Zerr, Inga

[["dc.bibliographiccitation.journal","Frontiers in Psychiatry"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Hirschel, Sina"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Manig, Anja"],["dc.contributor.author","Falk, Hannah Sönne"],["dc.contributor.author","Ernst, Marielle"],["dc.contributor.author","Vukovich, Ruth"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Bartels, Claudia"],["dc.date.accessioned","2021-04-14T08:23:48Z"],["dc.date.available","2021-04-14T08:23:48Z"],["dc.date.issued","2020"],["dc.description.abstract","Background IgLON5 disease is an autoimmune disorder that shares neuropathological aspects with a tauopathy. Its clinical spectrum is heterogeneous, and figural memory impairment as an initial phenomenon of IgLON5 syndrome has not yet been described. The rationale of this report is to highlight symptoms related to IgLON5 disease that have not been reported to date. This case report will thereby emphasize how important it is to initiate thorough diagnostic methods including cerebrospinal fluid analysis (CSF) before starting early immunotherapy. Methods We examined a 65-year-old Caucasian male via neuropsychological tests, magnetic resonance imaging (MRI), electroencephalography (EEG), neurography and polysomnography. He also underwent two lumbar punctures from which we determined specific autoantibodies in cerebrospinal (CSF) and peripheral blood (PB). Results The patient presented initially complaining of memory loss, gradual dysphagia and sleeping dysfunction. Neuropsychological testing at first presentation and follow-up revealed subtle figural and working memory impairment. At onset and at his 6-month follow-up, we detected IgLON5 antibodies in CSF and PB. Furthermore, we identified in the CSF a blood–brain barrier disturbance at disease onset and follow-up, and markers of neuroaxonal damage such as mildly elevated phosphorylated Tau-181 protein with 86 pg/ml (normal range ≤ 61 pg/ml) at onset. Three months after his initial presentation, he was suffering from axonal neuropathy and transient ataxia in the extremities. Assuming a definitive autoimmune encephalitis-associated with anti-IgLON5 antibodies, we applied high-dose steroids monthly (1g methylprednisolone i.v. for five consecutive days) and his memory complaints, ataxia of extremities and peripheral neuropathy as well as sleeping dysfunction decreased. Conclusions Our findings broaden IgLON5 disease’s clinical spectrum to include predominant and discrete figural memory impairment together with sleeping dysfunction at disease onset. In addition, our report illustrates how important taking an elaborated diagnostic approach is to assuring an accurate diagnosis and the appropriate therapy if a patient presents with a persisting figural memory impairment and sleeping abnormalities so as to avoid overlooking IgLON5 disease and a potentially poor outcome."],["dc.identifier.doi","10.3389/fpsyt.2020.00576"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17685"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81054"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1664-0640"],["dc.relation.haserratum","/handle/2/83966"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Figural Memory Impairment in Conjunction With Neuropsychiatric Symptoms in IgLON5 Antibody-Associated Autoimmune Encephalitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","613"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Expert Review of Anti-infective Therapy"],["dc.bibliographiccitation.lastpage","630"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Ludewigs, Heike"],["dc.contributor.author","Zuber, Chantal"],["dc.contributor.author","Vana, Karen"],["dc.contributor.author","Nikles, Daphne"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Weiss, Stefan"],["dc.date.accessioned","2018-11-07T10:59:57Z"],["dc.date.available","2018-11-07T10:59:57Z"],["dc.date.issued","2007"],["dc.description.abstract","Prion diseases are lethal for both humans and animals, and affected individuals die after several months following a rapid disease progression. Although researchers have attempted for decades to develop effective therapeutics for the therapy of human prion disorders, until now no efficient drug has been available on the market for transmissible spongiform encephalopathy (TSE) treatment or cure. Approximately 200 patients worldwide have died or suffer from variant Creutzfeldt-Jakob disease (CJD). Incidences for sporadic and familial CJD are approximately 1.5-2 per million per year and one per 10 million per year, respectively, in Europe. This review summarizes classical and modern trials for the development of effective anti-TSE drugs, introduces potential effective delivery systems, such as lentiviral and adeno-associated virus systems for antiprion components, including antibodies and siRNAs, and presents vaccination trials. Most of the antiprion drugs target prion protein PrPc and/or PrPSc. Alternative targets are receptors and coreceptors for PrP, that is, the 37/67-kDa laminin receptor and heparan sulfate proteoglycanes. We review clinical trials for the treatment of TSEs and describe hindrances and chances for a breakthrough in therapy of prion disorders."],["dc.identifier.doi","10.1586/14787210.5.4.613"],["dc.identifier.isi","000250760000019"],["dc.identifier.pmid","17678425"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50817"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Future