Nave, Klaus-Armin

[["dc.bibliographiccitation.firstpage","673"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","674"],["dc.bibliographiccitation.volume","138"],["dc.contributor.author","Stumpf, Sina K."],["dc.contributor.author","Berghoff, Stefan A."],["dc.contributor.author","Trevisiol, Andrea"],["dc.contributor.author","Spieth, Lena"],["dc.contributor.author","Düking, Tim"],["dc.contributor.author","Schneider, Lennart V."],["dc.contributor.author","Schlaphoff, Lennart"],["dc.contributor.author","Dreha-Kulaczewski, Steffi"],["dc.contributor.author","Bley, Annette"],["dc.contributor.author","Burfeind, Dinah"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Mitkovski, Miso"],["dc.contributor.author","Ruhwedel, Torben"],["dc.contributor.author","Guder, Philipp"],["dc.contributor.author","Röhse, Heiko"],["dc.contributor.author","Denecke, Jonas"],["dc.contributor.author","Gärtner, Jutta"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Saher, Gesine"],["dc.date.accessioned","2019-11-04T14:10:22Z"],["dc.date.accessioned","2021-10-27T13:21:24Z"],["dc.date.available","2019-11-04T14:10:22Z"],["dc.date.available","2021-10-27T13:21:24Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1007/s00401-019-02064-2"],["dc.identifier.pmid","31482207"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16592"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92019"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","1432-0533"],["dc.relation.iserratumof","/handle/2/62293"],["dc.relation.issn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Correction to: Ketogenic diet ameliorates axonal defects and promotes myelination in Pelizaeus–Merzbacher disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","erratum_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","567"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","586"],["dc.bibliographiccitation.volume","61"],["dc.contributor.author","Werner, Hauke B."],["dc.contributor.author","Kraemer-Albers, Eva-Maria"],["dc.contributor.author","Strenzke, Nicola"],["dc.contributor.author","Saher, Gesine"],["dc.contributor.author","Tenzer, Stefan"],["dc.contributor.author","Ohno-Iwashita, Yoshiko"],["dc.contributor.author","Monasterio-Schrader, Patricia de"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Moser, Tobias"],["dc.contributor.author","Griffiths, Ian R."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.date.accessioned","2017-09-07T11:47:44Z"],["dc.date.available","2017-09-07T11:47:44Z"],["dc.date.issued","2013"],["dc.description.abstract","The formation of central nervous system myelin by oligodendrocytes requires sterol synthesis and is associated with a significant enrichment of cholesterol in the myelin membrane. However, it is unknown how oligodendrocytes concentrate cholesterol above the level found in nonmyelin membranes. Here, we demonstrate a critical role for proteolipids in cholesterol accumulation. Mice lacking the most abundant myelin protein, proteolipid protein (PLP), are fully myelinated, but PLP-deficient myelin exhibits a reduced cholesterol content. We therefore hypothesized that high cholesterol is not essential in the myelin sheath itself but is required for an earlier step of myelin biogenesis that is fully compensated for in the absence of PLP. We also found that a PLP-homolog, glycoprotein M6B, is a myelin component of low abundance. By targeting the Gpm6b-gene and crossbreeding, we found that single-mutant mice lacking either PLP or M6B are fully myelinated, while double mutants remain severely hypomyelinated, with enhanced neurodegeneration and premature death. As both PLP and M6B bind membrane cholesterol and associate with the same cholesterol-rich oligodendroglial membrane microdomains, we suggest a model in which proteolipids facilitate myelination by sequestering cholesterol. While either proteolipid can maintain a threshold level of cholesterol in the secretory pathway that allows myelin biogenesis, lack of both proteolipids results in a severe molecular imbalance of prospective myelin membrane. However, M6B is not efficiently sorted into mature myelin, in which it is 200-fold less abundant than PLP. Thus, only PLP contributes to the high cholesterol content of myelin by association and co-transport. (c) 2013 Wiley Periodicals, Inc."],["dc.identifier.doi","10.1002/glia.22456"],["dc.identifier.gro","3142368"],["dc.identifier.isi","000314981400010"],["dc.identifier.pmid","23322581"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7508"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: BMBF; European Commission"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0894-1491"],["dc.title","A critical role for the cholesterol-associated proteolipids PLP and M6B in myelination of the central nervous system"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["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","2205"],["dc.bibliographiccitation.issue","14"],["dc.bibliographiccitation.journal","FEBS