Gotzmann, Nadine

[["dc.bibliographiccitation.firstpage","710"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Alzheimer's & Dementia: The Journal of the Alzheimer's Association"],["dc.bibliographiccitation.lastpage","719"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Gotzmann, Nadine"],["dc.contributor.author","Golanska, Ewa"],["dc.contributor.author","Thüne, Katrin"],["dc.contributor.author","Zejneli, Orgeta"],["dc.contributor.author","Kanata, Eirini"],["dc.contributor.author","Knipper, Tobias"],["dc.contributor.author","Cramm, Maria"],["dc.contributor.author","Lange, Peter"],["dc.contributor.author","Zafar, Saima"],["dc.contributor.author","Sikorska, Beata"],["dc.contributor.author","Liberski, Pawel P."],["dc.contributor.author","Mitrova, Eva"],["dc.contributor.author","Varges, Daniela"],["dc.contributor.author","Schmidt, Christian"],["dc.contributor.author","Sklaviadis, Theodoros"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-10-08T13:38:00Z"],["dc.date.available","2018-10-08T13:38:00Z"],["dc.date.issued","2017-06"],["dc.description.abstract","Accurate diagnosis of prion diseases and discrimination from alternative dementias gain importance in the clinical routine, but partial overlap in cerebrospinal fluid (CSF) biomarkers impedes absolute discrimination in the differential diagnostic context. We established the clinical parameters for prion disease diagnosis for the quantification of CSF α-synuclein in patients with sporadic (n = 234) and genetic (n = 56) prion diseases, in cases with cognitive impairment/dementia or neurodegenerative disease (n = 278), and in the neurologic control group (n = 111). An optimal cutoff value of 680 pg/mL α-synuclein results in 94% sensitivity and 96% specificity when diagnosing sporadic Creutzfeldt-Jakob disease (CJD). Genetic CJD cases showed increased CSF α-synuclein values. No increased α-synuclein levels were detected in non-CJD cases with rapid progression course. Detection of α-synuclein in the CSF of patients with suspected CJD is a valuable diagnostic test reaching almost full discrimination from non-prion disease cases. These data highlight the utility of CSF α-synuclein quantification in front of classical CSF biomarkers in clinical routine."],["dc.fs.pkfprnr","61006"],["dc.identifier.doi","10.1016/j.jalz.2016.09.013"],["dc.identifier.fs","631450"],["dc.identifier.pmid","27870938"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15884"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1552-5279"],["dc.title","Evaluation of α-synuclein as a novel cerebrospinal fluid biomarker in different forms of prion diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","35"],["dc.bibliographiccitation.journal","Acta Neuropathologica Communication"],["dc.bibliographiccitation.lastpage","20"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Thüne, Katrin"],["dc.contributor.author","Sikorska, Beata"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Tahir, Waqas"],["dc.contributor.author","Fernández-Borges, Natalia"],["dc.contributor.author","Cramm, Maria"],["dc.contributor.author","Gotzmann, Nadine"],["dc.contributor.author","Carmona, Margarita"],["dc.contributor.author","Streichenberger, Nathalie"],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Zafar, Saima"],["dc.contributor.author","Schuetz, Anna-Lena"],["dc.contributor.author","Rajput, Ashish"],["dc.contributor.author","Andréoletti, Olivier"],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Liberski, Pawel P."],["dc.contributor.author","Torres, Juan Maria"],["dc.contributor.author","Ferrer, Isidre"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-01-09T14:57:08Z"],["dc.date.available","2018-01-09T14:57:08Z"],["dc.date.issued","2017-04-27"],["dc.description.abstract","Sporadic Creutzfeldt-Jakob disease (sCJD) is the most prevalent form of human prion disease and it is characterized by the presence of neuronal loss, spongiform degeneration, chronic inflammation and the accumulation of misfolded and pathogenic prion protein (PrPSc). The molecular mechanisms underlying these alterations are largely unknown, but the presence of intracellular neuronal calcium (Ca2+) overload, a general feature in models of prion diseases, is suggested to play a key role in prion pathogenesis.Here we describe the presence of massive regulation of Ca2+ responsive genes in sCJD brain tissue, accompanied by two Ca2+-dependent processes: endoplasmic reticulum stress and the activation of the cysteine proteases Calpains 1/2. Pathogenic Calpain proteins activation in sCJD is linked to the cleavage of their cellular substrates, impaired autophagy and lysosomal damage, which is partially reversed by Calpain inhibition in a cellular prion model. Additionally, Calpain 1 treatment enhances seeding activity of PrPSc in a prion conversion assay. Neuronal lysosomal impairment caused by Calpain over activation leads to the release of the lysosomal protease Cathepsin S that in sCJD mainly localises in axons, although massive Cathepsin S overexpression is detected in microglial cells. Alterations in Ca2+ homeostasis and activation of Calpain-Cathepsin axis already occur at pre-clinical stages of the disease as detected in a humanized sCJD mouse model.Altogether our work indicates that unbalanced Calpain-Cathepsin activation is a relevant contributor to the pathogenesis of sCJD at multiple molecular levels and a potential target for therapeutic intervention."