Stadelmann-Nessler, Christine

[["dc.bibliographiccitation.firstpage","856"],["dc.bibliographiccitation.issue","6518"],["dc.bibliographiccitation.journal","Science"],["dc.bibliographiccitation.lastpage","860"],["dc.bibliographiccitation.volume","370"],["dc.contributor.author","Cantuti-Castelvetri, Ludovico"],["dc.contributor.author","Ojha, Ravi"],["dc.contributor.author","Pedro, Liliana D."],["dc.contributor.author","Djannatian, Minou"],["dc.contributor.author","Franz, Jonas"],["dc.contributor.author","Kuivanen, Suvi"],["dc.contributor.author","van der Meer, Franziska"],["dc.contributor.author","Kallio, Katri"],["dc.contributor.author","Kaya, Tuğberk"],["dc.contributor.author","Anastasina, Maria"],["dc.contributor.author","Smura, Teemu"],["dc.contributor.author","Levanov, Lev"],["dc.contributor.author","Szirovicza, Leonora"],["dc.contributor.author","Tobi, Allan"],["dc.contributor.author","Kallio-Kokko, Hannimari"],["dc.contributor.author","Österlund, Pamela"],["dc.contributor.author","Joensuu, Merja"],["dc.contributor.author","Meunier, Frédéric A."],["dc.contributor.author","Butcher, Sarah J."],["dc.contributor.author","Winkler, Martin Sebastian"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Helenius, Ari"],["dc.contributor.author","Gokce, Ozgun"],["dc.contributor.author","Teesalu, Tambet"],["dc.contributor.author","Hepojoki, Jussi"],["dc.contributor.author","Vapalahti, Olli"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Balistreri, Giuseppe"],["dc.contributor.author","Simons, Mikael"],["dc.date.accessioned","2021-04-14T08:31:26Z"],["dc.date.available","2021-04-14T08:31:26Z"],["dc.date.issued","2020"],["dc.description.abstract","The causative agent of coronavirus disease 2019 (COVID-19) is the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). For many viruses, tissue tropism is determined by the availability of virus receptors and entry cofactors on the surface of host cells. In this study, we found that neuropilin-1 (NRP1), known to bind furin-cleaved substrates, significantly potentiates SARS-CoV-2 infectivity, an effect blocked by a monoclonal blocking antibody against NRP1. A SARS-CoV-2 mutant with an altered furin cleavage site did not depend on NRP1 for infectivity. Pathological analysis of olfactory epithelium obtained from human COVID-19 autopsies revealed that SARS-CoV-2 infected NRP1-positive cells facing the nasal cavity. Our data provide insight into SARS-CoV-2 cell infectivity and define a potential target for antiviral intervention."],["dc.identifier.doi","10.1126/science.abd2985"],["dc.identifier.pmid","33082293"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83594"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/73"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/8"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","TRR 274: Checkpoints of Central Nervous System Recovery"],["dc.relation","TRR 274 | A06: The role of lipid-sensing nuclear receptors as checkpoints in regulating phagocyte function during recovery from demyelinating injury"],["dc.relation.eissn","1095-9203"],["dc.relation.issn","0036-8075"],["dc.relation.workinggroup","RG Stadelmann-Nessler"],["dc.relation.workinggroup","RG Cantuti"],["dc.relation.workinggroup","RG Gokce (Systems Neuroscience – Cell Diversity)"],["dc.relation.workinggroup","RG Simons (The Biology of Glia in Development and Disease)"],["dc.rights","CC BY 4.0"],["dc.title","Neuropilin-1 facilitates SARS-CoV-2 cell entry and infectivity"],["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","127"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","131"],["dc.bibliographiccitation.volume","141"],["dc.contributor.author","Wildemann, Brigitte"],["dc.contributor.author","Jarius, Sven"],["dc.contributor.author","Franz, Jonas"],["dc.contributor.author","Ruprecht, Klemens"],["dc.contributor.author","Reindl, Markus"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2021-04-14T08:32:11Z"],["dc.date.available","2021-04-14T08:32:11Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1007/s00401-020-02236-5"],["dc.identifier.pmid","33078290"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83840"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/74"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/50"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","TRR 274: Checkpoints of Central Nervous System Recovery"],["dc.relation.eissn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.relation.workinggroup","RG Stadelmann-Nessler"],["dc.rights","CC BY 4.0"],["dc.title","MOG-expressing teratoma followed by MOG-IgG-positive optic neuritis"],["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","224"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica Communications"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Lohrberg, Melanie"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Franz, Jonas"],["dc.contributor.author","van der