# Multimodal MRI Assessment of neuroprotective effects of Ofatumumab on brain structure, function, and clinical correlates in Relapsing Multiple Sclerosis

## TL;DR

This study shows that Ofatumumab may protect the brain in relapsing multiple sclerosis by improving white matter and functional connectivity.

## Contribution

The study provides new evidence of Ofatumumab's neuroprotective effects using multimodal MRI in RMS patients.

## Key findings

- OFA treatment was associated with improved motor function and anxiety in RMS patients.
- TG patients showed increased white matter integrity and enhanced thalamocortical connectivity.
- NTG patients experienced gray matter atrophy, while TG patients had stable cognition.

## Abstract

Relapsing Multiple Sclerosis (RMS) is characterized by neuroinflammation and neurodegeneration, leading to disability. Ofatumumab (OFA), an anti-CD20 monoclonal antibody, has shown promise as a disease-modifying therapy. This study aimed to assess the neuroprotective effects of OFA in RMS using multimodal magnetic resonance imaging (MRI). We conducted a retrospective cohort study comparing 16 RMS patients receiving OFA for 1 year (Treatment Group, TG) with 8 treatment-naïve patients (No-Treatment Group, NTG). Participants underwent 3T MRI scans, including 3D T1-weighted, diffusion tensor imaging (DTI), and resting-state functional MRI (rs-fMRI). Clinical outcomes were measured using the Expanded Disability Status Scale (EDSS), timed 25-Foot Walk (T25FW), and cognitive assessments. Results showed significant improvements in motor function and anxiety in the TG, alongside increased white matter integrity and stable cognition. Notably, TG patients exhibited enhanced functional connectivity between the thalamus and cortex, as well as increased fractional anisotropy (FA) in key white matter tracts. In contrast, the NTG displayed gray matter atrophy. These preliminary findings suggest that OFA treatment may preserve brain structure and function in RMS, with potential neuroprotective effects mediated, through thalamocortical network modulation and white matter restoration.