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.doi","10.1186/s40478-017-0431-y"],["dc.identifier.pmid","28449707"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14726"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11612"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","2051-5960"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Altered Ca2+ homeostasis induces Calpain-Cathepsin axis activation in sporadic Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2305"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","2311"],["dc.bibliographiccitation.volume","262"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Shafiq, Mohsin"],["dc.contributor.author","Gomes da Cunha, Jose Eriton"],["dc.contributor.author","Gotzman, Nadine"],["dc.contributor.author","Zafar, Saima"],["dc.contributor.author","Thune, Katrin"],["dc.contributor.author","Mendes de Oliveira, Joao Ricardo"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:50:51Z"],["dc.date.available","2018-11-07T09:50:51Z"],["dc.date.issued","2015"],["dc.description.abstract","The identification of reliable diagnostic tools for the differential diagnosis between sporadic Creutzfeldt-Jakob Disease (sCJD) and Alzheimer's disease (AD) remains impeded by the existing clinical, neuropathological and molecular overlap between both diseases. The development of new tools for the quantitative measurement of biomarkers is gaining experimental momentum due to recent advances in high-throughput screening analysis and with the optimization of assays for their quantification in biological fluids, including cerebrospinal fluid (CSF). Electrochemiluminescence (ECL)-based immunoassays have demonstrated to achieve clinical quality performance in a variety of sample types due to its high sensitivity and dynamic range. Here, we quantified the CSF levels of Tau-protein, beta-amyloid 1-42 (A beta 42) and alpha-synuclein, as important biomarkers in CSF used in the differential diagnosis of neurodegenerative disorders in 12 AD, 12 sCJD and 12 control cases by singleplex ECL-based technology. Its performance has been compared to classical enzyme-linked immunosorbent assays (ELISA) to confront their clinical accuracy. ECL-based technology validates previous data obtained with ELISA and presents a higher performance in the discrimination of three analysed groups as determined by increased area under the curve (AUC) values for the three biomarkers. Importantly, alpha-synuclein levels detected by ECL allow an excellent discrimination between sCJD cases and AD and control cases, unveiling a new clinical approach for the differential diagnosis of sCJD."],["dc.identifier.doi","10.1007/s00415-015-7837-x"],["dc.identifier.isi","000363035800012"],["dc.identifier.pmid","26162713"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35791"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","1432-1459"],["dc.relation.issn","0340-5354"],["dc.title","Quantification of CSF biomarkers using an electrochemiluminescence-based detection system in the differential diagnosis of AD and sCJD"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Prion"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Ferrer, Isidro"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Frau-Mendez, Lida"],["dc.contributor.author","Fernandez-Vega, Ivan"],["dc.contributor.author","Thune, Katrin"],["dc.contributor.author","Antonio del Rio, Jose"],["dc.contributor.author","Schmizt, Matthias"],["dc.contributor.author","Ansoleaga, Belen"],["dc.contributor.author","Gotzmann, Nadine"],["dc.contributor.author","Cramm, Maria"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Jose Zarranz, Juan"],["dc.date.accessioned","2018-11-07T10:20:26Z"],["dc.date.available","2018-11-07T10:20:26Z"],["dc.date.issued","2016"],["dc.format.extent","S83"],["dc.identifier.isi","000374656300119"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41890"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Taylor & Francis Inc"],["dc.publisher.place","Philadelphia"],["dc.relation.issn","1933-690X"],["dc.relation.issn","1933-6896"],["dc.title","Identification of new molecular alterations in Fatal Familial Insomnia"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2271"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","2277"],["dc.bibliographiccitation.volume","263"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Gotzmann, Nadine"],["dc.contributor.author","Gmitterova, Karin"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T10:06:41Z"],["dc.date.available","2018-11-07T10:06:41Z"],["dc.date.issued","2016"],["dc.description.abstract","Several studies have addressed the utility of cerebrospinal (CSF) alpha-synuclein levels as a potential biomarker of alpha-synuclein aggregation disorders. However, its relevance in the differential diagnostic