Roser, Anna‐Elisa

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Clinical and Translational Medicine"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Caldi Gomes, Lucas"],["dc.contributor.author","Roser, Anna‐Elisa"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Pena Centeno, Tonatiuh"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Schilde, Lukas"],["dc.contributor.author","May, Caroline"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2021-06-01T09:41:18Z"],["dc.date.available","2021-06-01T09:41:18Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1002/ctm2.357"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84876"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","2001-1326"],["dc.relation.issn","2001-1326"],["dc.title","MicroRNAs from extracellular vesicles as a signature for Parkinson's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["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"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Pharmacology & Therapeutics"],["dc.bibliographiccitation.lastpage","21"],["dc.bibliographiccitation.volume","189"],["dc.contributor.author","Koch, Jan Christoph"],["dc.contributor.author","Tatenhorst, Lars"],["dc.contributor.author","Roser, Anna-Elisa"],["dc.contributor.author","Saal, Kim-Ann"],["dc.contributor.author","Tönges, Lars"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2020-12-10T15:20:44Z"],["dc.date.available","2020-12-10T15:20:44Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.pharmthera.2018.03.008"],["dc.identifier.issn","0163-7258"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72778"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","ROCK inhibition in models of neurodegeneration and its potential for clinical translation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","94"],["dc.bibliographiccitation.journal","Frontiers in Aging Neuroscience"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Roser, Anna-Elisa"],["dc.contributor.author","Toenges, Lars"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2018-11-07T10:25:07Z"],["dc.date.available","2018-11-07T10:25:07Z"],["dc.date.issued","2017"],["dc.description.abstract","Neurodegenerative diseases are characterized by the progressive degeneration of neurons in the central and peripheral nervous system (CNS, PNS), resulting in a reduced innervation of target structures and a loss of function. A shared characteristic of many neurodegenerative diseases is the infiltration of microglial cells into affected brain regions. During early disease stages microglial cells often display a rather neuroprotective phenotype, but switch to a more pro-inflammatory neurotoxic phenotype in later stages of the disease, contributing to the neurodegeneration. Activation of the Rho kinase (ROCK) pathway appears to be instrumental for the modulation of the microglial phenotype: increased ROCK activity in microglia mediates mechanisms of the inflammatory response and is associated with improved motility, increased production of reactive oxygen species (ROS) and release of inflammatory cytokines. Recently, several studies suggested inhibition of ROCK signaling as a promising treatment option for neurodegenerative diseases. In this review article, we discuss the contribution of microglial activity and phenotype switch to the pathophysiology of Parkinson's disease (PD) and Amyotrophic lateral sclerosis (ALS), two devastating neurodegenerative diseases without disease-modifying treatment options. Furthermore, we describe how ROCK inhibition can influence the microglial phenotype in disease models and explore ROCK inhibition as a future treatment option for PD and ALS."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.doi","10.3389/fnagi.2017.00094"],["dc.identifier.isi","000398234900001"],["dc.identifier.pmid","28420986"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14427"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42788"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Frontiers Media Sa"],["dc.relation.issn","1663-4365"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Modulation of Microglial Activity by Rho-Kinase (ROCK) Inhibition as Therapeutic Strategy in Parkinson's Disease and Amyotrophic Lateral Sclerosis"],["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.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","3"],["dc.bibliographiccitation.journal","Parkinsonism & Related Disorders"],["dc.bibliographiccitation.lastpage","9"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Boerger, Matthias"],["dc.contributor.author","Funke, Sebastian"],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Roser, Anna-Elisa"],["dc.contributor.author","Wuestemann, Ann-Katrin"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Grus, Franz"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2020-12-10T15:20:41Z"],["dc.date.available","2020-12-10T15:20:41Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.parkreldis.2019.03.001"],["dc.identifier.issn","1353-8020"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72763"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Proteomic analysis of tear fluid reveals disease-specific patterns in patients with Parkinson's disease – A pilot study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2810"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Cell Death and