Heinemann, Uta

[["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","654"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurology Neurosurgery & Psychiatry"],["dc.bibliographiccitation.lastpage","659"],["dc.bibliographiccitation.volume","85"],["dc.contributor.author","Krasnianski, Anna"],["dc.contributor.author","Juan, P. Sanchez"],["dc.contributor.author","Ponto, Claudia"],["dc.contributor.author","Bartl, Mario"],["dc.contributor.author","Heinemann, U."],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T09:39:44Z"],["dc.date.available","2018-11-07T09:39:44Z"],["dc.date.issued","2014"],["dc.description.abstract","Background In absence of a positive family history, the diagnosis of fatal familial insomnia (FFI) might be difficult because of atypical clinical features and low sensitivity of diagnostic tests. FFI patients usually do not fulfil the established classification criteria for Creutzfeldt-Jakob disease (CJD); therefore, a prion disease is not always suspected. Objective To propose an update of diagnostic pathway for the identification of patients for the analysis of D178-M129 mutation. Design and methods Data on 41 German FFI patients were analysed. Clinical symptoms and signs, MRI, PET, SPECT, polysomnography, EEG and cerebrospinal fluid biomarkers were studied. Results An algorithm was developed which correctly identified at least 81% of patients with the FFI diagnosis during early disease stages. It is based on the detection of organic sleep disturbances, either verified clinically or by a polysomnography, and a combination of vegetative and focal neurological signs and symptoms. Specificity of the approach was tested on three cohorts of patients (MM1 sporadic CJD patients, non-selected sporadic CJD and other neurodegenerative diseases). Conclusions The proposed scheme may help to improve the clinical diagnosis of FFI. As the sensitivity of all diagnostic tests investigated but polysomnography is low in FFI, detailed clinical investigation is of special importance."],["dc.identifier.doi","10.1136/jnnp-2013-305978"],["dc.identifier.isi","000336124400015"],["dc.identifier.pmid","24249784"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10971"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33354"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Bmj Publishing Group"],["dc.relation.issn","1468-330X"],["dc.relation.issn","0022-3050"],["dc.rights","CC BY-NC 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/3.0"],["dc.title","A proposal of new diagnostic pathway for fatal familial insomnia"],["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","139"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neurodegenerative Diseases"],["dc.bibliographiccitation.lastpage","144"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Gawinecka, Joanna"],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Sanchez-Juan, Pascual"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Heinemann, Uta"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:15:34Z"],["dc.date.available","2018-11-07T09:15:34Z"],["dc.date.issued","2012"],["dc.description.abstract","Background:The detection of a 14-3-3 elevated level in cerebrospinal fluid (CSF) is a part of the diagnostic criteria for probable sporadic Creutzfeldt-Jakob disease (sCJD), as defined by the WHO. However, some pathological conditions associated with acute neuronal damage may result in a positive 14-3-3 test and thereby reduce test specificity in sCJD. Objective: Desmoplakin has been previously identified as up-regulated CSF protein in sCJD and these studies aimed to investigate its diagnostic utility and compare it with two known CSF markers, 14-3-3 and tau. Methods and Results: We tested CSF levels of 14-3-3, tau and desmoplakin in 58 sCJD patients and 81 control patients including 45 cases with an elevated 14-3-3 level due to other disease than sCJD. We detected an elevated CSF level of desmoplakin in 78% of the sCJD patients, while 14-3-3 (88%) and tau (91%) showed a higher positive rate. However, the false positive rate of newly tested desmoplakin was significantly lower in comparison to 14-3-3 and tau, and it accounted for only 11% versus 56% and 35%, respectively. Further reduction of false positive rates was achieved by combination of elevated tau level with a positive desmoplakin test. Moreover, in the non-sCJD group, desmoplakin level did not correlate with the level of both above-mentioned CSF markers, whereas a clear correlation was observed in the sCJD group. Conclusion: Desmoplakin showed a low positive rate accompanied by a very low false positive rate. Thus, we conclude that desmoplakin is a promising candidate for supportive CSF marker to rule out 14-3-3 false positive cases in sCJD differential diagnosis. Copyright (C) 2011 S. Karger AG, Basel"],["dc.description.sponsorship","European Commission [KBBE-2007-2-4-06]"],["dc.identifier.doi","10.1159/000334499"],["dc.identifier.isi","000301700600004"],["dc.identifier.pmid","22213780"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9091"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27723"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","S. Karger AG"],["dc.relation.eissn","1660-2862"],["dc.relation.issn","1660-2854"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Desmoplakin