A mechanism that prevents certain nerve cells from ripening hinders the repair of damaged neurons sheaths in multiple sclerosis.
A molecular brake that remains pulled too long could contribute to the damage inflicted on neurons from multiple sclerosis. The discovery of the mechanism, which concerns the maturation of the cells that produce myelin (a protective sheath that envelops neurons and that is compromised by multiple sclerosis) could open the way to new therapies against this disease. The research was published on Cell.
Insulating tape
Myelin is a substance made of fats and proteins that envelops and isolates neurons and allows the efficient transmission of nerve impulses. In multiple sclerosis, an autoimmune neurodegenerative disease, the cells in charge of repairing damaged myelin, the oligodenendrocytes, are unable to achieve a state of maturation and do their work.
The oligodendrocytes belong to the cells of the glia, a large and “mixed” group of cells of the nervous tissue that support the development of neurons and which have long been neglected in the studies, in favor of the neurons themselves.
A malfunctioning brake
A group of scientists from the Case Western Reserve University of Cleveland, in Ohio, has identified a protein (called sox6) which acts as a brake, blocking the oligodendrocytes in an “immature” state. As a rule, this brake serves to prevent early production of myelin and ensure that the oligodendrocytes regeneger at the right time. But in multiple sclerosis, it seems to prevent the process of re -emiginization (new myelin production) of the neurons with the damaged sheath, determining the chronicity of the disease.
An exclusive feature of multiple sclerosis
An unusually high number of oligodendrocytes with … “stuck stoped” sox6 was found in data on the nerve tissues of people with multiple sclerosis, but not in that of patients with other neurodegenerative diseases such as Parkinson’s or Alzheimer’s. When scientists used a drug to reduce the Sox6 protein in the mice, within a few days the treated cells managed to mature: the brake was released and the oligodendrocytes finally ripe managed to produce myelin for neighboring neurons.
This seems to suggest, say the researchers, that these cells in those suffering from multiple sclerosis are only temporarily stalled, not necessarily damaged.
