:
Myelin is a specialized membrane allowing for saltatory conduction of action potentials in neurons, an
essential process to achieve the normal communication across the nervous system. Accordingly, in diseases characterized
by the loss of myelin and myelin forming cells -oligodendrocytes in the CNS-, patients show severe
neurological disabilities. After a demyelinated insult, microglia, astrocytes and oligodendrocyte precursor cells
invade the lesioned area initiating a spontaneous process of myelin repair (i.e. remyelination). A preserved hallmark
of this neuroinflammatory scenario is a local increase of oxidative stress, where several cytokines and
chemokines are released by glial and other cells. This generates an environment that determines cell interaction
resulting in oligodendrocyte maturity and the ability to synthesize new myelin. Herein we review the main features
of the regulatory aspect of these molecules based on recent findings and propose new putative signal molecules
involved in the remyelination process, focused in the etiology of Multiple Sclerosis, one of the main demyelinating
diseases causing disabilities in the population.
Experience in the demyelinating diseases unit after 2 years
