alpha-Synuclein: a Modulator During Inflammatory CNS Demyelination

This study investigates the role of alpha-Synuclein (aSyn) in demyelinating diseases of the central nervous system, such as multiple sclerosis. Demyelination involves the loss of the myelin sheath around nerve fibers, leading to neurological problems. The researchers used two different animal models to study demyelination: one mimicking multiple sclerosis (EAE) and another using a toxin (cuprizone). They examined mice with and without aSyn to see how it affects the disease process. The findings suggest that aSyn plays a role in modulating the immune response during demyelination. In the EAE model, mice lacking aSyn had less inflammation and myelin loss. However, in the cuprizone model, aSyn deficiency did not significantly affect demyelination or remyelination.

• 1
  In the EAE model, aSyn-deficient mice showed a significant reduction of CNS inflammation and decreased myelin loss during late-stage inflammatory demyelination.
• 2
  In the cuprizone model, myelination and neuroinflammatory patterns were not affected by aSyn deficiency during both demyelination and remyelination phases.
• 3
  The study suggests that aSyn regulates peripheral immune responses under neuroinflammatory conditions, thereby modulating degenerative events in late-stage demyelinating disease.