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The future is taking shape

Within the past 20 years, the number of MS drugs has increased considerably.

Lemtrada® was introduced in Belgium in 2015 and is a monoclonal antibody that destroys various types of lymphocytes. Mavenclad® was introduced on 1st August 2018 and inhibits the proliferation of activated lymphocytes. Finally, Ocrevus® was introduced on 1st March 2019. This monoclonal antibody destroys a specific group of lymphocytes known as B lymphocytes.

All three drugs have one thing in common: they were initially used to treat leukaemia or lymphoma. In the case of MS, they are used over longer periods and/or at lower doses, with the aim of changing or remodelling the functioning of the immune system. The results have been very encouraging, even though the risks of side effects are higher.

The hoped-for reconstitution of immunity occurs spontaneously, and we have no control over the new immunity, which we can only hope is no longer autoimmune. This calls for a degree of modesty. The other question is when these treatments should be used, and for which patients. Obviously, not all forms of MS require such aggressive treatment, and for this reason new disease-activity biomarkers could prove very useful. The biomarker in which researchers and neurologists currently place their highest hopes is a blood assay for neurofilament light chain (NfL), a protein specific to the nerve fibres of neurones. A high level signals axon degeneration and loss, either acute in the event of an attack, or chronic in the case of underlying cell death in the nervous system. Indeed, the disease continues to have a hidden side on which so far, we have been able to have little effect – the slow degeneration of the neuronal networks inside the brain and spinal cord, and hence the gradual progression of the symptoms of the disease.

Future medications will need to address neuroprotection and remyelination.

Although the results achieved thus far give cause for optimism, a great deal remains to be done before we are able to correct each of the pathological mechanisms of MS.

Prof. Dr. Christian Sindic