Dibaj, Payam

[["dc.bibliographiccitation.firstpage","447"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Cell Science"],["dc.bibliographiccitation.lastpage","458"],["dc.bibliographiccitation.volume","124"],["dc.contributor.author","Fitzner, Dirk"],["dc.contributor.author","Schnaars, Mareike"],["dc.contributor.author","van Rossum, Denise"],["dc.contributor.author","Krishnamoorthy, Gurumoorthy"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Bakhti, Mostafa"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Simons, Mikael"],["dc.date.accessioned","2018-11-07T08:59:39Z"],["dc.date.available","2018-11-07T08:59:39Z"],["dc.date.issued","2011"],["dc.description.abstract","The transfer of antigens from oligodendrocytes to immune cells has been implicated in the pathogenesis of autoimmune diseases. Here, we show that oligodendrocytes secrete small membrane vesicles called exosomes, which are specifically and efficiently taken up by microglia both in vitro and in vivo. Internalisation of exosomes occurs by a macropinocytotic mechanism without inducing a concomitant inflammatory response. After stimulation of microglia with interferon-gamma, we observe an upregulation of MHC class II in a subpopulation of microglia. However, exosomes are preferentially internalised in microglia that do not seem to have antigen-presenting capacity. We propose that the constitutive macropinocytotic clearance of exosomes by a subset of microglia represents an important mechanism through which microglia participate in the degradation of oligodendroglial membrane in an immunologically 'silent' manner. By designating the capacity for macropinocytosis and antigen presentation to distinct cells, degradation and immune function might be assigned to different subtypes of microglia."],["dc.description.sponsorship","ERC; EMBO YIP; German Research Council [SFB/TR43]"],["dc.identifier.doi","10.1242/jcs.074088"],["dc.identifier.isi","000286223600016"],["dc.identifier.pmid","21242314"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8034"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23953"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Company Of Biologists Ltd"],["dc.relation.issn","0021-9533"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Selective transfer of exosomes from oligodendrocytes to microglia by macropinocytosis"],["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","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.firstpage","323"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","European Neurology"],["dc.bibliographiccitation.lastpage","324"],["dc.bibliographiccitation.volume","83"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Schnegelsberg, Margret"],["dc.contributor.author","Kröger, Renate"],["dc.date.accessioned","2021-04-14T08:24:01Z"],["dc.date.available","2021-04-14T08:24:01Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1159/000508496"],["dc.identifier.pmid","32668437"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81136"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.publisher","S. Karger AG"],["dc.relation.eissn","1421-9913"],["dc.relation.issn","0014-3022"],["dc.rights","https://www.karger.com/Services/SiteLicenses"],["dc.title","Lyme Neuroborreliosis with Long Meningeal Enhancement and Ischemic Stroke"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","eLife"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Patzig, Julia"],["dc.contributor.author","Erwig, Michelle S"],["dc.contributor.author","Tenzer, Stefan"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Schaeren-Wiemers, Nicole"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Werner, Hauke B"],["dc.date.accessioned","2021-06-01T10:48:59Z"],["dc.date.available","2021-06-01T10:48:59Z"],["dc.date.issued","2016"],["dc.description.abstract","Myelination of axons facilitates rapid impulse propagation in the nervous system. The axon/myelin-unit becomes impaired in myelin-related disorders and upon normal aging. However, the molecular cause of many pathological features, including the frequently observed myelin outfoldings, remained unknown. Using label-free quantitative proteomics, we find that the presence of myelin outfoldings correlates with a loss of cytoskeletal septins in myelin. Regulated by phosphatidylinositol-(4,5)-bisphosphate (PI(4,5)P2)-levels, myelin septins (SEPT2/SEPT4/SEPT7/SEPT8) and the PI(4,5)P2-adaptor anillin form previously unrecognized filaments that extend longitudinally along myelinated axons. By confocal microscopy and immunogold-electron microscopy, these filaments are localized to the non-compacted adaxonal myelin compartment. Genetic disruption of these filaments in Sept8-mutant mice causes myelin outfoldings as a very specific neuropathology. Septin filaments thus serve an important function in scaffolding the axon/myelin-unit, evidently a late stage of myelin maturation. We propose that pathological or aging-associated diminishment of the septin/anillin-scaffold causes myelin outfoldings that impair the normal nerve conduction