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This retrospective cohort study investigated the neuroprotective effects of Ofatumumab (OFA), an anti-CD20 monoclonal antibody, in 16 patients with Relapsing Multiple Sclerosis (RMS) compared to 8 treatment-naïve patients using multimodal MRI. After 1 year, the OFA group showed improvements in motor function and anxiety, increased white matter integrity, stable cognition, enhanced thalamocortical functional connectivity, and increased fractional anisotropy (FA) in white matter tracts, while the control group exhibited gray matter atrophy. These findings suggest OFA may preserve brain structure and function in RMS.
Ofatumumab treatment in RMS patients may preserve brain structure and function, as evidenced by improved white matter integrity and thalamocortical connectivity compared to untreated patients.
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.