Meer, Franziska"],["dc.contributor.author","Ruhwedel, Torben"],["dc.contributor.author","Sirmpilatze, Nikoloz"],["dc.contributor.author","Dadarwal, Rakshit"],["dc.contributor.author","Handwerker, Ronja"],["dc.contributor.author","Esser, Daniel"],["dc.contributor.author","Wiegand, Kerstin"],["dc.contributor.author","Hagel, Christian"],["dc.contributor.author","Gocht, Andreas"],["dc.contributor.author","König, Fatima Barbara"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Barrantes-Freer, Alonso"],["dc.date.accessioned","2021-03-16T11:09:56Z"],["dc.date.available","2021-03-16T11:09:56Z"],["dc.date.issued","2020"],["dc.description.abstract","Demyelinated lesions in human pons observed after osmotic shifts in serum have been referred to as central pontine myelinolysis (CPM). Astrocytic damage, which is prominent in neuroinflammatory diseases like neuromyelitis optica (NMO) and multiple sclerosis (MS), is considered the primary event during formation of CPM lesions. Although more data on the effects of astrocyte-derived factors on oligodendrocyte precursor cells (OPCs) and remyelination are emerging, still little is known about remyelination of lesions with primary astrocytic loss. In autopsy tissue from patients with CPM as well as in an experimental model, we were able to characterize OPC activation and differentiation. Injections of the thymidine-analogue BrdU traced the maturation of OPCs activated in early astrocyte-depleted lesions. We observed rapid activation of the parenchymal NG2+ OPC reservoir in experimental astrocyte-depleted demyelinated lesions, leading to extensive OPC proliferation. One week after lesion initiation, most parenchyma-derived OPCs expressed breast carcinoma amplified sequence-1 (BCAS1), indicating the transition into a pre-myelinating state. Cells derived from this early parenchymal response often presented a dysfunctional morphology with condensed cytoplasm and few extending processes, and were only sparsely detected among myelin-producing or mature oligodendrocytes. Correspondingly, early stages of human CPM lesions also showed reduced astrocyte numbers and non-myelinating BCAS1+ oligodendrocytes with dysfunctional morphology. In the rat model, neural stem cells (NSCs) located in the subventricular zone (SVZ) were activated while the lesion was already partially repopulated with OPCs, giving rise to nestin+ progenitors that generated oligodendroglial lineage cells in the lesion, which was successively repopulated with astrocytes and remyelinated. These nestin+ stem cell-derived progenitors were absent in human CPM cases, which may have contributed to the inefficient lesion repair. The present study points to the importance of astrocyte-oligodendrocyte interactions for remyelination, highlighting the necessity to further determine the impact of astrocyte dysfunction on remyelination inefficiency in demyelinating disorders including MS."],["dc.description.sponsorship","Open-Access-Finanzierung durch die Universitätsmedizin Göttingen 2021"],["dc.identifier.doi","10.1186/s40478-020-01105-2"],["dc.identifier.pmid","33357244"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17715"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/80525"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/126"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/27"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","TRR 274: Checkpoints of Central Nervous System Recovery"],["dc.relation","TRR 274 | B02: Inflammatory neurodegeneration and repair mechanisms in childhood onset autoimmune and neurometabolic demyelinating CNS disease"],["dc.relation.eissn","2051-5960"],["dc.relation.issn","2051-5960"],["dc.relation.orgunit","Abteilung Ökosystemmodellierung"],["dc.relation.workinggroup","RG Möbius"],["dc.relation.workinggroup","RG Stadelmann-Nessler"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Lack of astrocytes hinders parenchymal oligodendrocyte precursor cells from reaching a myelinating state in osmolyte-induced demyelination"],["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","Frontiers in Medicine"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Tampe, Désirée"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Bösherz, Mark-Sebastian"],["dc.contributor.author","Franz, Jonas"],["dc.contributor.author","Hofmann-Winkler, Heike"],["dc.contributor.author","Pöhlmann, Stefan"],["dc.contributor.author","Kluge, Stefan"],["dc.contributor.author","Moerer, Onnen"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Winkler, Martin Sebastian"],["dc.date.accessioned","2021-07-05T14:57:53Z"],["dc.date.available","2021-07-05T14:57:53Z"],["dc.date.issued","2021"],["dc.description.abstract","Background: Acute kidney injury (AKI) is very common in severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) disease 2019 (COVID-19) and considered as a risk factor for COVID-19 severity. SARS-CoV-2 renal tropism has been observed in