TBI Biomarker may predict patient outcome
A preclinical study released by researchers at the university of California, Los Angeles, has show that certain brain lipid levels are significantly increased post TBI. The findings were published in the American Journal of Pathology.
Researchers measured the levels of LPA (lysophosphatidic acid) were significantly increased in TBI patients. LPA is also increased in response to cell death and axon injuries which are events that occur in severe and moderate TBI. This finding is promising as researchers say that LPA could be used a biomarker of brain damage, cellular pathology following TBI, and may also be useful in determining patient outcomes.
One of the greatest problems facing clinicians in the diagnosis of TBI is that the tests are very subjective, relying for the most part on patient self reporting of symptoms. There is still very little understanding of the brain mechanics. Tools such as a biomarker would allow for non-invasive assessments of brain damage, and measures of the LPA levels may allow for better predictors of when activity is safe to resume for patients of TBI.
The following is the Abstract of the full report which you can find here.
Matrix-Assisted Laser Desorption Ionization Mapping of Lysophosphatidic Acid Changes after Traumatic Brain Injury and the Relationship to Cellular Pathology
Lysophosphatidic acid (LPA) levels increase in the cerebrospinal fluid and blood within 24 hours after traumatic brain injury (TBI), indicating it may be a biomarker for subsequent cellular pathology. However, no data exist that document this association after TBI. We, therefore, acquired matrix-assisted laser desorption ionization imaging mass spectrometry data of LPA, major LPA metabolites, and hemoglobin from adult rat brains at 1 and 3 hours after controlled cortical impact injury. Data were semiquantitatively assessed by signal intensity analysis normalized to naïve rat brains acquired concurrently. Gray and white matter pathology was assessed on adjacent sections using immunohistochemistry for cell death, axonal injury, and intracellular LPA, to determine the spatiotemporal patterning of LPA corresponding to pathology. The results revealed significant increases in LPA and LPA precursors at 1 hour after injury and robust enhancement in LPA diffusively throughout the brain at 3 hours after injury. Voxel-wise analysis of LPA by matrix-assisted laser desorption ionization and β-amyloid precursor protein by immunohistochemistry in adjacent sections showed significant association, raising the possibility that LPA is linked to secondary axonal injury. Total LPA and metabolites were also present in remotely injured areas, including cerebellum and brain stem, and in particular thalamus, where intracellular LPA is associated with cell death. LPA may be a useful biomarker of cellular pathology after TBI.