Citation

Cacialli P. Int. J. Mol. Sci. 2021; 22(4): e1585.

Copyright

(Copyright © 2021, Molecular Diversity Preservation International)

DOI

10.3390/ijms22041585

PMID

unavailable

Abstract

Traumatic brain injury (TBI) remains the leading cause of long-term disability, which annually involves millions of individuals. Several studies on mammals reported that neurotrophins could play a significant role in both protection and recovery of function following neurodegenerative diseases such as stroke and TBI. This protective role of neurotrophins after an event of TBI has also been reported in the zebrafish model. Nevertheless, reparative mechanisms in mammalian brain are limited, and newly formed neurons do not survive for a long time. In contrast, the brain of adult fish has high regenerative properties after brain injury. The evident differences in regenerative properties between mammalian and fish brain have been ascribed to remarkable different adult neurogenesis processes. However, it is not clear if the specific role and time point contribution of each neurotrophin and receptor after TBI is conserved during vertebrate evolution. Therefore, in this review, I reported the specific role and time point of intervention for each neurotrophic factor and receptor after an event of TBI in zebrafish and mammals.

Language: en

Keywords

injury; brain; BDNF; NGF; NT3; NT4; TrkA; TrkB; TrkC; zebrafish