Drugs Ltd"],["dc.relation.issn","1478-7210"],["dc.title","Therapeutic approaches for prion disorders"],["dc.type","review"],["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.journal","European Neuropsychopharmacology"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Haust, Merle"],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Meller, J."],["dc.date.accessioned","2018-11-07T10:36:28Z"],["dc.date.available","2018-11-07T10:36:28Z"],["dc.date.issued","2003"],["dc.format.extent","S232"],["dc.identifier.doi","10.1016/S0924-977X(03)91847-5"],["dc.identifier.isi","000185412300253"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45332"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","16th Congress of the European-College-of-Neuropsychopharmacology"],["dc.relation.eventlocation","PRAGUE, CZECH REPUBLIC"],["dc.relation.issn","0924-977X"],["dc.title","Autoimmune thyroiditis (AIT) and affective disorders - a prospective pilot study"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Current Neurology and Neuroscience Reports"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Zarranz, Juan-José"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Ferrer, Isidro"],["dc.date.accessioned","2018-04-23T11:47:17Z"],["dc.date.available","2018-04-23T11:47:17Z"],["dc.date.issued","2017"],["dc.description.abstract","Purpose of Review Fatal familiar insomnia (FFI) is an autosomal dominant inherited prion disease caused by D178N mutation in the prion protein gene (PRNP D178N) accompanied by the presence of a methionine at the codon 129 polymorphic site on the mutated allele. FFI is characterized by severe sleep disorder, dysautonomia, motor signs and abnormal behaviour together with primary atrophy of selected thalamic nuclei and inferior olives, and expansion to other brain regions with disease progression. This article reviews recent research on the clinical and molecular aspects of the disease. Recent Findings New clinical and biomarker tools have been implemented in order to assist in the diagnosis of the disease. In addition, the generation of mouse models, the availability of ‘omics’ data in brain tissue and the use of new seeding techniques shed light on the molecular events in FFI pathogenesis. Biochemical studies in human samples also reveal that neuropathological alterations in vulnerable brain regions underlie severe impairment in key cellular processes such as mitochondrial and protein synthesis machinery. Summary Although the development of a therapy is still a major challenge, recent findings represent a step toward understanding of the clinical and molecular aspects of FFI."],["dc.identifier.doi","10.1007/s11910-017-0743-0"],["dc.identifier.gro","3142200"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13320"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","1528-4042"],["dc.title","Fatal Familial Insomnia: Clinical Aspects and Molecular Alterations"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","731"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","43"],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T10:28:17Z"],["dc.date.available","2018-11-07T10:28:17Z"],["dc.date.issued","2002"],["dc.identifier.doi","10.1007/s00108-002-0616-7"],["dc.identifier.isi","000176551100004"],["dc.identifier.pmid","12426728"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43393"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0020-9554"],["dc.title","Clinical aspects, diagnosis and some treatments of human prion diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","114"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","EMERGING INFECTIOUS DISEASES"],["dc.bibliographiccitation.lastpage","117"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Douet, Jean Yves"],["dc.contributor.author","Zafar, Saima"],["dc.contributor.author","Perret-Liaudet, Armand"],["dc.contributor.author","Lacroux, Caroline"],["dc.contributor.author","Lugan, Severine"],["dc.contributor.author","Aron, Naima"],["dc.contributor.author","Cassard, Herve"],["dc.contributor.author","Ponto, Claudia"],["dc.contributor.author","Corbiere, Fabien"],["dc.contributor.author","Torres, Juan Maria"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Andreoletti, Olivier"],["dc.date.accessioned","2018-11-07T09:46:58Z"],["dc.date.available","2018-11-07T09:46:58Z"],["dc.date.issued","2014"],["dc.description.abstract","We report the presence of infectivity in erythrocytes, leukocytes, and plasma of 1 person with variant Creutzfeldt-Jakob disease and in the plasma of 2 in 4 persons whose tests were positive for sporadic Creutzfeldt-Jakob disease. The measured infectivity levels were comparable to those reported in various animals with transmissible spongiform encephalopathies."],["dc.identifier.doi","10.3201/eid2001.130353"],["dc.identifier.isi","000329272100018"],["dc.identifier.pmid","24377668"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35003"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Centers Disease Control"],["dc.relation.issn","1080-6059"],["dc.relation.issn","1080-6040"],["dc.title","Detection of Infectivity in Blood of Persons with Variant and 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.firstpage","719"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","The