A recent scientific study has shed light on a possible molecular mechanism responsible for nerve cell damage in multiple sclerosis, a chronic autoimmune disease that affects the central nervous system.
Multiple sclerosis occurs when the immune system mistakenly attacks the protective sheath surrounding nerve fibers, known as myelin. This damage disrupts the transmission of electrical signals between the brain and the rest of the body, leading to a wide range of neurological symptoms.
Depending on which areas of the nervous system are affected, patients may experience vision problems, muscle weakness, numbness, fatigue, balance issues, and cognitive difficulties.
Although current therapies can help reduce relapse rates and slow disease progression, preventing the underlying nerve damage has remained a major scientific challenge due to the limited understanding of the molecular processes involved.
The new research highlights a specific cell-death mechanism known as Parthanatos, a biological pathway triggered by severe cellular stress and inflammation. Researchers suggest that this process may play a central role in the loss of neurons associated with inflammatory activity in the disease.
Their findings indicate that immune-mediated oxidative stress can damage neuronal DNA at early stages. This damage activates a cascade of molecular signals that ultimately lead to the death of nerve cells.
One key step in this pathway involves the release of a molecule called PAR within the cell’s cytoplasm. This event triggers the activation of another factor known as AIF, which then binds with a protein called MIF. The complex moves into the cell nucleus where it acts to break down genetic material, resulting in neuronal death.
Scientists believe that targeting this molecular pathway could provide a promising strategy for future therapies designed to protect nerve cells and slow the progression of multiple sclerosis.
For more details and the latest news, follow Masr Connect.
