Multiple sclerosis (MS) is a neurological disease where inflammation damages the insulating myelin sheath around nerves in the central nervous system. Early in the disease, the body tries to repair this damage by forming new myelin, but this process often fails in later stages, leading to neurodegeneration and worsening symptoms. A key factor in this failure is the malfunction of immune cells called macrophages and microglia. These cells can initially help by clearing debris and supporting repair, but when they absorb too much myelin, they turn "foamy" and become harmful, blocking repair due to toxic fat buildup. Our recent research points to tiny molecules called microRNAs, especially miR146a, as potential regulators of these immune cells. MiR146a may influence how these cells handle inflammation and fat metabolism, which could improve their ability to repair myelin. Understanding how miR146a works could pave the way for new treatments to help MS patients recover from nerve damage more effectively.