Hosang, Leon

[["dc.bibliographiccitation.firstpage","47"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Neuroscience"],["dc.bibliographiccitation.lastpage","60"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Berghoff, Stefan A."],["dc.contributor.author","Spieth, Lena"],["dc.contributor.author","Sun, Ting"],["dc.contributor.author","Hosang, Leon"],["dc.contributor.author","Schlaphoff, Lennart"],["dc.contributor.author","Depp, Constanze"],["dc.contributor.author","Düking, Tim"],["dc.contributor.author","Winchenbach, Jan"],["dc.contributor.author","Neuber, Jonathan"],["dc.contributor.author","Ewers, David"],["dc.contributor.author","Scholz, Patricia"],["dc.contributor.author","van der Meer, Franziska"],["dc.contributor.author","Cantuti-Castelvetri, Ludovico"],["dc.contributor.author","Sasmita, Andrew O."],["dc.contributor.author","Meschkat, Martin"],["dc.contributor.author","Ruhwedel, Torben"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Sankowski, Roman"],["dc.contributor.author","Prinz, Marco"],["dc.contributor.author","Huitinga, Inge"],["dc.contributor.author","Sereda, Michael W."],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Ischebeck, Till"],["dc.contributor.author","Simons, Mikael"],["dc.contributor.author","Stadelmann-Nessler, Christine"],["dc.contributor.author","Edgar, Julia M."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Saher, Gesine"],["dc.date.accessioned","2021-04-14T08:27:05Z"],["dc.date.available","2021-04-14T08:27:05Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1038/s41593-020-00757-6"],["dc.identifier.pmid","33349711"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82162"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/11"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","TRR 274: Checkpoints of Central Nervous System Recovery"],["dc.relation","TRR 274 | A04: The role of the meninges in the resolution of acute autoimmune CNS lesions"],["dc.relation.eissn","1546-1726"],["dc.relation.issn","1097-6256"],["dc.relation.workinggroup","RG Cantuti"],["dc.relation.workinggroup","RG Nave (Neurogenetics)"],["dc.relation.workinggroup","RG Odoardi (Echtzeitdarstellung neuroimmunologischer Prozesse)"],["dc.relation.workinggroup","RG Simons (The Biology of Glia in Development and Disease)"],["dc.relation.workinggroup","RG Stadelmann-Nessler"],["dc.title","Microglia facilitate repair of demyelinated lesions via post-squalene sterol synthesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","E3131"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","E3140"],["dc.bibliographiccitation.volume","112"],["dc.contributor.author","Huang, Xiaojie"],["dc.contributor.author","Stodieck, Sophia Katharina"],["dc.contributor.author","Goetze, Bianka"],["dc.contributor.author","Cui, Lei"],["dc.contributor.author","Wong, Man Ho"],["dc.contributor.author","Wenzel, Colin"],["dc.contributor.author","Hosang, Leon"],["dc.contributor.author","Dong, Yan"],["dc.contributor.author","Loewel, Siegrid"],["dc.contributor.author","Schlueter, Oliver M."],["dc.date.accessioned","2018-11-07T09:55:51Z"],["dc.date.available","2018-11-07T09:55:51Z"],["dc.date.issued","2015"],["dc.description.abstract","During critical periods, all cortical neural circuits are refined to optimize their functional properties. The prevailing notion is that the balance between excitation and inhibition determines the onset and closure of critical periods. In contrast, we show that maturation of silent glutamatergic synapses onto principal neurons was sufficient to govern the duration of the critical period for ocular dominance plasticity in the visual cortex of mice. Specifically, postsynaptic density protein-95 (PSD-95) was absolutely required for experience-dependent maturation of silent synapses, and its absence before the onset of critical periods resulted in lifelong juvenile ocular dominance plasticity. Loss of PSD-95 in the visual cortex after the closure of the critical period reinstated silent synapses, resulting in reopening of juvenile-like ocular dominance plasticity. Additionally, silent synapse-based ocular dominance plasticity was largely independent of the inhibitory tone, whose developmental maturation was independent of PSD-95. Moreover, glutamatergic synaptic transmission onto parvalbumin-positive interneurons was unaltered in PSD-95 KO mice. These findings reveal not only that PSD-95-dependent silent synapse maturation in visual cortical principal neurons terminates the