Carboni, Eleonora

[["dc.bibliographiccitation.firstpage","309"],["dc.bibliographiccitation.issue","2-3"],["dc.bibliographiccitation.journal","NeuroMolecular Medicine"],["dc.bibliographiccitation.lastpage","321"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Carboni, Eleonora"],["dc.contributor.author","Tatenhorst, Lars"],["dc.contributor.author","Tönges, Lars"],["dc.contributor.author","Barski, Elisabeth"],["dc.contributor.author","Dambeck, Vivian"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2018-04-23T11:49:32Z"],["dc.date.available","2018-04-23T11:49:32Z"],["dc.date.issued","2017"],["dc.description.abstract","Parkinson’s disease (PD) is the most common neurodegenerative movement disorder, and its causes remain unknown. A major hallmark of the disease is the increasing presence of aggregated alpha-synuclein (aSyn). Furthermore, there is a solid consensus on iron (Fe) accumulation in several regions of PD brains during disease progression. In our study, we focused on the interaction of Fe and aggregating aSyn in vivo in a transgenic mouse model overexpressing human aSyn bearing the A53T mutation (prnp.aSyn.A53T). We utilized a neonatal iron-feeding model to exacerbate the motor phenotype of the transgenic mouse model. Beginning from day 100, mice were treated with deferiprone (DFP), a ferric chelator that is able to cross the blood–brain barrier and is currently used in clinics as treatment for hemosiderosis. Our paradigm resulted in an impairment of the learning abilities in the rotarod task and the novel object recognition test. DFP treatment significantly improved the performance in both tasks. Although this was not accompanied by alterations in aSyn aggregation, our results support DFP as possible therapeutic option in PD."],["dc.identifier.doi","10.1007/s12017-017-8447-9"],["dc.identifier.gro","3142070"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13724"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","1535-1084"],["dc.title","Deferiprone Rescues Behavioral Deficits Induced by Mild Iron Exposure in a Mouse Model of Alpha-Synuclein Aggregation"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Clinical and Translational Medicine"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Caldi Gomes, Lucas"],["dc.contributor.author","Galhoz, Ana"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Roser, Anna‐Elisa"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Carboni, Eleonora"],["dc.contributor.author","Barski, Elisabeth"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Lohmann, Katja"],["dc.contributor.author","Klein, Christine"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2022-03-01T11:45:26Z"],["dc.date.available","2022-03-01T11:45:26Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1002/ctm2.692"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103325"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","2001-1326"],["dc.relation.issn","2001-1326"],["dc.title","Multi‐omic landscaping of human midbrains identifies disease‐relevant molecular targets and pathways in advanced‐stage Parkinson's disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1769"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","ACS Chemical Neuroscience"],["dc.bibliographiccitation.lastpage","1779"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Dučić, Tanja"],["dc.contributor.author","Carboni, Eleonora"],["dc.contributor.author","Lai, Barry"],["dc.contributor.author","Chen, Si"],["dc.contributor.author","Michalke, Bernhard"],["dc.contributor.author","Lazaro, Diana F."],["dc.contributor.author","Outeiro, Tiago F."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Barski, Elisabeth"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2017-09-07T11:43:30Z"],["dc.date.available","2017-09-07T11:43:30Z"],["dc.date.issued","2015"],["dc.description.abstract","Manganese (Mn) may foster aggregation of alpha-synuclein (alpha Syn) contributing to the pathogenesis of PD. Here, we examined the influence of aSyn overexpression on distribution and oxidation states of Mn in frozen-hydrated primary midbrain neurons (PMNs) by synchrotron-based Xray fluorescence (XRF) and X-ray absorption near edge structure spectroscopy (XANES). Overexpression of aSyn increased intracellular Mn levels, whereas levels of Ca, Zn, K, P, and S were significantly decreased. Mn oxidation states were not altered. A strong correlation between Cu-/Mn-levels as well as Fe-/Mn-levels was observed in alpha Syn-overexpressing cells. Subcellular resolution revealed a punctate or filament-like perinuclear and neuritic distribution of Mn, which resembled the expression of DMT1 and MnSOD. While overexpression of aSyn did not significantly alter the expression patterns of the most-expressed Mn transport proteins (DMT1, VGCC, Fpn1), it attenuated the Mn release from Mn-treated neurons. Thus, these data suggest that aSyn may act as an intracellular Mn store. In total, neurotoxicity in PD could be mediated via regulation of transition metal levels and the metal-binding capacity of aSyn, which could represent a promising therapeutic target for this neurodegenerative disorder."],["dc.identifier.doi","10.1021/acschemneuro.5b00093"],["dc.identifier.gro","3141816"],["dc.identifier.isi","000363435300012"],["dc.identifier.pmid","26284970"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1390"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1948-7193"],["dc.title","Alpha-Synuclein Regulates Neuronal Levels of Manganese and Calcium"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]