context of neurodegenerative and movement disorders is still a contentious subject. Here, we report total CSF alpha-synuclein levels in a cohort of clinically diagnosed alpha-synuclein-related disorders encompassing Parkinson's disease, Parkinson's disease dementia, dementia with Lewy bodies and multiple system atrophy in comparison to essential tremor and neurological control cases. alpha-synuclein levels in alpha-synuclein-related disorders were significantly lower than in controls (p < 0.001). However, in the differential diagnostic context, only Parkinson's disease cases presented significant lower alpha-synuclein levels compared to essential tremor and neurological controls. In cases with clinically diagnosed alpha-synuclein pathology, CSF alpha-synuclein levels showed a moderate positive correlation with CSF tau and p-tau, but not with A beta 42 levels. Due to elevated CSF tau levels in dementia with Lewy bodies samples, tau/alpha-synuclein ratio showed a good clinical accuracy in discriminating controls from dementia with Lewy bodies cases (AUC = 0.8776) compared to single alpha-synuclein (AUC = 0.7192) and tau (AUC = 0.7739) levels. In conclusion, alpha-synuclein alone lacks of clinical value as a biomarker of alpha-synuclein-related disorders, but in combination with total tau, it may improve the diagnosis of dementia with Lewy bodies."],["dc.identifier.doi","10.1007/s00415-016-8259-0"],["dc.identifier.isi","000386355000014"],["dc.identifier.pmid","27544498"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39140"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","1432-1459"],["dc.relation.issn","0340-5354"],["dc.title","Cerebrospinal alpha-synuclein in alpha-synuclein aggregation disorders: tau/alpha-synuclein ratio as potential biomarker for dementia with Lewy bodies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2417"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Human Molecular Genetics"],["dc.bibliographiccitation.lastpage","2436"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Thuene, Katrin"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Ansoleaga, Belen"],["dc.contributor.author","Frau-Mendez, Margalida A."],["dc.contributor.author","Cramm, Maria"],["dc.contributor.author","Tahir, Waqas"],["dc.contributor.author","Gotzmann, Nadine"],["dc.contributor.author","Berjaoui, Sara"],["dc.contributor.author","Carmona, Margarita"],["dc.contributor.author","Silva, Christopher J."],["dc.contributor.author","Fernandez-Vega, Ivan"],["dc.contributor.author","Jose Zarranz, Juan"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Ferrer, Isidro"],["dc.date.accessioned","2018-11-07T10:12:45Z"],["dc.date.available","2018-11-07T10:12:45Z"],["dc.date.issued","2016"],["dc.description.abstract","Fatal familial insomnia is a rare disease caused by a D178N mutation in combination with methionine (Met) at codon 129 in the mutated allele of PRNP (D178N-129M haplotype). FFI is manifested by sleep disturbances with insomnia, autonomic disorders and spontaneous and evoked myoclonus, among other symptoms. This study describes new neuropathological and biochemical observations in a series of eight patients with FFI. The mediodorsal and anterior nuclei of the thalamus have severe neuronal loss and marked astrocytic gliosis in every case, whereas the entorhinal cortex is variably affected. Spongiform degeneration only occurs in the entorhinal cortex. Synaptic and fine granular proteinase K digestion (PrPres) immunoreactivity is found in the entorhinal cortex but not in the thalamus. Interleukin 6, interleukin 10 receptor alpha subunit, colony stimulating factor 3 receptor and toll-like receptor 7 mRNA expression increases in the thalamus in FFI. PrPc levels are significantly decreased in the thalamus, entorhinal cortex and cerebellum in FFI. This is accompanied by a particular PrPc and PrPres band profile. Altered PrP solubility consistent with significantly reduced PrP levels in the cytoplasmic fraction and increased PrP levels in the insoluble fraction are identified in FFI cases. Amyloid-like deposits are only seen in the entorhinal cortex. The RT-QuIC assay reveals that all the FFI samples of the entorhinal cortex are positive, whereas the thalamus is positive only in three cases and the cerebellumin two cases. The present findings unveil particular neuropathological and neuroinflammatory profiles in FFI and novel characteristics of natural prion protein in FFI, altered PrPres and Scrapie PrP (abnormal and pathogenic PrP) patterns and region-dependent putative capacity of PrP seeding."],["dc.identifier.doi","10.1093/hmg/ddw108"],["dc.identifier.isi","000393062900005"],["dc.identifier.pmid","27056979"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40298"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1460-2083"],["dc.relation.issn","0964-6906"],["dc.title","Identification of new molecular alterations in fatal familial insomnia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2249"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Molecular