COVID-19 patients, suggesting that direct viral injury of the kidneys may contribute to AKI. We examined 20 adult cases with confirmed SARS-CoV-2 infection requiring ICU supportive care in a single-center prospective observational study and investigated whether urinary markers for viral infection (SARS-CoV-2 N) and shedded cellular membrane proteins (ACE2, TMPRSS2) allow identification of patients at risk for AKI and outcome of COVID-19. Objectives: The objective of the study was to evaluate whether urinary markers for viral infection (SARS-CoV-2 N) and shedded cellular membrane proteins (ACE2, TMPRSS2) allow identification of patients at risk for AKI and outcome of COVID-19. Results: Urinary SARS-CoV-2 N measured at ICU admission identified patients at risk for AKI in COVID-19 (HR 5.9, 95% CI 1.4–26, p = 0.0095 ). In addition, the combination of urinary SARS-CoV-2 N and plasma albumin measurements further improved the association with AKI (HR 11.4, 95% CI 2.7–48, p = 0.0016 ). Finally, combining urinary SARS-CoV-2 N and plasma albumin measurements associated with the length of ICU supportive care (HR 3.3, 95% CI 1.1–9.9, p = 0.0273 ) and premature death (HR 7.6, 95% CI 1.3–44, p = 0.0240 ). In contrast, urinary ACE2 and TMPRSS2 did not correlate with AKI in COVID-19. Conclusions: In conclusion, urinary SARS-CoV-2 N levels associate with risk for AKI and correlate with COVID-19 severity."],["dc.description.abstract","Background: Acute kidney injury (AKI) is very common in severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) disease 2019 (COVID-19) and considered as a risk factor for COVID-19 severity. SARS-CoV-2 renal tropism has been observed in COVID-19 patients, suggesting that direct viral injury of the kidneys may contribute to AKI. We examined 20 adult cases with confirmed SARS-CoV-2 infection requiring ICU supportive care in a single-center prospective observational study and investigated whether urinary markers for viral infection (SARS-CoV-2 N) and shedded cellular membrane proteins (ACE2, TMPRSS2) allow identification of patients at risk for AKI and outcome of COVID-19. Objectives: The objective of the study was to evaluate whether urinary markers for viral infection (SARS-CoV-2 N) and shedded cellular membrane proteins (ACE2, TMPRSS2) allow identification of patients at risk for AKI and outcome of COVID-19. Results: Urinary SARS-CoV-2 N measured at ICU admission identified patients at risk for AKI in COVID-19 (HR 5.9, 95% CI 1.4–26, p = 0.0095 ). In addition, the combination of urinary SARS-CoV-2 N and plasma albumin measurements further improved the association with AKI (HR 11.4, 95% CI 2.7–48, p = 0.0016 ). Finally, combining urinary SARS-CoV-2 N and plasma albumin measurements associated with the length of ICU supportive care (HR 3.3, 95% CI 1.1–9.9, p = 0.0273 ) and premature death (HR 7.6, 95% CI 1.3–44, p = 0.0240 ). In contrast, urinary ACE2 and TMPRSS2 did not correlate with AKI in COVID-19. Conclusions: In conclusion, urinary SARS-CoV-2 N levels associate with risk for AKI and correlate with COVID-19 severity."],["dc.identifier.doi","10.3389/fmed.2021.644715"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/87765"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-441"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","2296-858X"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Urinary Levels of SARS-CoV-2 Nucleocapsid Protein Associate With Risk of AKI and COVID-19 Severity: A Single-Center Observational Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","glia.24042"],["dc.bibliographiccitation.firstpage","2362"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","2377"],["dc.bibliographiccitation.volume","69"],["dc.contributor.affiliation","Bergner, Caroline G.; 1\r\nInstitute of Neuropathology, University Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Genc, Nafiye; 1\r\nInstitute of Neuropathology, University Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Hametner, Simon; 3\r\nDivision of Neuropathology and Neurochemistry, Department of Neurology\r\nMedical University Vienna\r\nVienna Austria"],["dc.contributor.affiliation","Franz, Jonas; 1\r\nInstitute of Neuropathology, University Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","van der Meer, Franziska; 1\r\nInstitute of Neuropathology, University Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Mitkovski, Miso; 6\r\nLight Microscopy Facility\r\nMax‐Planck Institute for Experimental Medicine\r\nGöttingen Germany"],["dc.contributor.affiliation","Weber, Martin S.; 2\r\nDepartment of Neurology\r\nUniversity Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Stoltenburg‐Didinger, Gisela; 7\r\nInstitute of Cell Biology and Neurobiology, Charité University Medicine\r\nBerlin Germany"],["dc.contributor.affiliation","Kühl, Jörn‐Sven; 8\r\nDepartment of Pediatric Oncology, Hematology, and Hemostaseology\r\nUniversity of Leipzig Medical