Letters"],["dc.bibliographiccitation.lastpage","2211"],["dc.bibliographiccitation.volume","585"],["dc.contributor.author","Kassmann, Celia M."],["dc.contributor.author","Quintes, Susanne"],["dc.contributor.author","Rietdorf, Jens"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Sereda, Michael Werner"],["dc.contributor.author","Nientiedt, Tobias"],["dc.contributor.author","Saher, Gesine"],["dc.contributor.author","Baes, Myriam"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.date.accessioned","2022-03-01T11:45:09Z"],["dc.date.available","2022-03-01T11:45:09Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1016/j.febslet.2011.05.032"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103228"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.issn","0014-5793"],["dc.title","A role for myelin-associated peroxisomes in maintaining paranodal loops and axonal integrity"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","7632"],["dc.bibliographiccitation.issue","22"],["dc.bibliographiccitation.journal","Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","7645"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Fuenfschilling, Ursula"],["dc.contributor.author","Jockusch, Wolf J."],["dc.contributor.author","Sivakumar, Nandhini"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Corthals, Kristina"],["dc.contributor.author","Li, Sai"],["dc.contributor.author","Quintes, Susanne"],["dc.contributor.author","Kim, Younghoon"],["dc.contributor.author","Schaap, Iwan Alexander Taco"],["dc.contributor.author","Rhee, Jeong-Seop"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Saher, Gesine"],["dc.date.accessioned","2018-11-07T09:10:14Z"],["dc.date.available","2018-11-07T09:10:14Z"],["dc.date.issued","2012"],["dc.description.abstract","Cholesterol is an essential membrane component enriched in plasma membranes, growth cones, and synapses. The brain normally synthesizes all cholesterol locally, but the contribution of individual cell types to brain cholesterol metabolism is unknown. To investigate whether cortical projection neurons in vivo essentially require cholesterol biosynthesis and which cell types support neurons, we have conditionally ablated the cholesterol biosynthesis in these neurons in mice either embryonically or postnatally. We found that cortical projection neurons synthesize cholesterol during their entire lifetime. At all stages, they can also benefit from glial support. Adult neurons that lack cholesterol biosynthesis are mainly supported by astrocytes such that their functional integrity is preserved. In contrast, microglial cells support young neurons. However, compensatory efforts of microglia are only transient leading to layer-specific neuronal death and the reduction of cortical projections. Hence, during the phase of maximal membrane growth and maximal cholesterol demand, neuronal cholesterol biosynthesis is indispensable. Analysis of primary neurons revealed that neurons tolerate only slight alteration in the cholesterol content and plasma membrane tension. This quality control allows neurons to differentiate normally and adjusts the extent of neurite outgrowth, the number of functional growth cones and synapses to the available cholesterol. This study highlights both the flexibility and the limits of horizontal cholesterol transfer in vivo and may have implications for the understanding of neurodegenerative diseases."],["dc.identifier.doi","10.1523/JNEUROSCI.1352-11.2012"],["dc.identifier.fs","596609"],["dc.identifier.isi","000304627100022"],["dc.identifier.pmid","22649242"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8454"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26441"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Soc Neuroscience"],["dc.relation.issn","0270-6474"],["dc.relation.orgunit","Fakultät für Physik"],["dc.title","Critical Time Window of Neuronal Cholesterol Synthesis during Neurite Outgrowth"],["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.firstpage","1143"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","1149"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Stepniak, Beata"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Tantra, Martesa"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.contributor.author","Pardo, Luis A."],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Mohd Jofrry, Sue"],["dc.contributor.author","Gurvich, Artem"],["dc.contributor.author","Jensen, Niels"],["dc.contributor.author","Ostmeier, Katrin"],["dc.contributor.author","Lühder, F."],["dc.contributor.author","Probst, Christian"],["dc.contributor.author","Martens, Henrik"],["dc.contributor.author","Gillis, M."],["dc.contributor.author","Saher, Gesine"],["dc.contributor.author","Assogna, F."],["dc.contributor.author","Spalletta, Gianfranco"],["dc.contributor.author","Stöcker, W."],["dc.contributor.author","Schulz, Thomas F."