Neurobiology"],["dc.bibliographiccitation.lastpage","2257"],["dc.bibliographiccitation.volume","55"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Karch, André"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Zafar, Saima"],["dc.contributor.author","Gotzmann, Nadine"],["dc.contributor.author","Sun, Ting"],["dc.contributor.author","Köchy, Silja"],["dc.contributor.author","Knipper, Tobias"],["dc.contributor.author","Cramm, Maria"],["dc.contributor.author","Golanska, Ewa"],["dc.contributor.author","Sikorska, Beata"],["dc.contributor.author","Liberski, Pawel P."],["dc.contributor.author","Sánchez-Valle, Raquel"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-04-23T11:47:18Z"],["dc.date.available","2018-04-23T11:47:18Z"],["dc.date.issued","2018"],["dc.description.abstract","The analysis of cerebrospinal fluid (CSF) biomarkers gains importance in the differential diagnosis of prion diseases. However, no single diagnostic tool or combination of them can unequivocally confirm prion disease diagnosis. Electrochemiluminescence (ECL)-based immunoassays have demonstrated to achieve high diagnostic accuracy in a variety of sample types due to their high sensitivity and dynamic range. Quantification of CSF α-synuclein (a-syn) by an in-house ECL-based ELISA assay has been recently reported as an excellent approach for the diagnosis of sporadic Creutzfeldt-Jakob disease (sCJD), the most prevalent form of human prion disease. In the present study, we validated a commercially available ECL-based a-syn ELISA platform as a diagnostic test for correct classification of sCJD cases. CSF a-syn was analysed in 203 sCJD cases with definite diagnosis and in 445 non-CJD cases. We investigated reproducibility and stability of CSF a-syn and made recommendations for its analysis in the sCJD diagnostic workup. A sensitivity of 98% and a specificity of 97% were achieved when using an optimal cut-off of 820 pg/mL a-syn. Moreover, we were able to show a negative correlation between a-syn levels and disease duration suggesting that CSF a-syn may be a good prognostic marker for sCJD patients. The present study validates the use of a-syn as a CSF biomarker of sCJD and establishes the clinical and pre-analytical parameters for its use in differential diagnosis in clinical routine. Additionally, the current test presents some advantages compared to other diagnostic approaches: it is fast, economic, requires minimal amount of CSF and a-syn levels are stable along disease progression."],["dc.identifier.doi","10.1007/s12035-017-0479-5"],["dc.identifier.gro","3142202"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14714"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13323"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.issn","0893-7648"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Validation of α-Synuclein as a CSF Biomarker for Sporadic Creutzfeldt-Jakob Disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Prion"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Ferrer, Isidro"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Frau-Mendez, Lida"],["dc.contributor.author","Fernandez-Vega, Ivan"],["dc.contributor.author","Thüne, Katrin"],["dc.contributor.author","Antonio del Rio, Jose"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Ansoleaga, Belen"],["dc.contributor.author","Gotzmann, Nadine"],["dc.contributor.author","Cramm, Maria"],["dc.contributor.author","Silva, Christopher J."],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Zarranz, Juan Jose"],["dc.date.accessioned","2018-11-07T10:20:03Z"],["dc.date.available","2018-11-07T10:20:03Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1093/hmg/ddw108"],["dc.identifier.isi","000383361400009"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41799"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1933-690X"],["dc.relation.issn","1933-6896"],["dc.title","Identification of new molecular alterations in Fatal Familial Insomnia (vol 10, pg S83, 2016)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","517"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Molecular Neurobiology"],["dc.bibliographiccitation.lastpage","537"],["dc.bibliographiccitation.volume","55"],["dc.contributor.author","Tahir, Waqas"],["dc.contributor.author","Zafar, Saima"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Arora, Amandeep Singh"],["dc.contributor.author","Thüne, Katrin"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Gotzmann, Nadine"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Torres, Juan Maria"],["dc.contributor.author","Andréoletti, Olivier"],["dc.contributor.author","Ferrer, Isidre"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2020-12-10T14:14:25Z"],["dc.date.available","2020-12-10T14:14:25Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1007/s12035-016-0294-4"],["dc.identifier.eissn","1559-1182"],["dc.identifier.issn","0893-7648"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71342"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Molecular Alterations in the Cerebellum of Sporadic Creutzfeldt–Jakob Disease Subtypes with DJ-1 as a Key Regulator of Oxidative Stress"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]