velocity."],["dc.description.abstract","Normal communication within the brain or between the brain and other parts of the body requires information to flow quickly around the nervous system. This information travels along nerve cells in the form of electrical signals. To speed up the signals, a part of the nerve cell called the axon is frequently wrapped in an electrically insulating sheath made up of a membrane structure called myelin. The myelin sheath becomes impaired as a result of disease or ageing. In order to understand what might produce these changes, Patzig et al. have used biochemical and microscopy techniques to study mice that had similar defects in their myelin sheaths. The study reveals that forming a normal myelin sheath around an axon requires a newly identified ‘scaffold’ made of a group of proteins called the septins. Combining with another protein called anillin, septins assemble into filaments in the myelin sheath. These filaments then knit together into a scaffold that grows lengthways along the myelin-wrapped axon. Without this scaffold, the myelin sheath grew defects known as outfoldings. Axons transmitted electrical signals much more slowly than normal when the septin scaffold was missing from the myelin sheath. Future studies are needed to understand the factors that control how the septin scaffold forms. This could help to reveal ways of reversing the changes that alter the myelin sheath during ageing and disease."],["dc.identifier.doi","10.7554/eLife.17119"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13756"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86124"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2050-084X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Septin/anillin filaments scaffold central nervous system myelin to accelerate nerve conduction"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e17910"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Steffens, Heinz"],["dc.contributor.author","Zschuentzsch, Jana"],["dc.contributor.author","Nadrigny, Fabien"],["dc.contributor.author","Schomburg, Eike D."],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Neusch, Clemens"],["dc.date.accessioned","2018-11-07T08:58:04Z"],["dc.date.available","2018-11-07T08:58:04Z"],["dc.date.issued","2011"],["dc.description.abstract","Mutations in the enzyme superoxide dismutase-1 (SOD1) cause hereditary variants of the fatal motor neuronal disease Amyotrophic lateral sclerosis (ALS). Pathophysiology of the disease is non-cell-autonomous: neurotoxicity is derived not only from mutant motor neurons but also from mutant neighbouring non-neuronal cells. In vivo imaging by two-photon laser-scanning microscopy was used to compare the role of microglia/macrophage-related neuroinflammation in the CNS and PNS using ALS-linked transgenic SOD1(G93A) mice. These mice contained labeled projection neurons and labeled microglia/macrophages. In the affected lateral spinal cord (in contrast to non-affected dorsal columns), different phases of microglia-mediated inflammation were observed: highly reactive microglial cells in preclinical stages (in 60-day-old mice the reaction to axonal transection was similar to 180% of control) and morphologically transformed microglia that have lost their function of tissue surveillance and injury-directed response in clinical stages (reaction to axonal transection was lower than 50% of control). Furthermore, unlike CNS microglia, macrophages of the PNS lack any substantial morphological reaction while preclinical degeneration of peripheral motor axons and neuromuscular junctions was observed. We present in vivo evidence for a different inflammatory activity of microglia and macrophages: an aberrant neuroinflammatory response of microglia in the CNS and an apparently mainly neurodegenerative process in the PNS."],["dc.identifier.doi","10.1371/journal.pone.0017910"],["dc.identifier.isi","000288545100043"],["dc.identifier.pmid","21437247"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8214"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23554"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","In Vivo Imaging Reveals Distinct Inflammatory Activity of CNS Microglia versus PNS Macrophages in a Mouse Model for ALS"],["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","95"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Physiological research / Academia Scientiarum Bohemoslovaca"],["dc.bibliographiccitation.lastpage","105"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Zschüntzsch, J."],["dc.contributor.author","Ebert, S."],["dc.contributor.author","Hülsmann, S."],["dc.contributor.author","Dibaj, P."],["dc.contributor.author","Neusch, C."],["dc.date.accessioned","2019-07-10T08:14:00Z"],["dc.date.available","2019-07-10T08:14:00Z"],["dc.date.issued","2013"],["dc.description.abstract","Heterologeous expression of Kir channels offers a tool to modulate excitability of neurons which provide insight into Kir channel functions in general. Inwardly-rectifying K(+) channels (Kir channels) are potential candidate proteins to