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Introduction
Multiple sclerosis (MS) is a chronic neurological condition caused by an autoimmune attack to the myelin sheath of the central nervous system axons. Several medications are capable of satisfactorily controlling neuroinflammation and preventing new outbreaks, but there is a lack of options that enhance endogenous remyelination and, thus, mitigate the neurodegeneration associated.
Objective
This study aims to evaluate the brain remyelination capacity promoted by natalizumab (NTZ) treatment compared to other first-line MS therapies.
Methods
Patients aged 18-45 years with relapsing-remitting MS and EDSS<5.5 that started NTZ, teriflunomide, dimethyl fumarate, beta-interferons or glatiramer acetate treatment up to 30 days before inclusion were recruited and then evaluated at baseline, 6 months and 1 year. Clinical and quality of life parameters were assessed, as well as MRI brain scans and laboratory markers. Advanced quantitative magnetic resonance imaging sequences include diffusion tensor imaging, magnetization transfer map and normalized leptokurtic diffusion map (NLDm) calculated from q-Space diffusion. Quantitative changes in baseline chronic lesions and new lesions, with or without gadolinium enhancement, were assessed at 6 months. The values were normalized to a scale of 0-100 arbitrary units (a.u.) and the RD values were inverted to indicate a higher myelin content as the a.u. increased.
Results
Twenty-seven patients were included (18 NTZ and 9 controls). The preliminary results showed a tendency towards greater remyelination, measured by the change in lesional NLD over 6 months, in the NTZ group (mean-2.4; sd 5.6; beta=7.51; p=0.018) compared to the control group (mean-5.6; sd 7.9; beta=7.51; p=0.018) after age, illness length, ethnicity and previous outbreaks characteristics correction.
Conclusion
This finding indicates an increased myelin content in the lesions of the NTZ patients compared to controls, suggesting possible remyelination enhance. Therefore, highly effective treatments as NTZ could improve the endogenous remyelination conditions, helping to stabilize neurological disability and reduce neurodegeneration.
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