Citation

Bagnato S, Boccagni C. Neural Regen. Res. 2020; 15(7): 1247-1248.

Copyright

(Copyright © 2020, Neural Regeneration Research, Shenyang, Liaoning Province, P.R. China, Publisher Wolters Kluwer)

DOI

10.4103/1673-5374.272574

PMID

unavailable

Abstract

Traumatic brain injury (TBI) is the paradigmatic example of acute brain injury, defined as sudden and unexpected structural and/or functional damage to the brain. In western countries, TBI is a main cause of prolonged disability, and it is even more impactful because it very often affects young people. Contrary to past belief, the cerebral damage caused by TBI is not limited to the short temporal phase following the mechanical insult. Indeed, moderate/severe TBI can trigger several mechanisms of neuronal damage that operate for months or years after the acute injury, potentially leading to neuronal loss and brain atrophy. Very little is currently known about these processes, and their real impacts in long-term survivors of TBI are largely underestimated. In this perspective, we discuss the existing evidence that moderate/severe TBI triggers various mechanisms capable of inducing prolonged neurodegeneration in humans.

In conclusion, although we currently know some of the neurobiological events operating in the chronic phase of moderate/severe TBI, several pieces must still be placed in their correct positions to compose a complete mosaic of events leading to neuronal loss and brain atrophy. Exhaustive knowledge of these mechanisms will be of the utmost importance for the development of the most appropriate neuroprotective strategies to prevent the long-term effects of moderate/severe TBI.

Language: en