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Cerebrospinal fluid proteome comparison between multiple sclerosis patients and controls
Author(s) -
Kroksveen A. C.,
Guldbrandsen A.,
Vedeler C.,
Myhr K. M.,
Opsahl J. A.,
Berven F. S.
Publication year - 2012
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/ane.12029
Subject(s) - multiple sclerosis , cerebrospinal fluid , pathogenesis , proteome , apolipoprotein e , proteomics , apolipoprotein b , biomarker , medicine , pathology , disease , biology , immunology , bioinformatics , biochemistry , gene , cholesterol
Objectives The aim of the present study was to identify proteins in cerebrospinal fluid ( CSF ) with different abundance between patients with relapsing‐remitting multiple sclerosis ( RRMS ) and controls. Such proteins may be diagnostic biomarkers and contribute with novel information about the disease pathogenesis. Materials and methods Cerebrospinal fluid from patients with RRMS ( n = 17) and controls ( n = 17) were trypsin digested and analyzed in a label‐free fashion using liquid chromatography mass spectrometry. The resulting data were analyzed using S earch GUI , P eptide S haker, and the P rogenesis software. Results Two hundred and ninety‐one proteins were identified, of which 32 were significantly differentially abundant between the patients with RRMS and controls ( P ‐value ≤ 0.05, two or more peptides quantified). Among these were proteins which previously have been linked to MS , including immunoglobulin subunits, vitamin D ‐binding protein, apolipoprotein D , kallikrein‐6, neuronal pentraxin receptor, Dickkopf‐related protein 3, and contactin‐1. Conclusion The study provides an overview of differentially abundant proteins between RRMS and controls, and a few of these are further discussed. It should be stressed that a larger verification study is needed to reveal the potential value of these proteins as biomarkers for RRMS and their involvement in the disease pathogenesis.