fig3

Figure 3. Schematic representation of the demyelination and remyelination processes. (a) in a basal condition, type A neuroblasts and oligodendrocyte precursor cells (OPCs) are continuously generated from neural stem cells, with neuroblasts being the great majority progeny; (b) after a demyelinating episode, nearby astrocytes and microglia are activated and release inflammatory mediators, increasing the permeability of the blood‑brain barrier (BBB). By releasing chemokines, astrocytes recruit more microglial cells to the demyelinated area; (c) which phagocyte dead cells and myelin debris, as do macrophages that have crossed the BBB. Astrocytes and macrophages act as antigen‑presenting cells to T lymphocytes that are then activated and attack the myelin sheath and dying cells. B lymphocytes produce autoantigens against myelin antigens functioning as opsonins; (d) microglia, macrophages, and astrocytes release mediators that mobilize parenchymal OPCs to proliferate, migrate, and differentiate into new myelinating oligodendrocytes in the demyelinated area. After a demyelinating episode, OPC production in the subventricular zone (SVZ) is favored in detriment of neuronal precursor cells. These SVZ‑derived OPCs migrate to the demyelinated areas where they differentiate into mature myelinating oligodendrocytes; (e) new myelinating oligodendrocytes form a thinner myelin sheath around the demyelinated axon