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A major consequence of traumatic brain and spinal cord injury is the loss of the myelin sheath, a cholesterol-rich layer of insulation that wraps around axons of the nervous system. In the central nervous system (CNS), myelin is produced and maintained by oligodendrocytes. Damage to the CNS may result in oligodendrocyte cell death and subsequent loss of myelin, which can have serious consequences for functional recovery. Demyelination impairs neuronal function by decelerating signal transmission along the axon and has been implicated in many neurodegenerative diseases. After a traumatic injury, mechanisms of endogenous remyelination in the CNS are limited and often fail, for reasons that remain poorly understood. One area of research focuses on enhancing this endogenous response. Existing techniques include the use of small molecules, RNA interference (RNAi), and monoclonal antibodies that target specific signaling components of myelination for recovery. Cell-based replacement strategies geared towards replenishing oligodendrocytes and their progenitors have been utilized by several groups in the last decade as well. In this review article, we discuss the effects of traumatic injury on oligodendrocytes in the CNS, the lack of endogenous remyelination, translational studies in rodent models promoting remyelination, and finally human clinical studies on remyelination in the CNS after injury.