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Updated: Sep 2, 2025
Author Spotlight: Unveiling the Pathway Linking Obesity to Autoimmune Inflammation in Multiple Sclerosis
Published on: February 23, 2024
Comparison of orexin-A and neurofilament light chain levels in patients with relapsing-remitting multiple sclerosis:
Ercan Saruhan1, Muammer Korkmaz2, Basak Altiparmak3
1Department of Medical Biochemistry, Faculty of Medicine, Mugla Sitki Kocman University, Mugla, Turkey.
Background And Purpose:
Multiple sclerosis is an autoimmune disease of the central nervous system, with myelin degeneration and Relapsing-Remitting Multiple Sclerosis (RRMS) as the most common type. The aim of this study was to determine the levels of Neurofilament Light Chain (NFL) and Orexin-A (OXA) in patients with RRMS and compare it with healthy control subjects' data.
Methods:
In this case-control study of 61 subjects, serum and cerebrospinal fluid samples were collected from 23 RRMS patients and 38 healthy control subjects. NFL and OXA levels were determined in cerebrospinal fluid and serum samples using enzyme-linked immunosorbent assay kits. Self-reported questionnaires were also administered to evaluate fatigue severity and impact. Receiver operating characteristic curve analysis was used to determine the optimal cut-off value of NFL and OXA.
Results:
The NFL and OXA concentrations in cerebro-spinal fluid of RRMS patients were significantly higher than those of the control group (p < 0.001), but no sig-nificant difference was found in the serum concentrations (p = 0.842, p = 0.597, respectively). The cut-off values were found to be 1.194 ng/ml for NFL and 77.81 pg/ml for OXA in cerebrospinal fluid. A positive correlation was found between the Expanded Disability Status Scale and Epworth Sleepiness Scale in RRMS patients (ρ = 0.49, p = 0.045).
Conclusion:
These results suggest that increased levels of both NFL and OXA in cerebrospinal fluid reflect neuronal destruction in RRMS. Further research of neurodegeneration should focus on neuropeptides to determine the possible roles in RRMS pathogenesis.
