Junker, Andreas

[["dc.bibliographiccitation.firstpage","3738"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","FEBS Letters"],["dc.bibliographiccitation.lastpage","3746"],["dc.bibliographiccitation.volume","585"],["dc.contributor.author","Junker, Andreas"],["dc.date.accessioned","2018-11-07T08:49:09Z"],["dc.date.available","2018-11-07T08:49:09Z"],["dc.date.issued","2011"],["dc.description.abstract","MicroRNAs (miRNAs) comprise a group of several hundred, small non-coding RNA molecules with a fundamental influence on the regulation of gene expression. Certain miRNAs are altered in blood cells of multiple sclerosis (MS), and active and inactive MS brain lesions have distinct miRNA expression profiles. Several miRNAs such as miR-155 or miR-326 are considerably overexpressed in active MS lesions versus controls, and mice lacking these miRNAs either through knock-out (miR-155) or by in vivo silencing (miR-326) show a reduction of symptoms in experimental autoimmune encephalomyelitis (EAE), a model system for multiple sclerosis. This review describes miRNAs regulated in the blood or in brain lesions of MS patients in the context of their previously described functions in physiology and pathophysiology. (C) 2011 Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies."],["dc.identifier.doi","10.1016/j.febslet.2011.03.052"],["dc.identifier.isi","000297318000019"],["dc.identifier.pmid","21453702"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11295"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21390"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1873-3468"],["dc.relation.issn","0014-5793"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","Pathophysiology of translational regulation by microRNAs in multiple sclerosis"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","760"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","18"],["dc.contributor.affiliation","Voigt, David; \t\t \r\n\t\t Institute of Neuropathology, University Medical Center, Robert-Koch-Straße 40, Göttingen 37075, Germany, david-voigt@gmx.net"],["dc.contributor.affiliation","Scheidt, Uta; \t\t \r\n\t\t Institute of Neuropathology, University Medical Center, Robert-Koch-Straße 40, Göttingen 37075, Germany, uscheidt@med.uni-goettingen.de"],["dc.contributor.affiliation","Derfuss, Tobias; \t\t \r\n\t\t Neurologic Clinic and Policlinic, University Hospital Basel, Basel 4031, Switzerland, tobias.derfuss@usb.ch"],["dc.contributor.affiliation","Brück, Wolfgang; \t\t \r\n\t\t Institute of Neuropathology, University Medical Center, Robert-Koch-Straße 40, Göttingen 37075, Germany, wbrueck@med.uni-goettingen.de"],["dc.contributor.affiliation","Junker, Andreas; \t\t \r\n\t\t Institute of Neuropathology, University Hospital Essen, Hufelandstr. 55, Essen 45122, Germany, andreas.junker@uk-essen.de"],["dc.contributor.author","Voigt, David"],["dc.contributor.author","Scheidt, Uta"],["dc.contributor.author","Derfuss, Tobias"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Junker, Andreas"],["dc.date.accessioned","2018-11-07T10:25:12Z"],["dc.date.available","2018-11-07T10:25:12Z"],["dc.date.issued","2017"],["dc.date.updated","2022-09-05T16:09:31Z"],["dc.description.abstract","Multiple sclerosis is a chronic inflammatory disease of the central nervous system, characterized by demyelination and axonal damage as well as neuronal degeneration. Since oxygen-derived free radicals are an important factor leading to tissue damage in inflammatory multiple sclerosis (MS) lesions, research on antioxidative systems is essential to identify endogenous factors which can possibly counteract oxidative damage. As an important scavenging enzyme family, peroxiredoxins (PRDXs) play a crucial role in preventing oxidative damage; however little is known about their expression and function in MS lesions. In the present study we examined the expression of PRDX2 in white matter lesions of MS patients with long-standing, chronic disease. PRDX2 expression was investigated by immunohistochemistry in the context of oxidative stress and inflammation (determined by microglia/macrophage and T cell infiltration) in ten MS autopsy cases as well as seven control autopsy cases. PRDX2 was found to be upregulated in white matter MS lesions mainly in astrocytes, and its expression level was positively correlated with the degree of inflammation and oxidative stress. Our data suggest that PRDX2 expression contributes to the resistance of astrocytes against oxidative damage."],["dc.identifier.doi","10.3390/ijms18040760"],["dc.identifier.isi","000402639400085"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14785"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42804"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Mdpi Ag"],["dc.relation.eissn","1422-0067"],["dc.relation.issn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Expression of the Antioxidative Enzyme Peroxiredoxin 2 in Multiple Sclerosis Lesions in Relation to Inflammation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","294"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","300"],["dc.bibliographiccitation.volume","80"],["dc.contributor.author","Gerdes, Lisa Ann"],["dc.contributor.author","Held, Kathrin"],["dc.contributor.author","Beltran, Eduardo"],["dc.contributor.author","Berking, Carola"],["dc.contributor.author","Prinz, Joerg C."],["dc.contributor.author","Junker, Andreas"],["dc.contributor.author","Tietze, Julia K."],["dc.contributor.author","Ertl-Wagner, Birgit"],["dc.contributor.author","Straube, Andreas"],["dc.contributor.author","Kuempfel, Tania"],["dc.contributor.author","Dornmair, Klaus"],["dc.contributor.author","Hohlfeld, Reinhard"],["dc.date.accessioned","2018-11-07T10:10:53Z"],["dc.date.available","2018-11-07T10:10:53Z"],["dc.date.issued","2016"],["dc.description.abstract","We investigated a patient who developed multiple sclerosis (MS) during treatment with the CTLA4-blocking antibody ipilimumab for metastatic melanoma. Initially he showed subclinical magnetic resonance imaging (MRI) changes (radiologically isolated syndrome). Two courses of ipilimumab were each followed by a clinical episode of MS, 1 of which was