Göbbels, Sandra

[["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.contributor.author","Butt, Umer Javed"],["dc.contributor.author","Steixner-Kumar, Agnes A."],["dc.contributor.author","Depp, Constanze"],["dc.contributor.author","Sun, Ting"],["dc.contributor.author","Hassouna, Imam"],["dc.contributor.author","Wüstefeld, Liane"],["dc.contributor.author","Arinrad, Sahab"],["dc.contributor.author","Zillmann, Matthias R."],["dc.contributor.author","Schopf, Nadine"],["dc.contributor.author","Fernandez Garcia-Agudo, Laura"],["dc.contributor.author","Mohrmann, Leonie"],["dc.contributor.author","Bode, Ulli"],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Hindermann, Martin"],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Katschinski, Dörthe M."],["dc.contributor.author","Miskowiak, Kamilla W."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2021-04-14T08:28:40Z"],["dc.date.available","2021-04-14T08:28:40Z"],["dc.date.issued","2021"],["dc.description.abstract","Physical activity and cognitive challenge are established non-invasive methods to induce comprehensive brain activation and thereby improve global brain function including mood and emotional well-being in healthy subjects and in patients. However, the mechanisms underlying this experimental and clinical observation and broadly exploited therapeutic tool are still widely obscure. Here we show in the behaving brain that physiological (endogenous) hypoxia is likely a respective lead mechanism, regulating hippocampal plasticity via adaptive gene expression. A refined transgenic approach in mice, utilizing the oxygen-dependent degradation (ODD) domain of HIF-1α fused to CreERT2 recombinase, allows us to demonstrate hypoxic cells in the performing brain under normoxia and motor-cognitive challenge, and spatially map them by light-sheet microscopy, all in comparison to inspiratory hypoxia as strong positive control. We report that a complex motor-cognitive challenge causes hypoxia across essentially all brain areas, with hypoxic neurons particularly abundant in the hippocampus. These data suggest an intriguing model of neuroplasticity, in which a specific task-associated neuronal activity triggers mild hypoxia as a local neuron-specific as well as a brain-wide response, comprising indirectly activated neurons and non-neuronal cells."],["dc.identifier.doi","10.1038/s41380-020-00988-w"],["dc.identifier.pmid","33564132"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82678"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/31"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/104"],["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 | C01: Oligodendroglial NMDA receptors and NMDAR1 autoantibodies as determinants of axonal integrity in neuropsychiatric disease"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | Z02: Integrative Datenanalyse und -interpretation. Generierung einer synaptisch-integrativen Datenstrategie (SynIDs)"],["dc.relation.eissn","1476-5578"],["dc.relation.issn","1359-4184"],["dc.relation.workinggroup","RG Ehrenreich (Clinical Neuroscience)"],["dc.relation.workinggroup","RG Nave (Neurogenetics)"],["dc.relation.workinggroup","RG Bonn"],["dc.rights","CC BY 4.0"],["dc.title","Hippocampal neurons respond to brain activity with functional hypoxia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","528"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.lastpage","539"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Hagemeyer, Nora"],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Hofer, Sabine"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Gerwig, Ulrike C."],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Wieser, Georg L."],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Gurvich, Artem"],["dc.contributor.author","Heckers, Stephan H."],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-08-25T10:14:17Z"],["dc.date.available","2017-08-25T10:14:17Z"],["dc.date.issued","2012"],["dc.description.abstract","Severe mental illnesses have been linked to white matter abnormalities, documented by postmortem studies. However, cause and effect have remained difficult to distinguish. CNP (2',3'-cyclic nucleotide 3'-phosphodiesterase) is among the oligodendrocyte/myelin-associated genes most robustly reduced on mRNA and protein level in brains of schizophrenic, bipolar or major depressive patients. This suggests that CNP reduction might be critical for a more general disease process and not restricted to a single diagnostic