critical period for ocular dominance plasticity but also indicate that, in general, once silent synapses are consolidated in any neural circuit, initial experience-dependent functional optimization and critical periods end."],["dc.identifier.doi","10.1073/pnas.1506488112"],["dc.identifier.isi","000356251800009"],["dc.identifier.pmid","26015564"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36839"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Progressive maturation of silent synapses governs the duration of a critical period"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","14241"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Berghoff, Stefan A."],["dc.contributor.author","Gerndt, Nina"],["dc.contributor.author","Winchenbach, Jan"],["dc.contributor.author","Stumpf, Sina Kristin"],["dc.contributor.author","Hosang, Leon"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Ruhwedel, Torben"],["dc.contributor.author","Boehler, Carolin"],["dc.contributor.author","Barrette, Benoit"],["dc.contributor.author","Stassart, Ruth"],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Edgar, Julia M."],["dc.contributor.author","Saher, Gesine"],["dc.date.accessioned","2018-11-07T10:28:16Z"],["dc.date.available","2018-11-07T10:28:16Z"],["dc.date.issued","2017"],["dc.description.abstract","Multiple Sclerosis (MS) is an inflammatory demyelinating disorder in which remyelination failure contributes to persistent disability. Cholesterol is rate-limiting for myelin biogenesis in the developing CNS; however, whether cholesterol insufficiency contributes to remyelination failure in MS, is unclear. Here, we show the relationship between cholesterol, myelination and neurological parameters in mouse models of demyelination and remyelination. In the cuprizone model, acute disease reduces serum cholesterol levels that can be restored by dietary cholesterol. Concomitant with blood-brain barrier impairment, supplemented cholesterol directly supports oligodendrocyte precursor proliferation and differentiation, and restores the balance of growth factors, creating a permissive environment for repair. This leads to attenuated axon damage, enhanced remyelination and improved motor learning. Remarkably, in experimental autoimmune encephalomyelitis, cholesterol supplementation does not exacerbate disease expression. These findings emphasize the safety of dietary cholesterol in inflammatory diseases and point to a previously unrecognized role of cholesterol in promoting repair after demyelinating episodes."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [SA 2014/2-1]; ERC Advanced grant"],["dc.identifier.doi","10.1038/ncomms14241"],["dc.identifier.isi","000392582700001"],["dc.identifier.pmid","28117328"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14258"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43386"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","2041-1723"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Dietary cholesterol promotes repair of demyelinated lesions in the adult brain"],["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","S2211124721013590"],["dc.bibliographiccitation.firstpage","109889"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cell Reports"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Berghoff, Stefan A."],["dc.contributor.author","Spieth, Lena"],["dc.contributor.author","Sun, Ting"],["dc.contributor.author","Hosang, Leon"],["dc.contributor.author","Depp, Constanze"],["dc.contributor.author","Sasmita, Andrew O."],["dc.contributor.author","Vasileva, Martina H."],["dc.contributor.author","Scholz, Patricia"],["dc.contributor.author","Zhao, Yu"],["dc.contributor.author","Krueger-Burg, Dilja"],["dc.contributor.author","Saher, Gesine"],["dc.date.accessioned","2021-12-01T09:23:54Z"],["dc.date.available","2021-12-01T09:23:54Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1016/j.celrep.2021.109889"],["dc.identifier.pii","S2211124721013590"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94788"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.issn","2211-1247"],["dc.title","Neuronal cholesterol synthesis is essential for repair of chronically demyelinated lesions in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","138"],["dc.bibliographiccitation.issue","7899"],["dc.bibliographiccitation.journal","Nature"],["dc.bibliographiccitation.lastpage","144"],["dc.bibliographiccitation.volume","603"],["dc.contributor.author","Hosang, Leon"],["dc.contributor.author","Canals, Roger