Brück, Wolfgang

[["dc.bibliographiccitation.firstpage","1590"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","1593"],["dc.bibliographiccitation.volume","257"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T08:39:53Z"],["dc.date.available","2018-11-07T08:39:53Z"],["dc.date.issued","2010"],["dc.description.abstract","The following review summarizes the progress in multiple sclerosis research published in the Journal of Neurology in 2009."],["dc.identifier.doi","10.1007/s00415-010-5689-y"],["dc.identifier.isi","000281250100031"],["dc.identifier.pmid","20689961"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5157"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19106"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0340-5354"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Advances in multiple sclerosis research in 2009"],["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","245"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Expert Review of Clinical Pharmacology"],["dc.bibliographiccitation.lastpage","256"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Zamvil, Scott S"],["dc.date.accessioned","2021-06-01T10:48:27Z"],["dc.date.available","2021-06-01T10:48:27Z"],["dc.date.issued","2012"],["dc.description.abstract","Laquinimod is a novel, small, orally administered medication that has demonstrated efficacy in the treatment of multiple sclerosis, a chronic inflammatory demyelinating disease of the CNS. In preclinical testing, laquinimod inhibited the development of both acute and chronic paralysis in the multiple sclerosis model, experimental autoimmune encephalomyelitis. Furthermore, laquinimod reduced inflammation, demyelination and axonal damage in experimental autoimmune encephalomyelitis in mice treated at disease induction or at clinical disease onset. Recent findings from the clinical trials indicate that laquinimod has significant effects in reducing relapse rate and has more pronounced effects in reducing sustained disability progression as well as brain atrophy, with a good safety profile. In conclusion, preclinical studies show that laquinimod's unique mechanisms of action, including its immunomodulatory and CNS-protective effects, translate into clinical benefits in relapsing-remitting multiple sclerosis patients."],["dc.identifier.doi","10.1586/ecp.12.12"],["dc.identifier.isi","000209288000009"],["dc.identifier.pmid","22697588"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85940"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Informa Healthcare"],["dc.relation.eissn","1751-2441"],["dc.relation.issn","1751-2433"],["dc.title","Laquinimod, a once-daily oral drug in development for the treatment of relapsing-remitting multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","148"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","158"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Popescu, Bogdan F. G."],["dc.contributor.author","Guo, Yong"],["dc.contributor.author","Jentoft, Mark E."],["dc.contributor.author","Parisi, Joseph E."],["dc.contributor.author","Lennon, Vanda A."],["dc.contributor.author","Pittock, Sean J."],["dc.contributor.author","Weinshenker, Brian G."],["dc.contributor.author","Wingerchuk, Dean M."],["dc.contributor.author","Giannini, Caterina"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Shuster, Elizabeth A."],["dc.contributor.author","Carter, Jonathan"],["dc.contributor.author","Boyd, Clara D."],["dc.contributor.author","Clardy, Stacey Lynn"],["dc.contributor.author","Cohen, Bruce A."],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.date.accessioned","2018-11-07T10:02:13Z"],["dc.date.available","2018-11-07T10:02:13Z"],["dc.date.issued","2015"],["dc.description.abstract","Objective: To assess, in a surgical biopsy cohort of active demyelinating lesions, the diagnostic utility of aquaporin-4 (AQP4) immunohistochemistry in identifying neuromyelitis optica (NMO) or NMO spectrum disorder (NMOSD) and describe pathologic features that should prompt AQP4 immunohistochemical analysis and AQP4-immunoglobulin G (IgG) serologic testing. Methods: This was a neuropathologic cohort study of 20 surgical biopsies (19 patients; 11 cord/9 brain), performed because of diagnostic uncertainty, interpreted as active demyelinating disease and containing 2 or more of the following additional features: tissue vacuolation, granulocytic infiltrates, or astrocyte injury. Results: AQP4 immunoreactivity was lost in 18 biopsies and increased in 2. Immunopathologic features of the AQP4 loss cohort were myelin vacuolation (18), dystrophic astrocytes and granulocytes (17), vascular hyalinization (16), macrophages containing glial fibrillary acid protein (GFAP)-positive debris (14), and Creutzfeldt-Peters cells (0). All 14 cases with available serum tested positive for AQP4-IgG after biopsy. Diagnosis at last follow-up was NMO/NMOSD (15) and longitudinally extensive transverse myelitis (1 each relapsing and single). Immunopathologic features of the AQP4 increased cohort were macrophages containing GFAP-positive debris and granulocytes (2), myelin vacuolation (1), dystrophic astrocytes (1), Creutzfeldt-Peters cells (1), and vascular hyalinization (1). Diagnosis