category. We show here that reduced expression of CNP is the primary cause of a distinct behavioural phenotype, seen only upon aging as an additional 'pro-inflammatory hit'. This phenotype is strikingly similar in Cnp heterozygous mice and patients with mental disease carrying the AA genotype at CNP SNP rs2070106. The characteristic features in both species with their partial CNP 'loss-of-function' genotype are best described as 'catatonia-depression' syndrome. As a consequence of perturbed CNP expression, mice show secondary low-grade inflammation/neurodegeneration. Analogously, in man, diffusion tensor imaging points to axonal loss in the frontal corpus callosum. To conclude, subtle white matter abnormalities inducing neurodegenerative changes can cause/amplify psychiatric diseases."],["dc.identifier.doi","10.1002/emmm.201200230"],["dc.identifier.gro","3150560"],["dc.identifier.pmid","22473874"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7776"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7334"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","A myelin gene causative of a catatonia-depression syndrome upon aging"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1752"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","1767"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Hassouna, I."],["dc.contributor.author","Ott, C."],["dc.contributor.author","Wüstefeld, L."],["dc.contributor.author","Offen, N."],["dc.contributor.author","Neher, R. A."],["dc.contributor.author","Mitkovski, M."],["dc.contributor.author","Winkler, D."],["dc.contributor.author","Sperling, S."],["dc.contributor.author","Fries, L."],["dc.contributor.author","Goebbels, S."],["dc.contributor.author","Vreja, I. C."],["dc.contributor.author","Hagemeyer, N."],["dc.contributor.author","Dittrich, M."],["dc.contributor.author","Rossetti, M. F."],["dc.contributor.author","Kröhnert, K."],["dc.contributor.author","Hannke, K."],["dc.contributor.author","Boretius, S."],["dc.contributor.author","Zeug, A."],["dc.contributor.author","Höschen, C."],["dc.contributor.author","Dandekar, T."],["dc.contributor.author","Dere, E."],["dc.contributor.author","Neher, E."],["dc.contributor.author","Rizzoli, S. O."],["dc.contributor.author","Nave, K.-A."],["dc.contributor.author","Sirén, A.-L."],["dc.contributor.author","Ehrenreich, H."],["dc.date.accessioned","2017-09-07T11:53:29Z"],["dc.date.available","2017-09-07T11:53:29Z"],["dc.date.issued","2016"],["dc.description.abstract","Recombinant human erythropoietin (EPO) improves cognitive performance in neuropsychiatric diseases ranging from schizophrenia and multiple sclerosis to major depression and bipolar disease. This consistent EPO effect on cognition is independent of its role in hematopoiesis. The cellular mechanisms of action in brain, however, have remained unclear. Here we studied healthy young mice and observed that 3-week EPO administration was associated with an increased number of pyramidal neurons and oligodendrocytes in the hippocampus of ~20%. Under constant cognitive challenge, neuron numbers remained elevated until >6 months of age. Surprisingly, this increase occurred in absence of altered cell proliferation or apoptosis. After feeding a 15N-leucine diet, we used nanoscopic secondary ion mass spectrometry, and found that in EPO-treated mice, an equivalent number of neurons was defined by elevated 15N-leucine incorporation. In EPO-treated NG2-Cre-ERT2 mice, we confirmed enhanced differentiation of preexisting oligodendrocyte precursors in the absence of elevated DNA synthesis. A corresponding analysis of the neuronal lineage awaits the identification of suitable neuronal markers. In cultured neurospheres, EPO reduced Sox9 and stimulated miR124, associated with advanced neuronal differentiation. We are discussing a resulting working model in which EPO drives the differentiation of non-dividing precursors in both (NG2+) oligodendroglial and neuronal lineages. As endogenous EPO expression is induced by brain injury, such a mechanism of adult neurogenesis may be relevant for central nervous system regeneration."],["dc.identifier.doi","10.1038/mp.2015.212"],["dc.identifier.fs","620695"],["dc.identifier.gro","3145088"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14225"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2785"],["dc.language.iso","en"],["dc.notes.intern","Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.issn","1359-4184"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Revisiting