Differentiation"],["dc.bibliographiccitation.lastpage","2827"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Vahsen, Björn Friedhelm"],["dc.contributor.author","Ribas, Vinicius Toledo"],["dc.contributor.author","Sundermeyer, Jonas"],["dc.contributor.author","Boecker, Alexander"],["dc.contributor.author","Dambeck, Vivian"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Shomroni, Orr"],["dc.contributor.author","Caldi Gomes, Lucas"],["dc.contributor.author","Tatenhorst, Lars"],["dc.contributor.author","Barski, Elisabeth"],["dc.contributor.author","Roser, Anna-Elisa"],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Salinas, Gabriela"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Koch, Jan Christoph"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2020-12-10T18:09:42Z"],["dc.date.available","2020-12-10T18:09:42Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1038/s41418-020-0543-y"],["dc.identifier.eissn","1476-5403"],["dc.identifier.issn","1350-9047"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73733"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Inhibition of the autophagic protein ULK1 attenuates axonal degeneration in vitro and in vivo, enhances translation, and modulates splicing"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","n/a"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","n/a"],["dc.contributor.author","Saal, Kim Ann"],["dc.contributor.author","Warth Pérez Arias, Carmina"],["dc.contributor.author","Roser, Anna‐Elisa"],["dc.contributor.author","Christoph Koch, Jan"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Rizzoli, Silvio O."],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2021-04-14T08:30:03Z"],["dc.date.available","2021-04-14T08:30:03Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract The Rho kinase (ROCK) signaling pathway is an attractive therapeutic target in neurodegeneration since it has been linked to the prevention of neuronal death and neurite regeneration. The isoquinoline derivative fasudil is a potent ROCK inhibitor, which is already approved for chronic clinical treatment in humans. However, the effects of chronic fasudil treatments on neuronal function are still unknown. We analyzed here chronic fasudil treatment in primary rat hippocampal cultures. Neurons were stimulated with 20 Hz field stimulation and we investigated pre‐synaptic mechanisms and parameters regulating synaptic transmission after fasudil treatment by super resolution stimulated emission depletion (STED) microscopy, live‐cell fluorescence imaging, and western blotting. Fasudil did not affect basic synaptic function or the amount of several synaptic proteins, but it altered the chronic dynamics of the synaptic vesicles. Fasudil reduced the proportion of the actively recycling vesicles, and shortened the vesicle lifetime, resulting overall in a reduction of the synaptic response upon stimulation. We conclude that fasudil does not alter synaptic structure, accelerates vesicle turnover, and decreases the number of released vesicles. This broadens the known spectrum of effects of this drug, and suggests new potential clinical uses. image"],["dc.description.abstract","Chronic treatment with the Rho kinase (ROCK) inhibitor fasudil did not affect basic synaptic protein abundance, but altered synaptic vesicles dynamics. In stimulated cultures, fasudil reduced synapsin1 phosphorylation and the size of the recycling pool. We propose that over‐active vesicles thus are degraded faster reducing the synaptic response upon stimulation. This broadens the spectrum of fasudil effects suggesting new clinical uses of this drug. image"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft http://dx.doi.org/10.13039/501100001659"],["dc.identifier.doi","10.1111/jnc.15274"],["dc.identifier.pmid","33341946"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83082"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/67"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | B09: Cytoskelettale Veränderungen tragen zu synapto-axonalen Fehlfunktionen in Morbus Parkinson bei"],["dc.relation","SFB 1286 | Z03: Unkomplizierte multispektrale, superauflösende Bildgebung durch zehnfache Expansionsmikroskopie"],["dc.relation.eissn","1471-4159"],["dc.relation.issn","0022-3042"],["dc.relation.workinggroup","RG Rizzoli (Quantitative Synaptology in Space and Time)"],["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","Rho‐kinase inhibition by fasudil modulates pre‐synaptic vesicle dynamics"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","9"],["dc.bibliographiccitation.journal","Molecular Therapy - Nucleic Acids"],["dc.bibliographiccitation.lastpage","22"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Roser, Anna-Elisa"],["dc.contributor.author","Caldi Gomes, Lucas"],["dc.contributor.author","Halder, Rashi"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Tönges, Lars"],["dc.contributor.author","Tatenhorst, Lars"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2020-12-10T15:20:36Z"],["dc.date.available","2020-12-10T15:20:36Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.omtn.2018.01.005"],["dc.identifier.issn","2162-2531"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72737"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","miR-182-5p and miR-183-5p Act as GDNF Mimics in Dopaminergic Midbrain Neurons"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]