Papel da neurogênese no traumatismo cranioencefálico

Abstract

Traumatic Brain Injury (TBI) is one of the major health problems worldwide. Emerging evidence has been pointed out TBI as a public health concern, especially by affecting individuals at working age (under 45 years old) and resulting in a significant socioeconomic burden. In Brazil, data related to the epidemiology of TBI are scarce. However, there are reports of high mortality rates, as well as significant hospitalization and treatment costs. Despite of the growing interest in TBI over the past years, the mechanisms underlying its pathophysiology remain to be fully revealed. Neurogenesis, a phenomenon related with new born neurons in specific regions of the central nervous system (CNS), seems to play a role in TBI pathogenesis. However, the neurogenesis real morphological and functional contribution in TBI remains controverse. In this context, the current review aimed to discuss the ermerging evidence provided by pre-clinical and clinical studies regarding neurogenesis role in TBI as well as potential therapeutic strategies focused in neurogenesis following the traumatic event. The literature search was performed using the PubMed, Scielo and Lilacs databases. The key terms employed were "traumatic brain injury" and "neurogenesis". The pre-clinical studies revealed a significant decrease in neurogenesis, especially in the hippocampus dentate gyrus, following TCE. In parallel with neurogenesis reduction, the animals also presented significant impaiment in cognitive tasks related with memory and learning. Interestingly, in a post-mortem clinical study, a significant increase in hipocampal neurogenesis was found following TBI, oppening a road to the hypothesis that the CNS presents an intrisic potential to compensate, at least in part, the neuronal loss after the traumatic event. However, the functional role of neurogenesis in TBI remains to be fully clarified and it was investigated only in 2 clinical studies, hampering more significant conclusions. Currently, there are no effective treatment to prevent TBI-associated cognitive and behavioral alterations. The more recent therapeutic approaches are limited to the primary lessions and there are no approved treatements focusing in minimize or prevent secondary damage. The studies based on neurogenesis as potential therapeutic strategy are inconclusive. Further studies are necessary to investigate whether treatments based on neurogenesis or other phenomenons like neuroplasticity might induce beneficial effects in TBI-associated cognitive and behavioral alterations.