The study found that people with relapsing‑remitting multiple sclerosis have lower blood levels of a tiny protein called MOTS‑c, which is linked to how mitochondria manage metabolism. Higher MOTS‑c levels seemed to protect against MS, and the test could tell apart patients from healthy folks fairly well, but the research didn’t give any dosing or treatment advice.

Background Multiple sclerosis (MS) is a major global problem, and as its pathogenesis is understood more clearly, therapeutic options expand accordingly. The mitochondrial open reading frame of the 12S rRNA-c (MOTS-c) is a novel mitochondria-derived protein acting on metabolic homeostasis. In this study, we aimed to investigate the role of serum MOTS-c in the pathophysiology of the disease in MS patients and to discuss the mechanism of MOTS-c. Methodology In total, 43 patients diagnosed with relapsing-remitting MS and 41 healthy controls were enrolled in the study. MOTS-c, fasting blood glucose, insulin, Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), lipid panel, and body mass index levels were assessed. Results The participants' MOTS-c levels remained significantly lower than that of the control group, while their fasting blood glucose and HOMA-IR values were higher. The multivariate logistic regression analysis established that increased MOTS-c levels could be a protective factor against the development of MS disease. The area under the receiver operating characteristic curve for MOTS-c was calculated as 0.782 (95% confidence interval = 0.684-0.879, p = 0.0001). Conclusions This study is the first to scrutinize MOTS-c levels in MS patients. We tried to provide clinical evidence that MOTS-c could act as a highly discriminative biomarker between MS patients and control groups, which may hold great promise for future therapeutic options.