1. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden;2. Department of Microbiology and Immunology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden;3. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, M?lndal, Sweden;4. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, M?lndal, Sweden;5. Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London, UK;6. UK Dementia Research Institute at UCL, London, UK;7. Department of Molecular and Clinical Medicine/Wallenberg Lab, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden;8. Health Metrics Unit, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden;9. Department of Clinical Chemistry and Transfusion Medicine, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
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 of MS and might play a role in the progression of the disease.
