miRNA 548a-3p as biomarker of NEDA-3 at 2 years in multiple sclerosis patients treated with fingolimod

Background Multiple sclerosis (MS) is a disabling autoimmune demyelinating disorder affecting young people and causing significant disability. In the last decade, different microRNA (miRNA) expression patterns have been associated to several treatment response therapies such as interferon and glatir...

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Veröffentlicht in:Journal of neuroinflammation Jg. 20; H. 1; S. 131 - 8
Hauptverfasser: Gonzalez-Martinez, Alicia, Patel, Rohit, Healy, Brian C., Lokhande, Hrishikesh, Paul, Anu, Saxena, Shrishti, Polgar-Turcsanyi, Mariann, Weiner, Howard L., Chitnis, Tanuja
Format: Journal Article
Sprache:Englisch
Veröffentlicht: London BioMed Central 30.05.2023
BioMed Central Ltd
Springer Nature B.V
BMC
Schlagworte:
Analysis
Biological markers
Biomarkers
Biomedical and Life Sciences
Biomedicine
Care and treatment
Copolymer 1
Demyelination
Diagnosis
Disability
Dosage and administration
EDSS
Fingolimod
Immunology
Long-term
Lymphocytes
Mann-Whitney U test
MicroRNA
MicroRNAs
miR-548a-3p
miRNA
Multiple sclerosis
NEDA-3
Neurobiology
Neurology
Neurosciences
Serum levels
United States
United States > US
Germany
Disability
RRMS
Multiple sclerosis
Biomarker
miR-548a-3p
miRNA
Long-term
NEDA-3
EDSS
ISSN:1742-2094, 1742-2094
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Zusammenfassung:Background Multiple sclerosis (MS) is a disabling autoimmune demyelinating disorder affecting young people and causing significant disability. In the last decade, different microRNA (miRNA) expression patterns have been associated to several treatment response therapies such as interferon and glatiramer acetate. Nowadays, there is increasing interest in the potential role of miRNA as treatment response biomarkers to the most recent oral and intravenous treatments. In this study, we aimed to evaluate serum miRNAs as biomarkers of No Evidence of Disease Activity (NEDA-3) at 2 years in patients with relapsing remitting MS (RRMS) treated with fingolimod. Main body A Discovery cohort of 31 RRMS patients treated with fingolimod were identified from the CLIMB study and classified as No Evidence of Disease Activity (NEDA-3) or Evidence of Disease Activity (EDA-3) after 2 years on treatment. Levels of miRNA expression were measured at 6 months using human serum miRNA panels and compared in EDA-3 and NEDA-3 groups using the Wilcoxon rank sum test. A set of differentially expressed miRNA was further validated in an independent cohort of 22 fingolimod-treated patients. We found that 548a-3p serum levels were higher levels in fingolimod-treated patients classified as NEDA-3, compared to the EDA-3 group in both the Discovery ( n  = 31; p  = 0.04) and Validation ( n  = 22; p  = 0.03) cohorts 6 months after treatment initiation; miR-548a-3p provided an AUC of 0.882 discriminating patients with NEDA-3 at 2 years in the Validation cohort. Conclusion Our results show differences in miR-548a-3p expression at 6 months after fingolimod start in patients with MS with NEDA-3 at 2 years. These results provide class III evidence of the use of miR-548a-3p as biomarker of NEDA-3 in patients with fingolimod.
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ISSN:1742-2094
1742-2094
DOI:10.1186/s12974-023-02811-z