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","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","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","312"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","DMW - Deutsche Medizinische Wochenschrift"],["dc.bibliographiccitation.lastpage","317"],["dc.bibliographiccitation.volume","127"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Ruge, D."],["dc.contributor.author","Krause, G."],["dc.contributor.author","Mehnert, W. H."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Poser, Sigrid"],["dc.date.accessioned","2018-11-07T10:31:53Z"],["dc.date.available","2018-11-07T10:31:53Z"],["dc.date.issued","2002"],["dc.description.abstract","Objective: Analogous to prospective studies in other countries, prevalance and symptoms of sporadic Creutzfeldt-Jakob disease (CJD) were recorded in order to assess irregularities in the incidence of the disease in Germany since the onset of bovine spongioform encephalopathy (BSE). Patients and methods: Since 1993 all suspected case of CJD reported in the Federal Republic of Germany have been analysed by a unified schema and classified by standardised criteria. In addition to voluntary reporting two other systems were accessed: (1) compulsory reporting to the Robert Koch Institute via the appropriate Health Department and (2) cause of death statistics of the Federal Office of Statistics. Results: Between June 1993 and May 2001, a total of 1247 patients with suspected CJD, obtained by the >>Study of the epidemiology and early diagnosis of human spongioform encephalopathies<< at Gottingen University, were examined. The suspected disease was confirmed by autopsy in 404 cases, the diagnosis of probable CJD was made in 369 cases on the basis of clinical data and additional investigation. At the beginning of the Gottingen Study in 1993 the incidence in Germany was 0.7 per mill. population, while in the year 2000 it had risen to 1.3 per mill. population. Corresponding increases in the number of cases since 1993 have been noted also by the Robert Koch Institute and the Federal Office of Statistics. Conclusions: The increased incidence can be explained primarily by a decrease in previously unknown cases. Concerted action as part of the Gottingen Study has increased the cooperation of associated clinics. In addition to sporadic cases of CJD, genetic and, more rarely, iatrogenic forms have been seen in Germany. But no cases of new variant CJD have been reported so far."],["dc.identifier.doi","10.1055/s-2002-20150"],["dc.identifier.isi","000173968100002"],["dc.identifier.pmid","11845386"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44217"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","0012-0472"],["dc.title","Epidemiology and clinical symptomatology of Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","371"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","378"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Redyk, Katharina"],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Krack, Lennart A."],["dc.contributor.author","von Ahsen, Nico"],["dc.contributor.author","Roeber, Sigrun"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T08:47:31Z"],["dc.date.available","2018-11-07T08:47:31Z"],["dc.date.issued","2010"],["dc.description.abstract","Objective: To characterize clinical features, CSF biomarkers and genetic polymorphisms of patients suffering from a rapidly progressing subtype of Alzheimer's dementia (rpAD). Methods: Retrospective analyses of 32 neuropathologically confirmed cases differentially diagnosed as AD out of a group with rapidly progressive dementia. CSF biomarkers (14-3-3, tau, beta-amyloid 1-42) and genetic markers (PRNP codon 129, apolipoprotein E, ApoE, polymorphism) were determined. Results: Median survival was 26 months, age at onset 73 years. Biomarkers: mean beta-amyloid 1-42: 266 pg/ml, median tau: 491 pg/ml, 14-3-3 positive: 31%. Genetic polymorphisms showed a predominance of methionine homozygosity at PRNP codon 129 and a low frequency of ApoE4 (38%, no homozygous patients). Thirty-five symptoms were studied. Frequent symptoms were myoclonus (75%), disturbed gait (66%) and rigidity (50%). Discussion: rpAD is associated with a diversity of neurological signs even able to mimic Creutz feldt-Jakob disease. Biomarkers and genetic profile differ from those seen in classical AD. The findings on biomarkers, symptomatology and genetics may aid the differential diagnostic process. Copyright (C) 2010 S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000278692"],["dc.identifier.isi","000278130700012"],["dc.identifier.pmid","20453509"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9103"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20975"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1420-8008"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Clinical