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:37Z"],["dc.date.available","2017-09-07T11:46:37Z"],["dc.date.issued","2014"],["dc.description.abstract","In 2007, a multifaceted syndrome, associated with anti-NMDA receptor autoantibodies (NMDAR-AB) of immunoglobulin-G isotype, has been described, which variably consists of psychosis, epilepsy, cognitive decline and extrapyramidal symptoms. Prevalence and significance of NMDAR-AB in complex neuropsychiatric disease versus health, however, have remained unclear. We tested sera of 2817 subjects (1325 healthy, 1081 schizophrenic, 263 Parkinson and 148 affective-disorder subjects) for presence of NMDAR-AB, conducted a genome-wide genetic association study, comparing AB carriers versus non-carriers, and assessed their influenza AB status. For mechanistic insight and documentation of AB functionality, in vivo experiments involving mice with deficient blood-brain barrier (ApoE(-/-)) and in vitro endocytosis assays in primary cortical neurons were performed. In 10.5% of subjects, NMDAR-AB (NR1 subunit) of any immunoglobulin isotype were detected, with no difference in seroprevalence, titer or in vitro functionality between patients and healthy controls. Administration of extracted human serum to mice influenced basal and MK-801-induced activity in the open field only in ApoE(-/-) mice injected with NMDAR-AB-positive serum but not in respective controls. Seropositive schizophrenic patients with a history of neurotrauma or birth complications, indicating an at least temporarily compromised blood-brain barrier, had more neurological abnormalities than seronegative patients with comparable history. A common genetic variant (rs524991, P=6.15E-08) as well as past influenza A (P=0.024) or B (P=0.006) infection were identified as predisposing factors for NMDAR-AB seropositivity. The >10% overall seroprevalence of NMDAR-AB of both healthy individuals and patients is unexpectedly high. Clinical significance, however, apparently depends on association with past or present perturbations of blood-brain barrier function."],["dc.identifier.doi","10.1038/mp.2013.110"],["dc.identifier.gro","3150565"],["dc.identifier.pmid","23999527"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7339"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","Neuropsychiatric disease relevance of circulating anti-NMDA receptor autoantibodies depends on blood-brain barrier integrity"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S115"],["dc.bibliographiccitation.issue","13"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","S116"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","de Monasterio-Schrader, P."],["dc.contributor.author","Werner, Hauke B."],["dc.contributor.author","Kraemer-Albers, Eva-Maria"],["dc.contributor.author","Strenzke, Nicola"],["dc.contributor.author","Saher, Gesine"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Tenzer, S."],["dc.contributor.author","Ohno-Iwashita, Y."],["dc.contributor.author","Moser, Tobias"],["dc.contributor.author","Griffiths, I. R."],["dc.contributor.author","Nave, K. A."],["dc.date.accessioned","2018-11-07T11:23:39Z"],["dc.date.available","2018-11-07T11:23:39Z"],["dc.date.issued","2009"],["dc.identifier.isi","000270075500479"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56236"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.publisher.place","Hoboken"],["dc.relation.conference","9th European Meeting on Glial Cells in Health and Disease"],["dc.relation.eventlocation","Paris, FRANCE"],["dc.relation.issn","0894-1491"],["dc.title","High-Level Expression of the Proteolipids Plp and M6b is Sufficient to Induce Oligodendroglial Process Outgrowth in Vitro and Required for Normal Myelination in Vivo"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1130"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Nature Medicine"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Saher, Gesine"],["dc.contributor.author","Rudolphi, Fabian"],["dc.contributor.author","Corthals, Kristina"],["dc.contributor.author","Ruhwedel, Torben"],["dc.contributor.author","Schmidt, Karl-Friedrich"],["dc.contributor.author","Loewel, Siegrid"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Barrette, Benoit"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.date.accessioned","2018-11-07T09:08:43Z"],["dc.date.available","2018-11-07T09:08:43Z"],["dc.date.issued","2012"],["dc.description.abstract","Duplication of PLP1 (proteolipid protein gene 1) and the subsequent overexpression of the myelin protein PLP (also known as DM20) in oligodendrocytes is the most frequent cause of Pelizaeus-Merzbacher disease (PMD), a fatal leukodystrophy(1) without therapeutic options(2,3). PLP binds cholesterol and is contained within membrane lipid raft microdomains(4). Cholesterol availability is the rate-limiting factor of central nervous