Researchers at the University of California, San Francisco Uncover Mechanism of Neuron Death in Multiple Sclerosis

Researchers at the University of California, San Francisco, have made a significant breakthrough in understanding the nature of multiple sclerosis (MS). Professor Fancy from the Weill Institute of Neuroscience announced that the team has identified a specific mechanism that explains the death of vulnerable neurons in the brains of patients. This discovery could transform the approach to treatment and prognosis of the disease.

A key factor in neurodegeneration associated with multiple sclerosis is the loss of myelin. Myelin is a specialized sheath that covers nerve fibers (axons). Scientists compare its role to that of plastic insulation on electrical wires: it protects the fibers and ensures the rapid and efficient transmission of impulses between different parts of the brain. These myelinated axons form the white matter of the brain, located beneath its outer layers.

When myelin is damaged, the white matter begins to deteriorate, leading to the disruption of connections between neurons. This process causes the characteristic symptoms of multiple sclerosis, including vision disturbances, numbness in the limbs, muscle weakness, painful spasms, and loss of balance.

The disease has a complex structure and is divided into four main types. Relapsing-remitting MS is the most common form, characterized by periods of symptom exacerbation alternating with phases of partial or complete recovery. Secondary-progressive MS is a stage that often follows the relapsing type, marked by a gradual and relentless decline in condition. Primary-progressive MS is diagnosed in a small number of patients and is characterized by disease progression from the very beginning without clear periods of remission.

Professor Fancy emphasizes that understanding why certain neurons become vulnerable and die after the loss of the myelin sheath is critically important. Since the disease manifests differently in each patient—from prolonged stability to rapid development of disability—the identified mechanism will allow scientists to develop more targeted therapeutic methods aimed at preserving the integrity of white matter and protecting nerve fibers from irreversible destruction.

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