis identified expression of c-myc as an independent predictive factor of death from disease. (C) 2000 Wiley-Liss, Inc."],["dc.identifier.isi","000089667200001"],["dc.identifier.pmid","11008200"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39216"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0020-7136"],["dc.title","c-myc expression in medulloblastoma and its prognostic value"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","298"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The Lancet Neurology"],["dc.bibliographiccitation.lastpage","299"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Giaccone, Giorgio"],["dc.contributor.author","Arzberger, Thomas"],["dc.contributor.author","Alafuzoff, Irina"],["dc.contributor.author","Al-Sarraj, Safa"],["dc.contributor.author","Budka, Herbert"],["dc.contributor.author","Duyckaerts, Charles"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Ferrer, Isidro"],["dc.contributor.author","Ironside, James W."],["dc.contributor.author","Kovacs, Gabor G."],["dc.contributor.author","Meyronet, David"],["dc.contributor.author","Parchi, Piero"],["dc.contributor.author","Patsouris, Efstratios"],["dc.contributor.author","Revesz, Tomas"],["dc.contributor.author","Riederer, Peter"],["dc.contributor.author","Rozemuller, Annemieke"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Winblad, Bengt"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.date.accessioned","2018-11-07T08:57:37Z"],["dc.date.available","2018-11-07T08:57:37Z"],["dc.date.issued","2011"],["dc.description.sponsorship","Medical Research Council [G0900580, MC_G0901943]"],["dc.identifier.isi","000289185000011"],["dc.identifier.pmid","21435593"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23439"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","1474-4422"],["dc.title","New lexicon and criteria for the diagnosis of Alzheimer's 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.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"]]