Published 2021

Read in Norwegian

Publication details

Journal : Scientific Reports , vol. 11 , p. 1–19 , 2021

International Standard Numbers :
Printed : 2045-2322
Electronic : 2045-2322

Publication type : Academic article

Contributors : Mosleth, Ellen F.; Vedeler, Christian Alexander; Liland, Kristian Hovde; McLeod, Anette; Bringeland, Gerd Haga; Kroondijk, Liesbeth; Berven, Frode Steingrimsen; Lysenko, Artem; Rawlings, Christopher J.; El-Hajj Eid, Karim; Opsahl, Jill Anette; Gjertsen, Bjørn Tore; Myhr, Kjell-Morten; Gavasso, Sonia

If you have questions about the publication, you may contact Nofima’s Chief Librarian.

Kjetil Aune
Chief Librarian


Despite 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.