Cugota"],["dc.contributor.author","van der Flier, Felicia Joy"],["dc.contributor.author","Hollensteiner, Jacqueline"],["dc.contributor.author","Daniel, Rolf"],["dc.contributor.author","Flügel, Alexander"],["dc.contributor.author","Odoardi, Francesca"],["dc.date.accessioned","2022-04-01T10:00:47Z"],["dc.date.available","2022-04-01T10:00:47Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1038/s41586-022-04427-4"],["dc.identifier.pii","4427"],["dc.identifier.pmid","35197636"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105512"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/58"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation","TRR 274: Checkpoints of Central Nervous System Recovery"],["dc.relation","TRR 274 | A03: Checkpoints determining recovery from acute autoimmune CNS grey matter lesions"],["dc.relation","TRR 274 | A04: The role of the meninges in the resolution of acute autoimmune CNS lesions"],["dc.relation.eissn","1476-4687"],["dc.relation.issn","0028-0836"],["dc.relation.workinggroup","RG Flügel"],["dc.relation.workinggroup","RG Odoardi (Echtzeitdarstellung neuroimmunologischer Prozesse)"],["dc.rights.uri","https://www.springer.com/tdm"],["dc.title","The lung microbiome regulates brain autoimmunity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","eabo7639"],["dc.bibliographiccitation.issue","37"],["dc.bibliographiccitation.journal","Science Advances"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Düking, Tim"],["dc.contributor.author","Spieth, Lena"],["dc.contributor.author","Berghoff, Stefan A."],["dc.contributor.author","Piepkorn, Lars"],["dc.contributor.author","Schmidke, Annika M."],["dc.contributor.author","Mitkovski, Miso"],["dc.contributor.author","Kannaiyan, Nirmal"],["dc.contributor.author","Hosang, Leon"],["dc.contributor.author","Scholz, Patricia"],["dc.contributor.author","Shaib, Ali H."],["dc.contributor.author","Saher, Gesine"],["dc.date.accessioned","2022-10-04T10:21:32Z"],["dc.date.available","2022-10-04T10:21:32Z"],["dc.date.issued","2022"],["dc.description.abstract","To maintain homeostasis, the body, including the brain, reprograms its metabolism in response to altered nutrition or disease. However, the consequences of these challenges for the energy metabolism of the different brain cell types remain unknown. Here, we generated a proteome atlas of the major central nervous system (CNS) cell types from young and adult mice, after feeding the therapeutically relevant low-carbohydrate, high-fat ketogenic diet (KD) and during neuroinflammation. Under steady-state conditions, CNS cell types prefer distinct modes of energy metabolism. Unexpectedly, the comparison with KD revealed distinct cell type–specific strategies to manage the altered availability of energy metabolites. Astrocytes and neurons but not oligodendrocytes demonstrated metabolic plasticity. Moreover, inflammatory demyelinating disease changed the neuronal metabolic signature in a similar direction as KD. Together, these findings highlight the importance of the metabolic cross-talk between CNS cells and between the periphery and the brain to manage altered nutrition and neurological disease."],["dc.description.abstract","Differential metabolic flexibility of brain cells facilitates managing nutritional or pathologic challenges."],["dc.identifier.doi","10.1126/sciadv.abo7639"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114437"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-600"],["dc.relation.eissn","2375-2548"],["dc.title","Ketogenic diet uncovers differential metabolic plasticity of brain cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e2006838"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","PLOS Biology"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Favaro, Plinio D."],["dc.contributor.author","Huang, Xiaojie"],["dc.contributor.author","Hosang, Leon"],["dc.contributor.author","Stodieck, Sophia"],["dc.contributor.author","Cui, Lei"],["dc.contributor.author","Liu, Yu-Zhang"],["dc.contributor.author","Engelhardt, Karl-Alexander"],["dc.contributor.author","Schmitz, Frank"],["dc.contributor.author","Dong, Yan"],["dc.contributor.author","Löwel, Siegrid"],["dc.contributor.author","Schlüter, Oliver M."],["dc.date.accessioned","2019-07-09T11:49:59Z"],["dc.date.available","2019-07-09T11:49:59Z"],["dc.date.issued","2018"],["dc.description.abstract","The disc-large (DLG)-membrane-associated guanylate