Abstract
CNS myelination is a well-known biological phenomenon related to increase in action potential conduction speed and synaptic integration. Demyelination or abnormal myelination has been related to seizures and epilepsy either in patients or animal models. Although its role in fastening action potential propagation has been confirmed, few additional biological functions of CNS myelin has been described. Among these, myelin proteins such as NogoA were demonstrated to block axon elongation and synaptic potentiation. In light of our novel data on NogoA role in synaptogenesis, we propose a mechanism by which CNS myelin might regulate epileptogenesis both in multiple sclerosis and polymicrogyria.