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dc.contributor.authorMosleth, Ellen Færgestad
dc.date.accessioned2021-09-28T08:47:59Z
dc.date.available2021-09-28T08:47:59Z
dc.date.created2021-09-27T11:23:58Z
dc.date.issued2021
dc.identifier.issn2045-2322
dc.identifier.urihttps://hdl.handle.net/11250/2784026
dc.description.abstractDespite intensive research, the aetiology of multiple sclerosis (MS) remains unknown. Cerebrospinal fluid proteomics has the potential to reveal mechanisms of MS pathogenesis, but analyses must account for disease heterogeneity. We previously reported explorative multivariate analysis by hierarchical clustering of proteomics data of MS patients and controls, which resulted in two groups of individuals. Grouping reflected increased levels of intrathecal inflammatory response proteins and decreased levels of proteins involved in neural development in one group relative to the other group. MS patients and controls were present in both groups. Here we reanalysed these data and we also reanalysed data from an independent cohort of patients diagnosed with clinically isolated syndrome (CIS), who have symptoms of MS without evidence of dissemination in space and/or time. Some, but not all, CIS patients had intrathecal inflammation. The analyses reported here identified a common protein signature of MS/CIS that was not linked to elevated intrathecal inflammation. The signature included low levels of complement proteins, semaphorin-7A, reelin, neural cell adhesion molecules, inter-alpha-trypsin inhibitor heavy chain H2, transforming growth factor beta 1, follistatin-related protein 1, malate dehydrogenase 1 cytoplasmic, plasma retinol-binding protein, biotinidase, and transferrin, all known to play roles in neural development. Low levels of these proteins suggest that MS/CIS patients suffer from abnormally low oxidative capacity that results in disrupted neural development from an early stage of the disease.
dc.language.isoeng
dc.titleCerebrospinal fluid proteome shows disrupted neuronal development in multiple sclerosis
dc.typePeer reviewed
dc.typeJournal article
dc.description.versionpublishedVersion
dc.source.volume11
dc.source.journalScientific Reports
dc.identifier.doi10.1038/s41598-021-82388-w
dc.identifier.cristin1938948
dc.relation.projectNofima AS: 202101
dc.relation.projectNorges forskningsråd: 314599
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1


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