title: Traumatic brain injury: recent advances in plasticity and regeneration.
abstract: OBJECTIVE
  There is an urgent need for effective therapies to restore neurologic function and decrease disability following traumatic brain injury (TBI). Here, emerging findings on the mechanisms of post-TBI neural repair and regeneration, as well as therapeutic implications, are selectively reviewed.
  
  
  RESULTS
  Recent discoveries include the characterization of the inhibitory signaling systems within the injury site, postinjury stem cell niche activation, the role of serotonin signaling in repair, and environment enrichment. A potentially transformative finding has been the identification of exosomes, nano-sized extracellular vesicles which have key roles in cell signaling, and might serve as novel biomarkers and as vehicles for targeted delivery of repair-inducing molecules.
  
  
  CONCLUSIONS
  In the experimental setting, post-TBI repair can be promoted by modulation of inhibitory signaling, neurotrophic factor administration, and amplified serotonin signaling; additional strategies include mobilization of endogenous stem cell populations, exogenous cell-based therapies, and environmental enhancement. Feasibility, safety, and efficacy of these approaches need further investigation in humans. Studies are also needed to evaluate biomarkers based on molecular traces of neural repair and regeneration, which could transform prognostic and predictive modeling of post-TBI recovery trajectories.
authors.affiliation: aDepartments of Neurology bAnesthesiology Critical Care Medicine cNeurological Surgery, Johns Hopkins University School of Medicine.
authors.forename: J Kent
authors.initials: JK
authors.lastname: Werner
authors.forename: Robert D
authors.initials: RD
authors.lastname: Stevens
mesh_terms: D001930:Brain Injuries / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D055354:Exosomes / Q000502:physiology*; D006801:Humans; D009416:Nerve Regeneration / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*