Roser, Anna‐Elisa

[["dc.bibliographiccitation.artnumber","jnc.15461"],["dc.bibliographiccitation.firstpage","554"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","573"],["dc.bibliographiccitation.volume","159"],["dc.contributor.affiliation","Dauer née Joppe, Karina; 1Department of Neurology University Medical Center Goettingen Goettingen Germany"],["dc.contributor.affiliation","Caldi Gomes, Lucas; 1Department of Neurology University Medical Center Goettingen Goettingen Germany"],["dc.contributor.affiliation","Zhang, Shuyu; 3Department of Neurology School of Medicine University Hospital rechts der IsarTechnical University of Munich Munich Germany"],["dc.contributor.affiliation","Parvaz, Mojan; 3Department of Neurology School of Medicine University Hospital rechts der IsarTechnical University of Munich Munich Germany"],["dc.contributor.affiliation","Carboni, Eleonora; 1Department of Neurology University Medical Center Goettingen Goettingen Germany"],["dc.contributor.affiliation","Roser, Anna‐Elisa; 1Department of Neurology University Medical Center Goettingen Goettingen Germany"],["dc.contributor.affiliation","El DeBakey, Hazem; 4Department of Neurology University Hospital of Wuerzburg Wuerzburg Germany"],["dc.contributor.affiliation","Bähr, Mathias; 1Department of Neurology University Medical Center Goettingen Goettingen Germany"],["dc.contributor.affiliation","Vogel‐Mikuš, Katarina; 6Biotechnical faculty University of Ljubljana Ljubljana Slovenia"],["dc.contributor.affiliation","Wang Ip, Chi; 4Department of Neurology University Hospital of Wuerzburg Wuerzburg Germany"],["dc.contributor.affiliation","Becker, Stefan; 8Department of NMR Based Structural BiologyMax Planck Institute for Biophysical Chemistry Goettingen Germany"],["dc.contributor.affiliation","Zweckstetter, Markus; 1Department of Neurology University Medical Center Goettingen Goettingen Germany"],["dc.contributor.author","Tatenhorst, Lars"],["dc.contributor.author","Caldi Gomes, Lucas"],["dc.contributor.author","Zhang, Shuyu"],["dc.contributor.author","Parvaz, Mojan"],["dc.contributor.author","Carboni, Eleonora"],["dc.contributor.author","Roser, Anna‐Elisa"],["dc.contributor.author","El DeBakey, Hazem"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Dauer née Joppe, Karina"],["dc.contributor.author","Vogel‐Mikuš, Katarina"],["dc.contributor.author","Wang Ip, Chi"],["dc.contributor.author","Becker, Stefan"],["dc.contributor.author","Zweckstetter, Markus"],["dc.date.accessioned","2021-07-05T14:57:43Z"],["dc.date.available","2021-07-05T14:57:43Z"],["dc.date.issued","2021"],["dc.date.updated","2022-03-21T09:42:08Z"],["dc.description.abstract","Abstract Regional iron accumulation and α‐synuclein (α‐syn) spreading pathology within the central nervous system are common pathological findings in Parkinson's disease (PD). Whereas iron is known to bind to α‐syn, facilitating its aggregation and regulating α‐syn expression, it remains unclear if and how iron also modulates α‐syn spreading. To elucidate the influence of iron on the propagation of α‐syn pathology, we investigated α‐syn spreading after stereotactic injection of α‐syn preformed fibrils (PFFs) into the striatum of mouse brains after neonatal brain iron enrichment. C57Bl/6J mouse pups received oral gavage with 60, 120, or 240 mg/kg carbonyl iron or vehicle between postnatal days 10 and 17. At 12 weeks of age, intrastriatal injections of 5‐µg PFFs were performed to induce seeding of α‐syn aggregates. At 90 days post‐injection, PFFs‐injected mice displayed long‐term memory deficits, without affection of motor behavior. Interestingly, quantification of α‐syn phosphorylated at S129 showed reduced α‐syn pathology and attenuated spreading to connectome‐specific brain regions after brain iron enrichment. Furthermore, PFFs injection caused intrastriatal microglia accumulation, which was alleviated by iron in a dose‐dependent way. In primary cortical neurons in a microfluidic chamber model in vitro, iron application did not alter trans‐synaptic α‐syn propagation, possibly indicating an involvement of non‐neuronal cells in this process. Our study suggests that α‐syn PFFs may induce cognitive deficits in mice independent of iron. However, a redistribution of α‐syn aggregate pathology and reduction of striatal microglia accumulation in the mouse brain may be mediated via iron‐induced alterations of the brain connectome. image"],["dc.description.abstract","Brain iron accumulation and α‐synuclein (α‐syn) spreading pathology are common pathological findings in Parkinson's disease. To elucidate the influence of iron on α‐syn propagation, we investigated α‐syn spreading after stereotactic injection of α‐syn preformed fibrils (PFFs) into the striatum of C57Bl/6 mice after neonatal brain iron enrichment. 