adult neurogenesis and the role of erythropoietin for neuronal and oligodendroglial differentiation in the hippocampus"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2025"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","2040"],["dc.bibliographiccitation.volume","64"],["dc.contributor.author","Poggi, Giulia"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Moschny, Nicole"],["dc.contributor.author","Baudewig, Jürgen"],["dc.contributor.author","Ruhwedel, Torben"],["dc.contributor.author","Hassouna, Imam"],["dc.contributor.author","Wieser, Georg L."],["dc.contributor.author","Werner, Hauke B."],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:44:51Z"],["dc.date.available","2017-09-07T11:44:51Z"],["dc.date.issued","2016"],["dc.description.abstract","Subtle white matter abnormalities have emerged as a hallmark of brain alterations in magnetic resonance imaging or upon autopsy of mentally ill subjects. However, it is unknown whether such reduction of white matter and myelin contributes to any disease-relevant phenotype or simply constitutes an epiphenomenon, possibly even treatment-related. Here, we have re-analyzed Mbp heterozygous mice, the unaffected parental strain of shiverer, a classical neurological mutant. Between 2 and 20 months of age, Mbp+/- versus Mbp+/+ littermates were deeply phenotyped by combining extensive behavioral/cognitive testing with MRI, 1H-MR spectroscopy, electron microscopy, and molecular techniques. Surprisingly, Mbp-dependent myelination was significantly reduced in the prefrontal cortex. We also noticed a mild but progressive hypomyelination of the prefrontal corpus callosum and low-grade inflammation. While most behavioral functions were preserved, Mbp+/- mice exhibited defects of sensorimotor gating, as evidenced by reduced prepulse-inhibition, and a late-onset catatonia phenotype. Thus, subtle but primary abnormalities of CNS myelin can be the cause of a persistent cortical network dysfunction including catatonia, features typical of neuropsychiatric conditions."],["dc.identifier.doi","10.1002/glia.23039"],["dc.identifier.gro","3150347"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14054"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7101"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.issn","0894-1491"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Cortical network dysfunction caused by a subtle defect of myelination"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","734"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Clinical Investigation"],["dc.bibliographiccitation.lastpage","745"],["dc.bibliographiccitation.volume","128"],["dc.contributor.author","Janova, Hana"],["dc.contributor.author","Arinrad, Sahab"],["dc.contributor.author","Balmuth, Evan"],["dc.contributor.author","Mitjans, Marina"],["dc.contributor.author","Hertel, Johannes"],["dc.contributor.author","Habes, Mohamad"],["dc.contributor.author","Bittner, Robert A."],["dc.contributor.author","Pan, Hong"],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Gerwig, Ulrike C."],["dc.contributor.author","Langner, Sönke"],["dc.contributor.author","Werner, Hauke B."],["dc.contributor.author","Kittel-Schneider, Sarah"],["dc.contributor.author","Homuth, Georg"],["dc.contributor.author","Davatzikos, Christos"],["dc.contributor.author","Völzke, Henry"],["dc.contributor.author","West, Brian L."],["dc.contributor.author","Reif, Andreas"],["dc.contributor.author","Grabe, Hans Jörgen"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.date.accessioned","2020-12-10T18:38:19Z"],["dc.date.available","2020-12-10T18:38:19Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1172/JCI97032"],["dc.identifier.eissn","1558-8238"],["dc.identifier.issn","0021-9738"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77272"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Microglia ablation alleviates myelin-associated catatonic signs in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","869"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","GLIA"],["dc.bibliographiccitation.lastpage","880"],["dc.bibliographiccitation.volume","61"],["dc.contributor.author","Wieser, Georg L."],["dc.contributor.author","Gerwig, Ulrike C."],["dc.contributor.author","Adamcio, Bartosz"],["dc.contributor.author","Barrette, Benoit"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Goebbels, Sandra"],["dc.date.accessioned","2017-09-07T11:46:35Z"],["dc.date.available","2017-09-07T11:46:35Z"],["dc.date.issued","2013"],["dc.description.abstract","Oligodendrocytes