Published online Jan 26, 2020. doi: 10.4252/wjsc.v12.i1.8
Peer-review started: August 9, 2019
First decision: August 30, 2019
Revised: November 25, 2019
Accepted: December 13, 2019
Article in press: December 13, 2019
Published online: January 26, 2020
Processing time: 142 Days and 16 Hours
Poor recovery of neuronal functions is one of the most common healthcare challenges for patients with different types of brain injuries and/or neurodegenerative diseases. Therapeutic interventions face two major challenges: (1) How to generate neurons de novo to replenish the neuronal loss caused by injuries or neurodegeneration (restorative neurogenesis) and (2) How to prevent or limit the secondary tissue damage caused by long-term accumulation of glial cells, including microglia, at injury site (glial scar). In contrast to mammals, zebrafish have extensive regenerative capacity in numerous vital organs, including the brain, thus making them a valuable model to improve the existing therapeutic approaches for human brain repair. In response to injuries to the central nervous system (CNS), zebrafish have developed specific mechanisms to promote the recovery of the lost tissue architecture and functionality of the damaged CNS. These mechanisms include the activation of a restorative neurogenic program in a specific set of glial cells (ependymoglia) and the resolution of both the glial scar and inflammation, thus enabling proper neuronal specification and survival. In this review, we discuss the cellular and molecular mechanisms underlying the regenerative ability in the adult zebrafish brain and conclude with the potential applicability of these mechanisms in repair of the mammalian CNS.
Core tip: Poor recovery of neuronal functions is one of the most common healthcare challenges for patients with different types of brain injuries. In contrast to mammals, zebrafish have developed specific mechanisms to activate a restorative neurogenic program in a specific set of glial cells (ependymoglia) and to resolve both the glial scar and inflammation, thus enabling proper neuronal specification and survival. In this review, we discuss these mechanisms and their potential applicability for the repair of the mammalian central nervous system.