Features of Rapidly Progressive Alzheimer's 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","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","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","207"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Prion"],["dc.bibliographiccitation.lastpage","212"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Zuber, Chantal"],["dc.contributor.author","Mitteregger, Gerda"],["dc.contributor.author","Pace, Claudia"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Weiss, Stefan"],["dc.date.accessioned","2018-11-07T11:01:18Z"],["dc.date.available","2018-11-07T11:01:18Z"],["dc.date.issued","2007"],["dc.description.abstract","We identified the 37kDa/67kDa laminin receptor (LRP/LR) as a cell surface receptor for the cellular prion protein (PrPc) and the infectious prion protein (PrPSc). Recently, we showed that anti-LRP/LR antibody W3 cured scrapie infected N2a cells. Here, we demon strate that W3 delivered by passive immunotransfer into C57BL/6 mice reduced the PrPSc content in the spleen significantly by 66%, demonstrating an impairment of the peripheral PrPSc propagation. In addition, we observed a 1.8-fold increase in survival of anti-LRP/LR antibody W3 treated mice (mean survival of 31 days) compared to preimmune serum treated control animals (mean survival of 17 days). We conclude that the significant effect of anti-LRP/LR antibody W3 on the reduction of peripheral PrPSc propagation might be due to the blockage of the prion receptor LRP/LR which is required, as previously shown in vitro, for PrPSc propagation in vivo."],["dc.identifier.isi","000261468700006"],["dc.identifier.pmid","19164931"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51121"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.relation.issn","1933-6896"],["dc.title","Anti-LRP/LR Antibody W3 Hampers Peripheral PrPSc Propagation in Scrapie Infected Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","79"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Biologicals"],["dc.bibliographiccitation.lastpage","97"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Seitz, Rainer"],["dc.contributor.author","von Auer, Friedger"],["dc.contributor.author","Bluemel, Johannes"],["dc.contributor.author","Burger, Reinhard"],["dc.contributor.author","Buschmann, Anne"],["dc.contributor.author","Dietz, Klaus"],["dc.contributor.author","Heiden, Margarethe"],["dc.contributor.author","Hitzler, Walter E."],["dc.contributor.author","Klamm, Horst"],["dc.contributor.author","Kreil, Thomas"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Nuebling, Micha"],["dc.contributor.author","Offergeld, Ruth"],["dc.contributor.author","Pauli, Georg"],["dc.contributor.author","Schottstedt, Volkmar"],["dc.contributor.author","Volkers, Peter"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T11:03:22Z"],["dc.date.available","2018-11-07T11:03:22Z"],["dc.date.issued","2007"],["dc.description.abstract","Variant Creutzfeldt-Jakob disease (vCJD) is an at present inevitably lethal neurodegenerative disease which can only be diagnosed definitely post mortem. The majority of the approximately 200 victims to date have resided in the UK where most contaminated beef materials entered the food chain. Three cases in the UK demonstrated that vCJD can be transmitted by blood transfusion. Since BSE and vCJD have spread to several countries outside the UK, it appears advisable that specific risk assessments be carried out in different countries and geographic areas. This review explains the approach adopted by Germany in assessing the risk and considering precautionary measures. A fundamental premise is that the feeding chain of cattle and the food chain have been successfully and permanently cleared from contaminated material. This raises the question of whether transmissions via blood transfusions could have the potential to perpetuate vCJD in mankind. A model calculation based on actual population data showed, however, that this would not be the case. Moreover, an exclusion of transfusion recipients from blood donation would add very little to the safety of blood transfusions, but would have a considerable impact on blood supply. Therefore, an exclusion of transfusion recipients was not recommended in Germany. (c) 2007 The International Association for Biologicals. Published by Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.biologicals.2007.01.002"],["dc.identifier.isi","000245673600002"],["dc.identifier.pmid","17320412"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51603"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Ltd Elsevier Science Ltd"],["dc.relation.issn","1045-1056"],["dc.title","Impact of vCJD on blood supply"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]