hyperpolarise neuronal cell membranes. However, heterologeous expression of inwardly-rectifying K(+) channels has previously proven to be difficult. This was mainly due to a high toxicity of the respective Kir channel expression. We investigated the putative role of a predominantly glial-expressed, weakly rectifying Kir channel (Kir4.1 channel subunit; KCNJ10) in modulating electrophysiological properties of a motoneuron-like cell culture (NSC34). Transfection procedures using an EGFP-tagged Kir4.1 protein in this study proved to have no toxic effects on NSC34 cells. Using whole cell-voltage clamp, a substantial increase of inward rectifying K(+) currents as well as hyperpolarisation of the cell membrane was observed in Kir4.1-transfected cells. Na(+) inward currents, observed in NSC34 controls, were absent in Kir4.1-EGFP motoneuronal cells. The Kir4.1-transfection did not influence the NaV1.6 sodium channel expression. This study demonstrates the general feasibility of a heterologeous expression of a weakly inward-rectifying K(+) channel (Kir4.1 subunit) and shows that in vitro overexpression of Kir4.1 shifts electrophysiological properties of neuronal cells to a more glial-like phenotype and may therefore be a candidate tool to dampen excitability of neurons in experimental paradigms."],["dc.identifier.pmid","23173681"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8473"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61403"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1802-9973"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.title","Heterologeous expression of a glial Kir channel (KCNJ10) in a neuroblastoma spinal cord (NSC-34) cell line."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e43963"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","PlosOne"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Zschüntzsch, Jana"],["dc.contributor.author","Steffens, Heinz"],["dc.contributor.author","Scheffel, Jörg"],["dc.contributor.author","Göricke, Bettina"],["dc.contributor.author","Weishaupt, Jochen H."],["dc.contributor.author","Le Meur, Karim"],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Schomburg, Eike D."],["dc.contributor.author","Neusch, Clemens"],["dc.date.accessioned","2019-07-09T11:53:39Z"],["dc.date.available","2019-07-09T11:53:39Z"],["dc.date.issued","2012"],["dc.description.abstract","Mutations in SOD1 cause hereditary variants of the fatal motor neuron disease amyotrophic lateral sclerosis (ALS). Pathophysiology of the disease is non-cell-autonomous, with toxicity deriving also from glia. In particular, microglia contribute to disease progression. Methylene blue (MB) inhibits the effect of nitric oxide, which mediates microglial responses to injury. In vivo 2P-LSM imaging was performed in ALS-linked transgenic SOD1G93A mice to investigate the effect of MB on microglia-mediated inflammation in the spinal cord. Local superfusion of the lateral spinal cord with MB inhibited the microglial reaction directed at a laser-induced axon transection in control and SOD1G93A mice. In vitro, MB at high concentrations inhibited cytokine and chemokine release from microglia of control and advanced clinical SOD1G93A mice. Systemic MB-treatment of SOD1G93A mice at early preclinical stages significantly delayed disease onset and motor dysfunction. However, an increase of MB dose had no additional effect on disease progression; this was unexpected in view of the local anti-inflammatory effects. Furthermore, in vivo imaging of systemically MB-treated mice also showed no alterations of microglia activity in response to local lesions. Thus although systemic MB treatment had no effect on microgliosis, instead, its use revealed an important influence on motor neuron survival as indicated by an increased number of lumbar anterior horn neurons present at the time of disease onset. Thus, potentially beneficial effects of locally applied MB on inflammatory events contributing to disease progression could not be reproduced in SOD1G93A mice via systemic administration, whereas systemic MB application delayed disease onset via neuroprotection."],["dc.format.extent","13"],["dc.identifier.doi","10.1371/journal.phone.0043963"],["dc.identifier.fs","592827"],["dc.identifier.pmid","22952827"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7861"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60471"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Influence of Methylene Blue on Microglia-Induced Inflammation and Motor Neuron Degeneration in the SOD1G93A Model for ALS"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neurology International"],["dc.bibliographiccitation.volume","13"],["dc.contributor.affiliation","Dibaj, Payam; \t\t \r\n\t\t Center for Rare Diseases Göttingen (ZSEG), University Medical Center Göttingen, Georg August University, 37075 Göttingen, Germany, payam.dibaj@med.uni-goettingen.de\t\t \r\n\t\t Department of Neurogenetics, Max-Planck-Institute for Experimental Medicine, 37075 Göttingen, Germany, payam.dibaj@med.uni-goettingen.de\t\t \r\n\t\t