90 days post‐injection, PFFs injected mice displayed memory deficits, reduced α‐syn pathology and spreading to connectome‐specific regions after brain iron enrichment. Our study suggests that α‐syn PFFs may induce cognitive deficits in mice independent of iron. However, a redistribution of α‐syn pathology may be mediated via iron‐induced alterations of the brain connectome. image"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft http://dx.doi.org/10.13039/501100001659"],["dc.description.sponsorship","MPI"],["dc.identifier.doi","10.1111/jnc.15461"],["dc.identifier.pmid","34176164"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/87716"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/315"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-441"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation.eissn","1471-4159"],["dc.relation.issn","0022-3042"],["dc.relation.workinggroup","RG Bähr (Neurobiological Research Laboratory)"],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made."],["dc.title","Brain iron enrichment attenuates α‐synuclein spreading after injection of preformed fibrils"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","625"],["dc.bibliographiccitation.journal","Frontiers in Neuroscience"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Roser, Anna-Elisa"],["dc.contributor.author","Caldi Gomes, Lucas"],["dc.contributor.author","Schünemann, Jonas"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2019-07-09T11:45:52Z"],["dc.date.available","2019-07-09T11:45:52Z"],["dc.date.issued","2018"],["dc.description.abstract","Parkinson’s disease (PD) is the second most common neurodegenerative disorder worldwide. Its main neuropathological hallmarks are the degeneration of dopaminergic neurons in the substantia nigra and alpha-synuclein containing protein inclusions, called Lewy Bodies. The diagnosis of idiopathic PD is still based on the assessment of clinical criteria, leading to an insufficient diagnostic accuracy. Additionally, there is no biomarker available allowing the prediction of the disease course or monitoring the response to therapeutic approaches. So far, protein biomarker candidates such as alpha-synuclein have failed to improve diagnosis of PD. Circulating microRNAs (miRNAs) in body fluids are promising biomarker candidates for PD, as they are easily accessible by nonor minimally-invasive procedures and changes in their expression are associated with pathophysiological processes relevant for PD. Advances in miRNA analysis methods resulted in numerous recent publications on miRNAs as putative biomarkers. Here, we discuss the applicability of different body fluids as sources for miRNA biomarkers, highlight technical aspects of miRNA analysis and give an overview on published studies investigating circulating miRNAs as biomarker candidates for diagnosis of PD and other Parkinsonian syndromes."],["dc.identifier.arxiv","30233304"],["dc.identifier.doi","10.3389/fnins.2018.00625"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15332"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59325"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/34"],["dc.language.iso","en"],["dc.notes.intern","DeepGreen Import"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | B09: Cytoskelettale Veränderungen tragen zu synapto-axonalen Fehlfunktionen in Morbus Parkinson bei"],["dc.relation.eissn","1662-453X"],["dc.relation.issn","1662-453X"],["dc.relation.workinggroup","RG Lingor (Translational Neurodegeneration)"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.subject.ddc","610"],["dc.title","Circulating miRNAs as Diagnostic Biomarkers for Parkinson’s Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","overview_ja"],["dspace.entity.type","Publication"]]