Center\r\nLeipzig Germany"],["dc.contributor.affiliation","Köhler, Wolfgang; 9\r\nDepartment of Neurology\r\nUniversity of Leipzig Medical Center\r\nLeipzig Germany"],["dc.contributor.affiliation","Brück, Wolfgang; 1\r\nInstitute of Neuropathology, University Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Gärtner, Jutta; 10\r\nDepartment of Pediatrics and Adolescent Medicine\r\nUniversity Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.author","Bergner, Caroline G."],["dc.contributor.author","Genc, Nafiye"],["dc.contributor.author","Hametner, Simon"],["dc.contributor.author","Franz, Jonas"],["dc.contributor.author","Mitkovski, Miso"],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Stoltenburg‐Didinger, Gisela"],["dc.contributor.author","Kühl, Jörn‐Sven"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","van der Meer, Franziska"],["dc.contributor.author","Köhler, Wolfgang"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Gärtner, Jutta"],["dc.date.accessioned","2021-08-12T07:45:04Z"],["dc.date.available","2021-08-12T07:45:04Z"],["dc.date.issued","2021"],["dc.date.updated","2022-03-21T10:48:21Z"],["dc.description.abstract","Abstract Cerebral disease manifestation occurs in about two thirds of males with X‐linked adrenoleukodystrophy (CALD) and is fatally progressive if left untreated. Early histopathologic studies categorized CALD as an inflammatory demyelinating disease, which led to repeated comparisons to multiple sclerosis (MS). The aim of this study was to revisit the relationship between axonal damage and myelin loss in CALD. We applied novel immunohistochemical tools to investigate axonal damage, myelin loss and myelin repair in autopsy brain tissue of eight CALD and 25 MS patients. We found extensive and severe acute axonal damage in CALD already in prelesional areas defined by microglia loss and relative myelin preservation. In contrast to MS, we did not observe selective phagocytosis of myelin, but a concomitant decay of the entire axon‐myelin unit in all CALD lesion stages. Using a novel marker protein for actively remyelinating oligodendrocytes, breast carcinoma‐amplified sequence (BCAS) 1, we show that repair pathways are activated in oligodendrocytes in CALD. Regenerating cells, however, were affected by the ongoing disease process. We provide evidence that—in contrast to MS—selective myelin phagocytosis is not characteristic of CALD. On the contrary, our data indicate that acute axonal injury and permanent axonal loss are thus far underestimated features of the disease that must come into focus in our search for biomarkers and novel therapeutic approaches."],["dc.description.abstract","MAIN POINTS This study characterizes CALD as an axonopathic disease. Microglia cell death in CALD early lesion formation is associated with severe axonal damage. Microglia homeostasis may be linked to axonal energy metabolism. image"],["dc.description.sponsorship","Association Européenne contre les Leucodystrophies http://dx.doi.org/10.13039/501100008731"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft http://dx.doi.org/10.13039/501100001659"],["dc.description.sponsorship","Deutsche Multiple Sklerose Gesellschaft http://dx.doi.org/10.13039/501100007458"],["dc.description.sponsorship","Gemeinnützige Hertie‐Stiftung http://dx.doi.org/10.13039/501100003493"],["dc.description.sponsorship","National Multiple Sclerosis Society http://dx.doi.org/10.13039/100000890"],["dc.identifier.doi","10.1002/glia.24042"],["dc.identifier.pmid","34137074"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88362"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/269"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/37"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-448"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","TRR 274: Checkpoints of Central Nervous System Recovery"],["dc.relation","TRR 274 | B01: The role of inflammatory cytokine signaling for efficient remyelination in multiple sclerosis"],["dc.relation","TRR 274 | B02: Inflammatory neurodegeneration and repair mechanisms in childhood onset autoimmune and neurometabolic demyelinating CNS disease"],["dc.relation.eissn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.relation.workinggroup","RG Gärtner"],["dc.relation.workinggroup","RG Stadelmann-Nessler"],["dc.relation.workinggroup","RG Brück"],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made."],["dc.title","Concurrent axon and myelin destruction differentiates X‐linked adrenoleukodystrophy from multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Neurology"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","von Gottberg, Philipp"],["dc.contributor.author","Franz, Jonas"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Weber, Martin S."],["dc.date.accessioned","2021-04-14T08:27:59Z"],["dc.date.available","2021-04-14T08:27:59Z"],["dc.date.issued","2021"],["dc.description.abstract","Fingolimod