World Journal of Biological Psychiatry"],["dc.bibliographiccitation.lastpage","728"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Martins-De-Souza, Daniel"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Gawinecka, Joanna"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Turck, Christoph W."],["dc.date.accessioned","2018-11-07T08:41:14Z"],["dc.date.available","2018-11-07T08:41:14Z"],["dc.date.issued","2010"],["dc.description.abstract","Objectives. To identify proteins differentially expressed in schizophrenia patients, we collected 50 mu l cerebrospinal fluid from 17 first-episode schizophrenia patients and 10 healthy controls. Methods. Their proteins were separated by two-dimensional gel electrophoresis without using any depletion method and identified by mass spectrometry. Results. Approximately 550 spots were detected, six of which had significantly different intensities in schizophrenia compared to control specimens. We were able to validate in individual samples the upregulation of apolipoprotein E, apolipoprotein A1 and prostaglandin-H2 D-isomerase by Western blot analyses and detect the downregulation of transthyretin, TGF-beta receptor type-1 and coiled-coil domain-containing protein 3 precursor. Conclusions. These findings may help to elucidate the disease mechanisms and confirm the hypothesis of disturbed cholesterol and phospholipid metabolism in schizophrenia, and thus reveal the final role players. Moreover, a grouped protein expression analysis of apolipoprotein E, apolipoprotein A-I, and prostaglandin-H2 D-isomerase in cerebrospinal fluid from patients might be a potential diagnostic tool for schizophrenia."],["dc.identifier.doi","10.3109/15622971003758748"],["dc.identifier.isi","000280009300005"],["dc.identifier.pmid","20446881"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19420"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Informa Healthcare"],["dc.relation.issn","1562-2975"],["dc.title","Different apolipoprotein E, apolipoprotein A1 and prostaglandin-H2 D-isomerase levels in cerebrospinal fluid of schizophrenia patients and healthy controls"],["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.issue","2"],["dc.bibliographiccitation.journal","Prion"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Kiesel, Petra"],["dc.contributor.author","Gibson, Toby J."],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Bodemer, Monika"],["dc.contributor.author","Kaup, Franz-Josef"],["dc.contributor.author","Bodemer, Walter"],["dc.contributor.author","Zischler, Hans"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T08:44:50Z"],["dc.date.available","2018-11-07T08:44:50Z"],["dc.date.issued","2010"],["dc.description.abstract","Alu DNA elements were long considered to be of no biological significance and thus have been only poorly defined. However, in the past Alu DNA elements with well-defined nucleotide sequences have been suspected to contribute to disease, but the role of Alu DNA element transcripts has rarely been investigated. For the first time, we determined in a real-time approach Alu DNA element transcription in buffy coat cells isolated from the blood of humans suffering from sporadic Creutzfeldt-Jakob disease (sCJD) and other neurodegenerative disorders. The reverse transcribed Alu transcripts were amplified and their cDNA sequences were aligned to genomic regions best fitted to database genomic Alu DNA element sequences deposited in the UCSC and NCBI data bases. Our cloned Alu RNA/cDNA sequences were widely distributed in the human genome and preferably belonged to the \"young\" Alu Y family. We also observed that some RNA/cDNA clones could be aligned to several chromosomes because of the same degree of identity and score to resident genomic Alu DNA elements. These elements, called paralogues, have purportedly been recently generated by retrotransposition. Along with cases of sCJD we also included cases of dementia and Alzheimer disease (AD). Each group revealed a divergent pattern of transcribed Alu elements. Chromosome 2 was the most preferred site in sCJD cases, besides chromosome 17; in AD cases chromosome 11 was overrepresented whereas chromosomes 2, 3 and 17 were preferred active Alu loci in controls. Chromosomes 2, 12 and 17 gave rise to Alu transcripts in dementia cases. The detection of putative Alu paralogues widely differed depending on the disease. A detailed data search revealed that some cloned Alu transcripts originated from RNA polymerase III transcription since the genomic sites of their Alu elements were found between genes. Other Alu DNA elements could be located close to or within coding regions of genes. In general, our observations suggest that identification and genomic localization of active Alu DNA elements could be further developed as a surrogate marker for differential gene expression in disease. A sufficient number of cases are necessary for statistical significance before Alu DNA elements can be considered useful to differentiate neurodegenerative diseases from controls."],["dc.identifier.isi","000280388200006"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20288"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.relation.issn","1933-6896"],["dc.title","Transcription of Alu DNA elements in blood cells of sporadic Creutzfeldt-Jakob disease (sCJD)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]