About this Research Topic
Traumatic brain injury (TBI) is a major public health and socio-economic problem worldwide. It is the leading cause of death and disability, especially among children and young adults. Motor and cognitive deficits are well-known sequelae of TBI, which lead to long-term functional impairment and decrease in quality of life. More recently, it has been recognized that behavioral problems, including psychiatric disorders, also represent a significant source of distress in TBI patients.
Although molecular and cellular mechanisms involved in TBI pathophysiology are not fully understood, a growing body of evidence supports the involvement of a wide range of pathways including inflammatory response, oxidative stress, excitotoxicity, biochemical and metabolic changes that are also associated with cognitive, motor, and behavioral outcomes. For instance, TBI induces a complex inflammatory response characterized by fast proliferation and migration of brain resident immune cells (microglia) and circulating monocytes to the lesion site, with consequent production of inflammatory mediators that influence neuronal activity. Microglial cells remain activated for weeks, months or even years following a TBI event, which has been associated with increased expression of inflammatory cytokines, such as IL-1β and TNF, and long-term cognitive dysfunction. Therefore, TBI treatment should not focus only in the acute phase but also on chronic processes that may influence the development of TBI long-term cognitive and behavioral changes.
Currently, there is no treatment that prevents or minimizes TBI neurological and psychiatric sequelae. The understanding of the mechanisms underlying TBI pathophysiology may pave the way for the identification of biomarkers and potential therapeutic targets that ultimately will lead to efficacious therapeutic strategies. Biomarkers can also help stratifying patients and defining therapeutic and outcome prognosis.
In this Research Topic, we aim to approach the diverse field of TBI, especially regarding potential cellular and molecular mechanisms, diagnostic and prognostic biomarkers as well as promise therapeutic strategies, for readers with a general interest in neurotrauma.
Although molecular and cellular mechanisms involved in TBI pathophysiology are not fully understood, a growing body of evidence supports the involvement of a wide range of pathways including inflammatory response, oxidative stress, excitotoxicity, biochemical and metabolic changes that are also associated with cognitive, motor, and behavioral outcomes. For instance, TBI induces a complex inflammatory response characterized by fast proliferation and migration of brain resident immune cells (microglia) and circulating monocytes to the lesion site, with consequent production of inflammatory mediators that influence neuronal activity. Microglial cells remain activated for weeks, months or even years following a TBI event, which has been associated with increased expression of inflammatory cytokines, such as IL-1β and TNF, and long-term cognitive dysfunction. Therefore, TBI treatment should not focus only in the acute phase but also on chronic processes that may influence the development of TBI long-term cognitive and behavioral changes.
Currently, there is no treatment that prevents or minimizes TBI neurological and psychiatric sequelae. The understanding of the mechanisms underlying TBI pathophysiology may pave the way for the identification of biomarkers and potential therapeutic targets that ultimately will lead to efficacious therapeutic strategies. Biomarkers can also help stratifying patients and defining therapeutic and outcome prognosis.
In this Research Topic, we aim to approach the diverse field of TBI, especially regarding potential cellular and molecular mechanisms, diagnostic and prognostic biomarkers as well as promise therapeutic strategies, for readers with a general interest in neurotrauma.
Keywords: Traumatic Brain Injury, Biomarkers, Cognition, Psychiatric disorders, Neuroimage
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