Traumatic brain injury (TBI) continues to be a critical health condition, especially for the newly born, the elderly, and victims of motor vehicle accidents, sports concussions, war blasts, etc. Due to the extremely complicated nature of primary and secondary sequelae following injury, little can be inferred from human clinical studies concerning TBI pathogenesis and progression. Instead, mouse models have overwhelmed the animal research on TBI, for reasons ranging from the lack of serious ethical concerns to the statistical advantages of producing relatively large sample size groups. Studies on rodents are nonetheless burdened with several limitations, such as non-standardized categorization of severity, use of neuroprotective anesthetics and a different time-course progression of post-TBI damage in rodents compared to humans. Moreover, short- and long-term dysregulation of neuronal and glial cells at the perilesional region are often neglected at the expense of studying biomarkers that are more readily detected in the bloodstream.
This Research Topic aims to highlight the relevance and shortcomings of existing TBI mouse models, mainly those based on weight drop, fluid percussion injury, controlled cortical impact injury, and blast injury. It is even more pertinent to acknowledge the limitations of recently introduced models, such as penetrating ballistic-like brain injury and CHIMERA models. Moreover, deregulation of intracellular mechanisms in affected brain cells ought to be studied along pathways of apoptosis, DNA damage, oxidative stress, glucose metabolism, calcium influx, neuronal plasticity, and others. Such processes can be investigated by state-of-the-art techniques including RNA sequencing, optogenetics, in vivo electrophysiology and neuroproteomics. A focused approach of this sort – investigating the cellular context in mouse models following neurotrauma – will likely bring animal research a step closer to useful translational applications.
The scope of this Research Topic encompasses all attempts at unraveling TBI damage in rodents, ranging from rapid short-term molecular changes in the perilesional area, to persistent long-term outcomes that set the stage to more serious neurodegenerative phenotypes. Equally relevant are reports on pharmacological and neurotherapeutic interventions that can potentially ameliorate defects following brain injury. We also welcome updated reviews on existing molecular discrepancies of TBI in rodents vs. humans. In addition, perspectives on how to next reconcile the two bodies of literature (i.e. in mice and humans) can help guide researchers to new translational avenues. All in all, the aim of this collection is to serve as a reference that will help resolve much of the concerns on reproducibility and basic-to-clinical aspects of TBI pathology.
Traumatic brain injury (TBI) continues to be a critical health condition, especially for the newly born, the elderly, and victims of motor vehicle accidents, sports concussions, war blasts, etc. Due to the extremely complicated nature of primary and secondary sequelae following injury, little can be inferred from human clinical studies concerning TBI pathogenesis and progression. Instead, mouse models have overwhelmed the animal research on TBI, for reasons ranging from the lack of serious ethical concerns to the statistical advantages of producing relatively large sample size groups. Studies on rodents are nonetheless burdened with several limitations, such as non-standardized categorization of severity, use of neuroprotective anesthetics and a different time-course progression of post-TBI damage in rodents compared to humans. Moreover, short- and long-term dysregulation of neuronal and glial cells at the perilesional region are often neglected at the expense of studying biomarkers that are more readily detected in the bloodstream.
This Research Topic aims to highlight the relevance and shortcomings of existing TBI mouse models, mainly those based on weight drop, fluid percussion injury, controlled cortical impact injury, and blast injury. It is even more pertinent to acknowledge the limitations of recently introduced models, such as penetrating ballistic-like brain injury and CHIMERA models. Moreover, deregulation of intracellular mechanisms in affected brain cells ought to be studied along pathways of apoptosis, DNA damage, oxidative stress, glucose metabolism, calcium influx, neuronal plasticity, and others. Such processes can be investigated by state-of-the-art techniques including RNA sequencing, optogenetics, in vivo electrophysiology and neuroproteomics. A focused approach of this sort – investigating the cellular context in mouse models following neurotrauma – will likely bring animal research a step closer to useful translational applications.
The scope of this Research Topic encompasses all attempts at unraveling TBI damage in rodents, ranging from rapid short-term molecular changes in the perilesional area, to persistent long-term outcomes that set the stage to more serious neurodegenerative phenotypes. Equally relevant are reports on pharmacological and neurotherapeutic interventions that can potentially ameliorate defects following brain injury. We also welcome updated reviews on existing molecular discrepancies of TBI in rodents vs. humans. In addition, perspectives on how to next reconcile the two bodies of literature (i.e. in mice and humans) can help guide researchers to new translational avenues. All in all, the aim of this collection is to serve as a reference that will help resolve much of the concerns on reproducibility and basic-to-clinical aspects of TBI pathology.