system myelin synthesis(5). Transgenic mice with extra copies of the Plp1 gene(6) are accurate models of PMD. Dysmyelination(6-8) followed by demyelination(9,10), secondary inflammation and axon damage contribute to the severe motor impairment in these mice(9,10). The finding that in Plp1-transgenic oligodendrocytes, PLP and cholesterol accumulate in late endosomes and lysosomes (endo/lysosomes)(9,11-13), prompted us to further investigate the role of cholesterol in PMD. Here we show that cholesterol itself promotes normal PLP trafficking and that dietary cholesterol influences PMD pathology. In a preclinical trial, PMD mice were fed a cholesterol-enriched diet. This restored oligodendrocyte numbers and ameliorated intracellular PLP accumulation. Moreover, myelin content increased, inflammation and gliosis were reduced and motor defects improved. Even after onset of clinical symptoms, cholesterol treatment prevented disease progression. Dietary cholesterol did not reduce Plp1 overexpression but facilitated incorporation of PLP into myelin membranes. These findings may have implications for therapeutic interventions in patients with PMD."],["dc.identifier.doi","10.1038/nm.2833"],["dc.identifier.isi","000306121600044"],["dc.identifier.pmid","22706386"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26092"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1078-8956"],["dc.title","Therapy of Pelizaeus-Merzbacher disease in mice by feeding a cholesterol-enriched diet"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1489"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","1501"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Pan, Hong"],["dc.contributor.author","Oliveira, Bárbara"],["dc.contributor.author","Saher, Gesine"],["dc.contributor.author","Dere, Ekrem"],["dc.contributor.author","Tapken, Daniel"],["dc.contributor.author","Mitjans, Marina"],["dc.contributor.author","Seidel, Jan"],["dc.contributor.author","Wesolowski, Janina"],["dc.contributor.author","Wakhloo, Debia"],["dc.contributor.author","Klein-Schmidt, Christina"],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Schwabe, Kerstin"],["dc.contributor.author","Trippe, Ralf"],["dc.contributor.author","Mätz-Rensing, Kerstin"],["dc.contributor.author","Berghoff, Stefan"],["dc.contributor.author","Al-Krinawe, Yazeed"],["dc.contributor.author","Martens, Henrik"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Kaup, Franz-Josef"],["dc.contributor.author","Mischke, Reinhard"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Krauss, Joachim K."],["dc.contributor.author","Hollmann, Michael"],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2020-12-10T18:09:36Z"],["dc.date.available","2020-12-10T18:09:36Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1038/s41380-017-0011-3"],["dc.identifier.eissn","1476-5578"],["dc.identifier.issn","1359-4184"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15575"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73703"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC-SA 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-sa/4.0"],["dc.title","Uncoupling the widespread occurrence of anti-NMDAR1 autoantibodies from neuropsychiatric disease in a novel autoimmune model"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMC Neuroscience"],["dc.bibliographiccitation.lastpage","9"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Fünfschilling, Ursula"],["dc.contributor.author","Saher, Gesine"],["dc.contributor.author","Xiao, Le"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.date.accessioned","2019-07-09T11:41:50Z"],["dc.date.available","2019-07-09T11:41:50Z"],["dc.date.issued","2007"],["dc.description.abstract","Background: Cholesterol, an essential component of all mammalian plasma membranes, is highly enriched in the brain. Both during development and in the adult, brain cholesterol is derived from local cholesterol synthesis and not taken up from the circulation. However, the contribution of neurons and glial cells to total brain cholesterol metabolism is unknown.Results: Using conditional gene inactivation in the mouse, we disrupted the squalene synthase gene (fdft1), which is critical for cholesterol synthesis, in cerebellar granule cells and some precerebellar nuclei. Mutant mice showed no histological signs of neuronal degeneration, displayed ultrastructurally normal synapses, and exhibited normal motor coordination. This revealed that these adult neurons do not require cell-autonomous cholesterol synthesis for survival or function."],["dc.identifier.doi","10.1186/1471-2202-8-1"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/1246"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58528"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.subject.ddc","619"],["dc.title","Survival of adult neurons lacking cholesterol synthesis in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]