represents a highly effective disease-modifying drug in patients with active relapsing-remitting multiple sclerosis (RRMS). Its immunosuppressive effects can mediate adverse events like increased risk of cancer development or appearance of opportunistic infections. Progressive multifocal leukoencephalopathy (PML)–representing a severe opportunistic infection–has been only infrequently described during Fingolimod treatment. Here, we present a case of a 63-year-old women with pre-diagnosed RRMS who presented with new multiple cerebral lesions in a routine MRI scan, also including a tumefactive lesion in the left parietal lobe, eventually leading to the diagnosis of brain metastases derived by an adenocarcinoma of the lung. Additionally, a JCV-DNA-PCR in the cerebrospinal fluid revealed positive results, corresponding to a paraclinical progressive multifocal leukoencephalopathy. In conclusion, adverse events potentially associated with immunosuppression can occur during Fingolimod treatment. In this context, the occurrence of cancer and opportunistic infections should be carefully monitored. Here, we report a case in which JCV-DNA-PCR in the cerebrospinal fluid suggests asymptomatic PML and simultaneously lung cancer brain metastases developed. While it is rather unlikely that either event occurred as an adverse event of fingolimod treatment, a contributing effect cannot be formally excluded."],["dc.identifier.doi","10.3389/fneur.2021.561158"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17790"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82468"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1664-2295"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Case Report: Findings Suggestive of Paraclinical Progressive Multifocal Leukoencephalopathy and Lung Cancer-Derived Brain Metastases in an MS Patient Treated With Fingolimod"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e2113835118"],["dc.bibliographiccitation.issue","48"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences"],["dc.bibliographiccitation.volume","118"],["dc.contributor.author","Eckermann, Marina"],["dc.contributor.author","Schmitzer, Bernhard"],["dc.contributor.author","van der Meer, Franziska"],["dc.contributor.author","Franz, Jonas"],["dc.contributor.author","Hansen, Ove"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Salditt, Tim"],["dc.date.accessioned","2022-01-11T14:05:50Z"],["dc.date.available","2022-01-11T14:05:50Z"],["dc.date.issued","2021"],["dc.description.abstract","We have studied the three-dimensional (3D) cytoarchitecture of the human hippocampus in neuropathologically healthy and Alzheimer’s disease (AD) individuals, based on phase-contrast X-ray computed tomography of postmortem human tissue punch biopsies. In view of recent findings suggesting a nuclear origin of AD, we target in particular the nuclear structure of the dentate gyrus (DG) granule cells. Tissue samples of 20 individuals were scanned and evaluated using a highly automated approach of measurement and analysis, combining multiscale recordings, optimized phase retrieval, segmentation by machine learning, representation of structural properties in a feature space, and classification based on the theory of optimal transport. Accordingly, we find that the prototypical transformation between a structure representing healthy granule cells and the pathological state involves a decrease in the volume of granule cell nuclei, as well as an increase in the electron density and its spatial heterogeneity. The latter can be explained by a higher ratio of heterochromatin to euchromatin. Similarly, many other structural properties can be derived from the data, reflecting both the natural polydispersity of the hippocampal cytoarchitecture between different individuals in the physiological context and the structural effects associated with AD pathology."],["dc.identifier.doi","10.1073/pnas.2113835118"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/97758"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/369"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/53"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-507"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","TRR 274: Checkpoints of Central Nervous System Recovery"],["dc.relation","TRR 274 | B01: The role of inflammatory cytokine signaling for efficient remyelination in multiple sclerosis"],["dc.relation.eissn","1091-6490"],["dc.relation.issn","0027-8424"],["dc.relation.orgunit","Institut für Röntgenphysik"],["dc.relation.workinggroup","RG Salditt (Structure of Biomolecular Assemblies and X-Ray Physics)"],["dc.relation.workinggroup","RG Stadelmann-Nessler"],["dc.rights","CC BY-NC-ND 4.0"],["dc.subject.gro","biomedical tomography"],["dc.title","Three-dimensional virtual histology of the human hippocampus based on phase-contrast computed tomography"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]