as a Potential Candidate for Cerebrospinal Fluid Marker to Rule Out 14-3-3 False Positive Rates in Sporadic Creutzfeldt-Jakob Disease Differential Diagnosis"],["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","263"],["dc.bibliographiccitation.issue","5-6"],["dc.bibliographiccitation.journal","Neurodegenerative Diseases"],["dc.bibliographiccitation.lastpage","269"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Gmitterova, Karin"],["dc.contributor.author","Heinemann, U."],["dc.contributor.author","Gawinecka, Joanna"],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Valkovic, P."],["dc.contributor.author","Benetin, J."],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T08:35:12Z"],["dc.date.available","2018-11-07T08:35:12Z"],["dc.date.issued","2009"],["dc.description.abstract","Background: The 8-hydroxy-2 deoxyguanosine (8-OHdG) is a product of nucleoside oxidation of DNA and a reliable marker of oxidative stress markers. Increased levels of oxidative stress have been reported in the cerebrospinal fluid (CSF) of patients with various neurodegenerative disorders. Objective: In search of a biochemical indicator of Parkinson's disease (PD), we analyzed the levels 8-OHdG in the CSF of 99 patients, using ELISA to assess the differences between various neurodegenerative disorders. Results: Statistically significant higher CSF levels (p = 0.022) of 8-OHdG in non-demented PD patients as compared to the control group were observed. No differences between CSF 8-OHdG levels and age at the time of lumbar puncture, presence or severity of dementia, or gender were found. Conclusions: 8-OHdG levels could be potentially useful in the neurochemically supported diagnosis of PD. Copyright (C) 2009 S. Karger AG, Basel"],["dc.description.sponsorship","European Commission [SP5A-CT-2007-044438]"],["dc.identifier.doi","10.1159/000237221"],["dc.identifier.isi","000274466900008"],["dc.identifier.pmid","19955696"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9327"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18007"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1660-2854"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","8-OHdG in Cerebrospinal Fluid as a Marker of Oxidative Stress in Various Neurodegenerative Diseases"],["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"]]

[["dc.bibliographiccitation.artnumber","e84405"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Karch, Andre"],["dc.contributor.author","Manthey, Henrike"],["dc.contributor.author","Ponto, Claudia"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Heinemann, Uta"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:16:26Z"],["dc.date.available","2018-11-07T09:16:26Z"],["dc.date.issued","2013"],["dc.description.abstract","Background: Since more than a decade ApoE is known to be a strong risk factor for Alzheimer's disease (AD); however, molecular pathways mediating this risk are still unclear. In recent years it has been hypothesized that ApoE might play a role in the disintegration of blood-brain barrier (BBB). In the present study we addressed the question if ApoE genotypes might be associated with BBB function measured by albumin ratio (Q(Alb)) in a large cohort of patients with different types of dementia. Methods: Five hundred twenty (520) patients with Creutzfeldt-Jakob disease (CJD, n = 350), Alzheimer's disease (n = 71) and cerebral small vessel disease (n = 99) were assessed for their ApoE genotype. BBB function was measured in all patients using Q(Alb) and was compared between ApoE genotypes. Dominant and additive genetic models were assumed in order to investigate the potential effect of ApoE on BBB function. Results: We observed no systematic differences in Q(Alb) between ApoE genotypes within the present study. Increased Q(Alb) levels were shown for those without E3 allele in the subgroup of CJD patients when assuming a dominant genetic model (p = 0.035). This could not be confirmed for patients with other forms of dementia (p = 0.234). Discussion: Although there was some evidence for a protective effect of E3 alleles in CJD patients, this study does not support the hypothesis of a systematic role of ApoE genotypes in BBB function in individuals with a diagnosis of dementia. Thus, changes in BBB function do not seem to contribute to the increased risk of cognitive decline associated with certain ApoE genotypes. The interpretation of the results of this study must take into account that BBB function was only assessed by measuring Q(Alb) which has been shown to be a good marker for overall BBB integrity but might not reflect all qualities of the barrier."],["dc.identifier.doi","10.1371/journal.pone.0084405"],["dc.identifier.isi","000329117900091"],["dc.identifier.pmid","24386372"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9577"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27934"],["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","Investigating the Association of ApoE Genotypes with Blood-Brain Barrier Dysfunction Measured by Cerebrospinal Fluid-Serum Albumin Ratio in a Cohort of Patients with Different Types of Dementia"],["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"]]