Center for Neurology, Asklepios Hospitals Schildautal, 38723 Seesen, Germany, payam.dibaj@med.uni-goettingen.de"],["dc.contributor.affiliation","Seeger, Dagmar; \t\t \r\n\t\t Pain Clinic, Center for Anesthesiology, University Medical Center Göttingen, Georg August University, 37075 Göttingen, Germany, dseeger@med.uni-goettingen.de"],["dc.contributor.affiliation","Gärtner, Jutta; \t\t \r\n\t\t Center for Rare Diseases Göttingen (ZSEG), University Medical Center Göttingen, Georg August University, 37075 Göttingen, Germany, gaertnj@med.uni-goettingen.de\t\t \r\n\t\t Department of Pediatrics and Pediatric Neurology, University Medical Center Göttingen, Georg August University, 37075 Göttingen, Germany, gaertnj@med.uni-goettingen.de"],["dc.contributor.affiliation","Petzke, Frank; \t\t \r\n\t\t Pain Clinic, Center for Anesthesiology, University Medical Center Göttingen, Georg August University, 37075 Göttingen, Germany, frank.petzke@med.uni-goettingen.de"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Seeger, Dagmar"],["dc.contributor.author","Gärtner, Jutta"],["dc.contributor.author","Petzke, Frank"],["dc.date.accessioned","2022-04-05T11:39:45Z"],["dc.date.available","2022-04-05T11:39:45Z"],["dc.date.issued","2021-02-25"],["dc.date.updated","2022-09-06T03:56:43Z"],["dc.description.abstract","A 60-year-old man suffering from recurrent attacks of yawning-fatigue-syndrome, triggered by mild exercise of his right leg since a temporary lumbar disc herniation 9 years ago, was initially treated with the oral µ-opioid-receptor agonist tilidine before each bout of exercise (see Dibaj et al. 2019 JAMA Neurology 2019;77:254). During the first few months, this treatment continuously prolonged the time without exercise-triggered yawning and fatigue. In the next few months of treatment, exercise was increased in a graded manner to alleviate the yawning-fatigue-syndrome. The number of repetitions of the physical exercises was gradually increased without taking the opioid beforehand. After several months, almost the same effort level without medication could be achieved by graded activity as before under the influence of opioid medication. Graded physical activity can thus disrupt complex pathophysiological mechanisms leading to yawning and fatigue."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3390/neurolint13010008"],["dc.identifier.pmid","33668800"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/106399"],["dc.language.iso","en"],["dc.relation.eissn","2035-8377"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.relation.orgunit","Max-Planck-Institut für Experimentelle Medizin"],["dc.relation.orgunit","Klinik für Anästhesiologie"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Follow-Up of a Case of Dopamine-Mediated Yawning-Fatigue-Syndrome Responsive to Opioids, Successful Desensitization via Graded Activity Treatment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","eLife"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Erwig, Michelle S."],["dc.contributor.author","Patzig, Julia"],["dc.contributor.author","Steyer, Anna M."],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Heilmann, Mareike"],["dc.contributor.author","Heilmann, Ingo"],["dc.contributor.author","Jung, Ramona B."],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Werner, Hauke B."],["dc.date.accessioned","2019-08-02T06:29:41Z"],["dc.date.available","2019-08-02T06:29:41Z"],["dc.date.issued","2019"],["dc.description.abstract","Myelin serves as an axonal insulator that facilitates rapid nerve conduction along axons. By transmission electron microscopy, a healthy myelin sheath comprises compacted membrane layers spiraling around the cross-sectioned axon. Previously we identified the assembly of septin filaments in the innermost non-compacted myelin layer as one of the latest steps of myelin maturation in the central nervous system (CNS) (Patzig et al., 2016). Here we show that loss of the cytoskeletal adaptor protein anillin (ANLN) from oligodendrocytes disrupts myelin septin assembly, thereby causing the emergence of pathological myelin outfoldings. Since myelin outfoldings are a poorly understood hallmark of myelin disease and brain aging we assessed axon/myelin-units in Anln-mutant mice by focused ion beam-scanning electron microscopy (FIB-SEM); myelin outfoldings were three-dimensionally reconstructed as large sheets of multiple compact membrane layers. We suggest that anillin-dependent assembly of septin filaments scaffolds mature myelin sheaths, facilitating rapid nerve conduction in the healthy CNS."],["dc.identifier.doi","10.7554/eLife.43888"],["dc.identifier.pmid","30672734"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15932"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/62262"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","2050-084X"],["dc.relation.issn","2050-084X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Anillin facilitates septin assembly to prevent pathological outfoldings of central nervous system myelin"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]