The molecule that slows the progression of multiple sclerosis opens the way to new therapies.
Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system. It is characterized by an inflammatory reaction in the white matter of the brain and spinal cord. In most cases, this disease progresses through focal inflammatory flare-ups with the appearance of one or more neurological signs during the flare-up. Their occurrences are unpredictable and their frequency and intensity vary for each patient. The severity and time to progression of the disease therefore vary from one patient to another.
In a study published in Science Translational Medicine, neurologist Alexandre Prat and researchers lift the veil on a molecule called ALCAM (Activated Leukocyte Cell Adhesion Molecule). The results of their work, carried out in vitro in humans and live in mice, could lead to the development of a new generation of therapies to treat this autoimmune disease.
Fatigue, lack of coordination, vision problems and cognitive impairment
Normally, the blood-brain barrier protects our brain from attacks. It prevents, for example, immune system cells such as lymphocytes from invading our central nervous system. In people with MS, this border is permeable, so that large numbers of lymphocytes infiltrate the brain.
B lymphocytes are responsible for the progressive phase of multiple sclerosis. This leads to the deterioration of tissues, including the myelin sheath that usually protects neurons and ensures the transmission of nerve impulses. Certain drugs, commonly called anti-B lymphocytes, slow down its development and reduce the resulting disability. Multiple sclerosis can indeed cause symptoms such as extreme fatigue, lack of coordination, vision problems, cognitive impairment and mood changes.
Decrease the penetration of lymphocytes into the nervous system
By targeting the ALCAM molecule, the lymphocytes continue to circulate in the patient’s body, and continue to defend it against infections, but without reaching the brain. “This molecule reduces the penetration of B lymphocytes into the central nervous system. By blocking this molecule in mice, the entry of B cells into the brain was reduced and thus slowed the progression of the disease.
“The ALCAM molecule is expressed more strongly on the B lymphocytes of people with multiple sclerosis. By specifically targeting this molecule, we will now be able to explore other therapeutic pathways to treat the disease”, explains Dr.Prat.
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