Abstract
Traumatic brain injury (TBI) is understood as an interplay between the initial injury, subsequent secondary injuries, and a complex host response all of which are highly heterogeneous. An understanding of the underlying biology suggests a number of windows where mechanistically inspired interventions could be targeted. Unfortunately, biologically plausible therapies have to-date failed to translate into clinical practice. While a number of stereotypical pathways are now understood to be involved, current clinical characterization is too crude for it to be possible to characterize the biological phenotype in a truly mechanistically meaningful way. In this review, we examine current and emerging technologies for fuller biochemical characterization by the simultaneous measurement of multiple, diverse biomarkers. We describe how clinically available techniques such as cerebral microdialysis can be leveraged to give mechanistic insights into TBI pathobiology and how multiplex proteomic and metabolomic techniques can give a more complete description of the underlying biology. We also describe spatially resolved label-free multiplex techniques capable of probing structural differences in chemical signatures. Finally, we touch on the bioinformatics challenges that result from the acquisition of such large amounts of chemical data in the search for a more mechanistically complete description of the TBI phenotype.
Highlights
In broad terms, we understand the biology of traumatic brain injury (TBI) as being the result of an interplay between the biomechanics of the initial insult and resulting injury, the effects of the subsequent resuscitative treatments and the host response
Top ranking serum metabolites associated with Traumatic brain injury (TBI) were found highly correlated with their MD levels suggesting possible sensitivity to blood–brain barrier (BBB) damage, as well as protective response and altered metabolism post-TBI
This study showed that matrix metalloproteinases (MMPs)-9 concentrations are increased in pericontusional brain early post-TBI, likely reflecting post- traumatic proteolytic breakdown of the BBB which correlates with hemorrhagic progression and vasogenic edema [18]
Summary
We understand the biology of traumatic brain injury (TBI) as being the result of an interplay between the biomechanics of the initial insult and resulting injury, the effects of the subsequent resuscitative treatments and the host response. These latter factors are important; even the best available prognostic models predict only a small part of the observed variability in outcome [1]. The molecular signatures generated by emerging experimental techniques are complex and new approaches will likely be needed to make sense of the large amount of data that are becoming available.
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