at last follow-up was multiple sclerosis (MS) and both tested AQP4-IgG seronegative after biopsy. Conclusions: AQP4 immunohistochemistry with subsequent AQP4-IgG testing has diagnostic utility in identifying cases of NMO/NMOSD. This study highlights the importance of considering NMOSD in the differential diagnosis of tumefactive brain or spinal cord lesions. AQP4-IgG testing may avert biopsy and avoid ineffective therapies if these patients are erroneously treated for MS."],["dc.identifier.isi","000347996400012"],["dc.identifier.pmid","25503621"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38185"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","Diagnostic utility of aquaporin-4 in the analysis of active demyelinating lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1853-1857"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Oncology Letters"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Böhrnsen, Florian"],["dc.contributor.author","Enders, Christina"],["dc.contributor.author","Ludwig, Hans-Christoph"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Füzesi, Laszlo"],["dc.contributor.author","Gutenberg, Angelika"],["dc.date.accessioned","2018-06-26T08:12:45Z"],["dc.date.available","2018-06-26T08:12:45Z"],["dc.date.issued","2015-09"],["dc.description.abstract","Tumors of the pineal region (PR) are rare and can be subdivided into four main histomorphological groups: Pineal-parenchymal tumors (PPT), germ cell tumors (GCT), glial tumors and miscellaneous tumors. The appropriate pathological classification and grading of these malignancies is essential for determining the clinical management and prognosis. However, an early diagnosis is often delayed due to unspecific clinical symptoms, and histological support is not always decisive to identify the diversity of tumors of the PR. The present study aimed to characterize 18 tumors of the PR using comparative genomic hybridization. All the tumors were primarily surgically resected without any previous irradiation or chemotherapy. In addition to chromosomal aberrations in PPT and different GCTs of the PR, the present study described, for the first time, the chromosomal changes in a few rare entities (solitary-fibrous and neuroendocrine tumors) of the PR. The tumors in the study, regardless of histology and World Health Organization grade, were characterized by frequent gains at 7, 9q, 12q, 16p, 17 and 22q, and losses at 13q. While the detection of chromosomal aberrations in these tumors appears not to be indicative enough of histological entities and their grade of malignancy, the present data may be of use to select genes of interest for higher resolution genomic analyses."],["dc.identifier.doi","10.3892/ol.2015.3383"],["dc.identifier.pmid","26622764"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15149"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.title","Common molecularcytogenetic alterations in tumors originating from the pineal region"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e1906"],["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","e1913"],["dc.bibliographiccitation.volume","97"],["dc.contributor.author","Tobin, W. Oliver"],["dc.contributor.author","Kalinowska-Lyszczarz, Alicja"],["dc.contributor.author","Weigand, Stephen D."],["dc.contributor.author","Guo, Yong"],["dc.contributor.author","Tosakulwong, Nirubol"],["dc.contributor.author","Parisi, Joseph E."],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Frischer, Josa M."],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.date.accessioned","2021-12-01T09:22:30Z"],["dc.date.available","2021-12-01T09:22:30Z"],["dc.date.issued","2021"],["dc.description.abstract","Background and Objectives The goal of this work was to compare clinical characteristics across immunopathologic subtypes of patients with multiple sclerosis. Methods Immunopathologic subtyping was performed on specimens from 547 patients with biopsy- or autopsy-confirmed CNS demyelination. Results The frequency of immunopathologic subtypes was 23% for pattern I, 56% for pattern II, and 22% for pattern III. Immunopatterns were similar in terms of age at autopsy/biopsy (median age 41 years, range 4–83 years, p = 0.16) and proportion female (54%, p = 0.71). Median follow-up after symptom onset was 2.3 years (range 0–38 years). In addition to being overrepresented among autopsy cases (45% vs 19% in biopsy cohort, p < 0.001), index attack-related disability was higher in pattern III vs II (median Expanded Disability Status Scale score 4 vs 3, p = 0.02). Monophasic clinical course was more common in patients with pattern III than pattern I or II (59% vs 33% vs 32%, p < 0.001). Similarly, patients with pattern III pathology were likely to have progressive disease compared to patients with patterns I or II when followed up for ≥5 years (24% overall, p = 0.49), with no differences in long-term survival, despite a more fulminant attack presentation. Conclusion All 3 immunopatterns can be detected in active lesions, although they are found less frequently later into the disease due to the lower number of active lesions. Pattern III is associated with a more fulminant initial attack than either pattern