make myelin for rapid impulse propagation and contribute to the long-term survival of myelinated axons. The mechanisms by which oligodendroglial dysfunction(s) contribute to slowly progressive neurodegeneration are not well understood. Here, we demonstrate in Cnp1 mutant mice that secondary axonal degeneration in the subcortical white matter is associated with an age-dependent activation of both, innate and adaptive immune responses, including an expansion of infiltrating CD8+ T cells. While the detrimental role of lymphocytes in inherited myelin diseases is known, the role of activated microglia for the hypothetical cycle of inflammation/degeneration is unclear. We used a mild standardized cryolesion of the right parietal cortex to activate microglia at the vulnerable age of mouse puberty (postnatal day (P) 28). When applied to Cnp1 mutant mice, analyzed more than 3 months later, minor brain injury had acted as a “second hit” and significantly enhanced astrogliosis, microgliosis and axon degeneration, but not T cell infiltration. Interestingly, exacerbated neuropathological changes were also reflected by specific deterioration of working memory on top of an essentially normal basic behavior. We propose a model in which oligodendroglial dysfunctions can trigger a vicious cycle of neurodegeneration and low-grade inflammation that is amplified by nonspecific activators of the innate immune system. This interaction of genetic and environmental factors may be relevant for neuropsychiatric diseases associated with secondary neuroinflammation."],["dc.identifier.doi","10.1002/glia.22480"],["dc.identifier.gro","3150535"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7307"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","Neuroinflammation in white matter tracts of Cnp1 mutant mice amplified by a minor brain injury"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","581"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Neuron"],["dc.bibliographiccitation.lastpage","595"],["dc.bibliographiccitation.volume","59"],["dc.contributor.author","Brinkmann, Bastian G."],["dc.contributor.author","Agarwal, Amit"],["dc.contributor.author","Sereda, Michael W."],["dc.contributor.author","Garratt, Alistair N."],["dc.contributor.author","Müller, Thomas"],["dc.contributor.author","Wende, Hagen"],["dc.contributor.author","Stassart, Ruth M."],["dc.contributor.author","Nawaz, Schanila"],["dc.contributor.author","Humml, Christian"],["dc.contributor.author","Velanac, Viktorija"],["dc.contributor.author","Radyushkin, Konstantin"],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Fischer, Tobias M."],["dc.contributor.author","Franklin, Robin J."],["dc.contributor.author","Lai, Cary"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Birchmeier, Carmen"],["dc.contributor.author","Schwab, Markus H."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.date.accessioned","2017-09-07T11:46:36Z"],["dc.date.available","2017-09-07T11:46:36Z"],["dc.date.issued","2008-08-28"],["dc.description.abstract","Understanding the control of myelin formation by oligodendrocytes is essential for treating demyelinating diseases. Neuregulin-1 (NRG1) type III, an EGF-like growth factor, is essential for myelination in the PNS. It is thus thought that NRG1/ErbB signaling also regulates CNS myelination, a view suggested by in vitro studies and the overexpression of dominant-negative ErbB receptors. To directly test this hypothesis, we generated a series of conditional null mutants that completely lack NRG1 beginning at different stages of neural development. Unexpectedly, these mice assemble normal amounts of myelin. In addition, double mutants lacking oligodendroglial ErbB3 and ErbB4 become myelinated in the absence of any stimulation by neuregulins. In contrast, a significant hypermyelination is achieved by transgenic overexpression of NRG1 type I or NRG1 type III. Thus, NRG1/ErbB signaling is markedly different between Schwann cells and oligodendrocytes that have evolved an NRG/ErbB-independent mechanism of myelination control."],["dc.identifier.doi","10.1016/j.neuron.2008.06.028"],["dc.identifier.gro","3150555"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7329"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.subject","molneuro; devbio"],["dc.title","Neuregulin-1/ErbB signaling serves distinct functions in myelination of the peripheral and central nervous system"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]