accompanied by a massive increase of MRI activity. Brain biopsy confirmed active, T-cell type MS. Quantitative next generation sequencing of T-cell receptor genes revealed distinct oligoclonal CD4(+) and CD8(+) T-cell repertoires in the primary melanoma and cerebrospinal fluid. Our results pinpoint the coinhibitory molecule CTLA4 as an immunological checkpoint and therapeutic target in MS."],["dc.identifier.doi","10.1002/ana.24715"],["dc.identifier.isi","000382402600013"],["dc.identifier.pmid","27351142"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14028"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39943"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1531-8249"],["dc.relation.issn","0364-5134"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","CTLA4 as Immunological Checkpoint in the Development of Multiple Sclerosis"],["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","641"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Brain Pathology"],["dc.bibliographiccitation.lastpage","652"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Junker, Andreas"],["dc.contributor.author","Wozniak, Jadwiga"],["dc.contributor.author","Voigt, David"],["dc.contributor.author","Scheidt, Uta"],["dc.contributor.author","Antel, Jack"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2021-04-14T08:27:30Z"],["dc.date.available","2021-04-14T08:27:30Z"],["dc.date.issued","2020"],["dc.description.abstract","Abstract Cortical demyelinated lesions are frequent and widespread in chronic multiple sclerosis (MS) patients, and may contribute to disease progression. Inflammation and related oxidative stress have been proposed as central mediators of cortical damage, yet meningeal and cortical inflammation is not specific to MS, but also occurs in other diseases. The first aim of this study was to test whether cortical demyelination was specific for demyelinating CNS diseases compared to other CNS disorders with prominent meningeal and cortical inflammation. The second aim was to assess whether oxidative tissue damage was associated with the extent of neuroaxonal damage. We studied a large cohort of patients diagnosed with demyelinating CNS diseases and non‐demyelinating diseases of autoimmune, infectious, neoplastic or metabolic origin affecting the meninges and the cortex. Included were patients with MS, acute disseminated encephalomyelitis (ADEM), neuromyelitis optica (NMO), viral and bacterial meningoencephalitis, progressive multifocal leukoencephalopathy (PML), subacute sclerosing panencephalitis (SSPE), carcinomatous and lymphomatous meningitis and metabolic disorders such as extrapontine myelinolysis, thus encompassing a wide range of adaptive and innate cytokine signatures. Using myelin protein immunohistochemistry, we found cortical demyelination in MS, ADEM, PML and extrapontine myelinolysis, whereby each condition showed a disease‐specific histopathological pattern. Remarkably, extensive ribbon‐like subpial demyelination was only observed in MS, thus providing an important pathogenetic and diagnostic cue. Cortical oxidative injury was detected in both demyelinating and non‐demyelinating CNS disorders. Our data demonstrate that meningeal and cortical inflammation alone accompanied by oxidative stress are not sufficient to generate the extensive subpial cortical demyelination found in MS, but require other MS‐specific factors."],["dc.description.sponsorship","National Multiple Sclerosis Society http://dx.doi.org/10.13039/100000890"],["dc.identifier.doi","10.1111/bpa.12813"],["dc.identifier.eissn","1750-3639"],["dc.identifier.issn","1015-6305"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82309"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1750-3639"],["dc.relation.issn","1015-6305"],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited."],["dc.title","Extensive subpial cortical demyelination is specific to multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","17565"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.lastpage","17588"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Abdelhak, Ahmed"],["dc.contributor.author","Junker, Andreas"],["dc.contributor.author","Brettschneider, Johannes"],["dc.contributor.author","Kassubek, Jan"],["dc.contributor.author","Ludolph, Albert C."],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Tumani, Hayrettin"],["dc.date.accessioned","2018-11-07T09:53:26Z"],["dc.date.available","2018-11-07T09:53:26Z"],["dc.date.issued","2015"],["dc.description.abstract","Many neurodegenerative disorders share a common pathophysiological pathway involving axonal degeneration despite different etiological triggers. Analysis of cytoskeletal markers such as neurofilaments, protein tau and tubulin in cerebrospinal fluid (CSF) may be a useful approach to detect the process of axonal damage and its severity during disease course. In this article, we review the published literature regarding brain-specific CSF markers for cytoskeletal damage in primary progressive multiple sclerosis and amyotrophic lateral sclerosis in order to evaluate their utility as a biomarker for disease progression in conjunction with imaging and histological markers which might also be useful in other neurodegenerative diseases associated with affection of the upper motor neurons. A long-term benefit of such an approach could be facilitating early diagnostic and prognostic tools and assessment of treatment efficacy of disease modifying drugs."],["dc.description.sponsorship","BMBF-funded competence network multiple sclerosis (KKNMS)"],["dc.identifier.doi","10.3390/ijms160817565"],["dc.identifier.isi","000366826100046"],["dc.identifier.pmid","26263977"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12759"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36329"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Mdpi Ag"],["dc.relation.issn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Brain-Specific Cytoskeletal Damage Markers in Cerebrospinal Fluid: Is There a Common Pattern between Amyotrophic Lateral Sclerosis and Primary Progressive Multiple Sclerosis?"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]