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Mononuclear cell transcriptome changes associated with dimethyl fumarate in MS.

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  • 1Division of Brain Sciences (A.R.G., M.T.C., R.N.), Department of Medicine, Imperial College London; the Department of Neurology (K.K.), Weill Institute for Neurosciences, University of California, San Francisco; icometrix (W.v.H.), Begaultlaan, Leuven, Belgium; the Department of Neurology (S.E.B.), Weill Institute for Neurosciences, Institute for Human Genetics and Graduate Program in Bioinformatics, University of California, San Francisco; and Division of Brain Sciences (P.M.M.), Department of Medicine, the Centre for Neurotechnology and the UK Dementia Research Institute, Imperial College London.

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Dimethyl fumarate (DMF) treatment response in relapsing-remitting multiple sclerosis (RRMS) is linked to early gene expression changes. Short-term activation of Nrf2 and NFκB pathways in PBMCs predicts treatment success.

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Area of Science:

  • Genomics and Molecular Biology
  • Immunology
  • Neuroscience

Background:

  • Relapsing-remitting multiple sclerosis (RRMS) is an autoimmune disease affecting the central nervous system.
  • Dimethyl fumarate (DMF) is a therapeutic agent used to manage RRMS.
  • Understanding the molecular mechanisms underlying DMF treatment response is crucial for optimizing patient outcomes.

Purpose of the Study:

  • To identify short-term gene expression alterations in peripheral blood mononuclear cells (PBMCs) associated with DMF treatment response in RRMS patients.
  • To discover transcriptomic markers that predict medium-term treatment efficacy.

Main Methods:

  • Blood samples were collected from 24 RRMS patients and 7 healthy controls at baseline, 6 weeks, and 15 months.
  • Next-generation RNA sequencing was performed on PBMCs to analyze gene expression profiles.
  • Differential gene expression analysis was used to compare responders (NEDA-4 positive) and non-responders.

Main Results:

  • Responders showed 478 differentially expressed genes (DEGs) at 6 weeks, enriched for nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and nuclear factor κB (NFκB) pathways.
  • Non-responders exhibited no significant DEGs at 6 weeks compared to baseline.
  • At 15 months, non-responders had 1,264 DEGs, enriched for T-cell signaling, while responders showed minimal changes.

Conclusions:

  • Early PBMC transcriptome changes, specifically Nrf2 pathway activation and NFκB inhibition, distinguish patients who respond to DMF.
  • Gene expression stabilization may correlate with treatment-induced suppression of disease activity in RRMS.
  • These findings suggest potential early biomarkers for DMF treatment response.