I or II. Biopsied patients appear to have similar long-term outcomes regardless of their immunopatterns. Progressive disease is less associated with the initial immunopattern and suggests convergence into a final common pathway related to the chronically denuded axon."],["dc.description.abstract","Background and Objectives The goal of this work was to compare clinical characteristics across immunopathologic subtypes of patients with multiple sclerosis. Methods Immunopathologic subtyping was performed on specimens from 547 patients with biopsy- or autopsy-confirmed CNS demyelination. Results The frequency of immunopathologic subtypes was 23% for pattern I, 56% for pattern II, and 22% for pattern III. Immunopatterns were similar in terms of age at autopsy/biopsy (median age 41 years, range 4–83 years, p = 0.16) and proportion female (54%, p = 0.71). Median follow-up after symptom onset was 2.3 years (range 0–38 years). In addition to being overrepresented among autopsy cases (45% vs 19% in biopsy cohort, p < 0.001), index attack-related disability was higher in pattern III vs II (median Expanded Disability Status Scale score 4 vs 3, p = 0.02). Monophasic clinical course was more common in patients with pattern III than pattern I or II (59% vs 33% vs 32%, p < 0.001). Similarly, patients with pattern III pathology were likely to have progressive disease compared to patients with patterns I or II when followed up for ≥5 years (24% overall, p = 0.49), with no differences in long-term survival, despite a more fulminant attack presentation. Conclusion All 3 immunopatterns can be detected in active lesions, although they are found less frequently later into the disease due to the lower number of active lesions. Pattern III is associated with a more fulminant initial attack than either pattern I or II. Biopsied patients appear to have similar long-term outcomes regardless of their immunopatterns. Progressive disease is less associated with the initial immunopattern and suggests convergence into a final common pathway related to the chronically denuded axon."],["dc.identifier.doi","10.1212/WNL.0000000000012782"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94416"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","Clinical Correlation of Multiple Sclerosis Immunopathologic Subtypes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","194"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","CANCER GENETICS AND CYTOGENETICS"],["dc.bibliographiccitation.lastpage","197"],["dc.bibliographiccitation.volume","200"],["dc.contributor.author","Schaefer, Inga-Marie"],["dc.contributor.author","Martinez, Ramon"],["dc.contributor.author","Enders, Christina"],["dc.contributor.author","Loertzer, Hagen"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Rohde, Veit"],["dc.contributor.author","Fuezesi, Laszlo"],["dc.contributor.author","Gutenberg, Angelika"],["dc.date.accessioned","2018-11-07T08:41:20Z"],["dc.date.available","2018-11-07T08:41:20Z"],["dc.date.issued","2010"],["dc.identifier.doi","10.1016/j.cancergencyto.2010.04.013"],["dc.identifier.isi","000279373500019"],["dc.identifier.pmid","20620607"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19445"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0165-4608"],["dc.title","Molecular cytogenetics of malignant pheochromocytoma with cerebral metastasis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.volume","112"],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Schmidt, H."],["dc.contributor.author","Mack, Matthias"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Priller, Josef"],["dc.contributor.author","Prinz, Marco R."],["dc.date.accessioned","2018-11-07T09:16:23Z"],["dc.date.available","2018-11-07T09:16:23Z"],["dc.date.issued","2006"],["dc.format.extent","359"],["dc.identifier.isi","000240061000029"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27924"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","51st Annual Meeting of the German-Society-of-Neuropathology-and-Neuroanatomy"],["dc.relation.eventlocation","Mannheim, GERMANY"],["dc.relation.issn","0001-6322"],["dc.title","The presence of the chemokine receptor CCR2 on specific myeloid cells determines the outcome of autoimmune encephalomyelitis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2487"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","2500"],["dc.bibliographiccitation.volume","132"],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Mack, Matthias"],["dc.contributor.author","Schmidt, Hauke"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Djukic, Marija"],["dc.contributor.author","Zabel, Mark D."],["dc.contributor.author","Hille, Andrea"],["dc.contributor.author","Priller, Josef"],["dc.contributor.author","Prinz, Marco R."],["dc.date.accessioned","2018-11-07T11:24:34Z"],["dc.date.available","2018-11-07T11:24:34Z"],["dc.date.issued","2009"],["dc.description.abstract","The chemokine receptor CCR2 plays a vital role for the induction of autoimmunity in the central nervous system. However, it remains unclear how the pathogenic response is mediated by CCR2-bearing cells. By combining bone marrow chimerism with gene targeting we detected a mild disease-modulating role