Clinical Applications of Biomarkers of TBI

Biomarkers of neuronal, glial, and axonal damage such as neuron-specific enolase, S100B, and myelin basic protein, respectively, are readily detectable in biological samples such as serum or CSF and are being studied in patients with TBI. In addition, a number of studies have demonstrated that novel tools to assess simultaneously multiple biomarkers can provide unique insight such as details on specific molecular participants in cell death cascades, inflammation, or oxidative stress. Multifaceted cellular, biochemical, and molecular monitoring of proteins and lipids is desirable as an adjunct to guide therapy and improve outcome in TBI. Biomarkers are useful as diagnostic, prognostic, and monitoring adjuncts in neurointensive care (Kochanek et al. 2008).

TBI biomarkers may have clinical utility in stratifying injury severity level, predicting adverse secondary events or outcomes, and monitoring the effectiveness of therapeutic interventions. As a biomarker source, serum offers several advantages over CSF, including ease of accessibility and reduced risk to the patient. Screened pooled serum samples obtained from severe TBI patients and age-, sex- and race- matched volunteers have been studied for biomarkers (Hergenroeder et al. 2008). Labeling with mass-balanced isobaric tags (iTRAQ), and analysis by LC-MS/MS revealed 31 candidate biomarkers whose serum abundance was altered after TBI. Changes in two candidate biomarkers - CRP and retinol binding protein (RBP) - were robust indicators of injury even at very acute time points. Analysis of serum RBP4 levels at 24-36 h post-injury indicates it may predict subsequent increases in intracranial pressure (ICP) with a sensitivity of 86% and specificity of 88%. These results support the use of serum as a source for discovery of TBI biomarkers, and indicate that serum biomarkers may have utility for predicting secondary pathologies such as elevated ICP associated with TBI. Changes in the expression profile of biomarkers such as microRNA in peripheral blood mononuclear cells may reflect molecular alterations following TBI that contribute to the onset and progression of TBI phenotypes including chronic traumatic encephalopathy (Pasinetti et al. 2010).

 
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