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Sulfatide isoform pattern in cerebrospinal fluid discriminates progressive MS from relapsing-remitting MS

Journal article
Authors Lenka Novakova
Avadhesh Kumar Singh
Markus Axelsson
Marcus Ståhlman
Martin Adiels
Clas Malmeström
Henrik Zetterberg
Jan Borén
Jan Lycke
Susanna Cardell
Maria K. Blomqvist
Published in Journal of Neurochemistry
Volume 146
Issue 3
Pages 322-332
ISSN 0022-3042
Publication year 2018
Published at Wallenberg Laboratory
Institute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine
Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Institute of Biomedicine, Department of Microbiology and Immunology
Institute of Neuroscience and Physiology, Department of Clinical Neuroscience
Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 322-332
Language en
Links dx.doi.org/10.1111/jnc.14452
Keywords axonal loss, biomarkers, cerebrospinal fluid, demyelination, inflammation, mass spectrometry, fibrillary acidic protein, multiple-sclerosis, t-cells, mass-spectrometry, brain, myelin, leukodystrophy, demyelination, inflammation, autoimmunity, Biochemistry & Molecular Biology, Neurosciences & Neurology
Subject categories Biochemistry and Molecular Biology, Immunology in the medical area, Neurosciences

Abstract

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS). Several biomarkers including proteins and lipids have been reported in MS cerebrospinal fluid (CSF), reflecting different aspects of the pathophysiology particularly of relapsing-remitting MS (RRMS). Sulfatide, abundant in the myelin sheath and a proposed target for autoimmune attack in MS, has been reported altered in MS CSF. Here, we investigated the potential of CSF sulfatide and its isoforms as biomarkers in MS. A highly sensitive and quantitative mass spectrometry method was employed to determine levels of sulfatide isoforms in CSF from RRMS and progressive MS (PMS) patients, and healthy donors (HD). We demonstrate that levels of total CSF sulfatide and C24:1, C26:1, and C26:1-OH isoforms were significantly increased in PMS compared with RRMS patients and HD, while C23:0-OH was significantly decreased in CSF from PMS patients compared to the other two groups. Multivariate discriminant analysis showed that CSF sulfatide isoform pattern in PMS patients was distinct and non-overlapping with that of RRMS patients and HD. Sulfatide levels did not correlate with tested biomarkers or clinical parameters. The results suggest that CSF sulfatide isoform levels may be used to discriminate the phenotype ofMS and might play a role in the progression of the disease.

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