Meissner, Bettina

[["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","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","658"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","661"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Krasnianski, Anna"],["dc.contributor.author","Bartl, Mario"],["dc.contributor.author","Sanchez Juan, Pascual J."],["dc.contributor.author","Heinemann, Uta"],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Schulze-Sturm, Ulf"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T11:15:18Z"],["dc.date.available","2018-11-07T11:15:18Z"],["dc.date.issued","2008"],["dc.description.abstract","Our aim was to develop a detailed clinical description of fatal familial insomnia in a large patient group with respect to the M129V genotype. Data on 41 German fatal familial insomnia patients were analyzed. Clinical features, 14-3-3 proteins in the cerebrospinal fluid, magnetic resonance imaging, positron emission tomography, single-photon emission computed tomography, polysomnography, and electroencephalography were studied. Age at disease onset, disease duration, and clinical syndrome varied depending on the codon 129 genotype. Because the sensitivity of the most diagnostic tests is low in fatal familial insomnia, detailed clinical investigation is extremely important. Polysomnography may help to support the diagnosis."],["dc.identifier.doi","10.1002/ana.21358"],["dc.identifier.isi","000255960600015"],["dc.identifier.pmid","18360821"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6093"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54336"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0364-5134"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Fatal familial insomnia: Clinical features and early identification"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","35"],["dc.bibliographiccitation.journal","BMC Neurology"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Boesenberg-Grosse, Constanze"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Bodemer, Monika"],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Krasnianski, Anna"],["dc.contributor.author","Bartl, Mario"],["dc.contributor.author","Heinemann, Uta"],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Eigenbrod, Sabina"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Green, Alison"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:14:53Z"],["dc.date.available","2018-11-07T09:14:53Z"],["dc.date.issued","2006"],["dc.description.abstract","Background: Brain derived proteins such as 14-3-3, neuron-specific enolase (NSE), S 100b, tau, phosphorylated tau and A beta(1-42) were found to be altered in the cerebrospinal fluid (CSF) in Creutzfeldt-Jakob disease (CJD) patients. The pathogenic mechanisms leading to these abnormalities are not known, but a relation to rapid neuronal damage is assumed. No systematic analysis on brain-derived proteins in the CSF and neuropathological lesion profiles has been performed. Methods: CSF protein levels of brain-derived proteins and the degree of spongiform changes, neuronal loss and gliosis in various brain areas were analyzed in 57 CJD patients. Results: We observed three different patterns of CSF alteration associated with the degree of cortical and subcortical changes. NSE levels increased with lesion severity of subcortical areas. Tau and 14-3-3 levels increased with minor pathological changes, a negative correlation was observed with severity of cortical lesions. Levels of the physiological form of the prion protein (PrPc) and A beta(1-42) levels correlated negatively with cortical pathology, most clearly with temporal and occipital lesions. Conclusion: Our results indicate that the alteration of levels of brain-derived proteins in the CSF does not only reflect the degree of neuronal damage, but it is also modified by the localization on the brain pathology. Brain specific lesion patterns have to be considered when analyzing CSF neuronal proteins."],["dc.identifier.doi","10.1186/1471-2377-6-35"],["dc.identifier.isi","000240991000001"],["dc.identifier.pmid","16989662"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/1372"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27536"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2377"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Brain-derived proteins in the CSF, do they correlate with brain pathology in CJD?"],["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"]]