kinase (MAGUK) family of proteins forms a central signaling hub of the glutamate receptor complex. Among this family, some proteins regulate developmental maturation of glutamatergic synapses, a process vulnerable to aberrations, which may lead to neurodevelopmental disorders. As is typical for paralogs, the DLG-MAGUK proteins postsynaptic density (PSD)-95 and PSD-93 share similar functional domains and were previously thought to regulate glutamatergic synapses similarly. Here, we show that they play opposing roles in glutamatergic synapse maturation. Specifically, PSD-95 promoted, whereas PSD-93 inhibited maturation of immature α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid-type glutamate receptor (AMPAR)-silent synapses in mouse cortex during development. Furthermore, through experience-dependent regulation of its protein levels, PSD-93 directly inhibited PSD-95's promoting effect on silent synapse maturation in the visual cortex. The concerted function of these two paralogs governed the critical period of juvenile ocular dominance plasticity (jODP), and fine-tuned visual perception during development. In contrast to the silent synapse-based mechanism of adjusting visual perception, visual acuity improved by different mechanisms. Thus, by controlling the pace of silent synapse maturation, the opposing but properly balanced actions of PSD-93 and PSD-95 are essential for fine-tuning cortical networks for receptive field integration during developmental critical periods, and imply aberrations in either direction of this process as potential causes for neurodevelopmental disorders."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2018"],["dc.identifier.doi","10.1371/journal.pbio.2006838"],["dc.identifier.pmid","30586380"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15797"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15829"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59674"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1545-7885"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.subject.ddc","612"],["dc.title","An opposing function of paralogs in balancing developmental synapse maturation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","ENEURO.0289-17.2017"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","eneuro"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Hosang, Leon"],["dc.contributor.author","Yusifov, Rashad"],["dc.contributor.author","Löwel, Siegrid"],["dc.date.accessioned","2020-12-10T18:42:33Z"],["dc.date.available","2020-12-10T18:42:33Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1523/ENEURO.0289-17.2017"],["dc.identifier.eissn","2373-2822"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78003"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Long-Term Visual Training Increases Visual Acuity and Long-Term Monocular Deprivation Promotes Ocular Dominance Plasticity in Adult Standard Cage-Raised Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","118988"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Biochimica et Biophysica Acta. Molecular Cell Research"],["dc.bibliographiccitation.volume","1868"],["dc.contributor.author","Löhndorf, Anke"],["dc.contributor.author","Hosang, Leon"],["dc.contributor.author","Dohle, Wolfgang"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Waschkowski, Sissy-Alina"],["dc.contributor.author","Rosche, Anette"],["dc.contributor.author","Bauche, Andreas"],["dc.contributor.author","Winzer, Riekje"],["dc.contributor.author","Tolosa, Eva"],["dc.contributor.author","Guse, Andreas H."],["dc.date.accessioned","2021-06-01T09:41:11Z"],["dc.date.available","2021-06-01T09:41:11Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1016/j.bbamcr.2021.118988"],["dc.identifier.pmid","33581218"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84840"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/21"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation","TRR 274: Checkpoints of Central Nervous System Recovery"],["dc.relation","TRR 274 | A03: Checkpoints determining recovery from acute autoimmune CNS grey matter lesions"],["dc.relation.issn","0167-4889"],["dc.relation.workinggroup","RG Flügel"],["dc.relation.workinggroup","RG Odoardi (Echtzeitdarstellung neuroimmunologischer Prozesse)"],["dc.title","2-Methoxyestradiol and its derivatives inhibit store-operated Ca2+ entry in T cells: Identification of a new and potent inhibitor"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]