of CCR2 during experimental autoimmune encephalomyelitis, a model for central nervous system autoimmunity, on radio-resistant cells that was independent from targeted CCR2 expression on endothelia. Interestingly, absence of CCR2 on lymphocytes did not influence autoimmune demyelination. In contrast, engagement of CCR2 on accessory cells was required for experimental autoimmune encephalomyelitis induction. CCR2Ly-6C(hi) monocytes were rapidly recruited to the inflamed central nervous system and were crucial for the effector phase of disease. Selective depletion of this specific monocyte subpopulation through engagement of CCR2 strongly reduced central nervous system autoimmunity. Collectively, these data indicate a disease-promoting role of CCR2Ly-6C(hi) monocytes during autoimmune inflammation of the central nervous system."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft; Gemeinnutzige Hertie-Stiftung"],["dc.identifier.doi","10.1093/brain/awp144"],["dc.identifier.isi","000269963600019"],["dc.identifier.pmid","19531531"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56435"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.title","CCR2Ly-6C(hi) monocytes are crucial for the effector phase of autoimmunity in the central nervous system"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","235"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","245"],["dc.bibliographiccitation.volume","123"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Radue, Ernst-Wilhelm"],["dc.contributor.author","Oterino, Agustin"],["dc.contributor.author","Kuempfel, Tania"],["dc.contributor.author","Wiendl, Heinz"],["dc.contributor.author","Schippling, Sven"],["dc.contributor.author","Kuhle, Jens"],["dc.contributor.author","Sahraian, Mohammad Ali"],["dc.contributor.author","Gray, Francoise"],["dc.contributor.author","Jakl, Veronika"],["dc.contributor.author","Haeusler, Darius"],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T09:13:35Z"],["dc.date.available","2018-11-07T09:13:35Z"],["dc.date.issued","2012"],["dc.description.abstract","Natalizumab is an approved medication for highly active multiple sclerosis (MS). Progressive multifocal leukoencephalopathy (PML) may occur as a severe side effect of this drug. Here, we describe pathological and radiological characteristics of immune reconstitution inflammatory syndrome (IRIS), which occurs in natalizumab-associated PML after the cessation of therapy, and we differentiate it from ongoing PML. Brain biopsy tissue and MRI scans from five MS patients with natalizumab-associated PML were analyzed and their histology compared with non-MS PML. Histology showed an extensive CD8-dominated T cell infiltrate and numerous macrophages within lesions, and in nondemyelinated white and grey matter, in four out of five cases. Few or no virally infected cells were found. This was indicative of IRIS as known from HIV patients with PML. Outstandingly high numbers of plasma cells were present as compared to non-MS PML and typical MS lesions. MRI was compatible with IRIS, revealing enlarging lesions with a band-like or speckled contrast enhancement either at the lesion edge or within lesions. Only the fifth patient showed typical PML pathology, with low inflammation and high numbers of virally infected cells. This patient showed a similar interval between drug withdrawal and biopsy (3.5 months) to the rest of the cohort (range 2.5-4 months). MRI could not differentiate between PML-associated IRIS and ongoing PML. We describe in detail the histopathology of IRIS in natalizumab-associated PML. PML-IRIS, ongoing PML infection, and MS exacerbation may be impossible to discern clinically alone. MRI may provide some clues for distinguishing different pathologies that can be differentiated histologically. In our individual cases, biopsy helped to clarify diagnoses in natalizumab-associated PML."],["dc.identifier.doi","10.1007/s00401-011-0900-5"],["dc.identifier.isi","000301855900007"],["dc.identifier.pmid","22057786"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7121"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27215"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0001-6322"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Pathology of immune reconstitution inflammatory syndrome in multiple sclerosis with natalizumab-associated progressive multifocal leukoencephalopathy"],["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","81"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica Communications"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Rieckmann, Peter"],["dc.contributor.author","Kallmann, Boris-Alexander"],["dc.contributor.author","Brück, Wolfgang"],["dc.date.accessioned","2019-07-09T11:42:51Z"],["dc.date.available","2019-07-09T11:42:51Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1186/s40478-016-0352-1"],["dc.identifier.pmid","27503238"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13864"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58763"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Disseminated necrotizing leukoencephalopathy eight months after alemtuzumab treatment for multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]