FOR PROVIDERS

Blood tests are an essential method to determine the extent of a Traumatic Brain Injury (TBI). The blood test is best run from the moment a patient has an injury and after a few weeks of the trauma when the proteins “should have” decreased if there is no ongoing damage to the brain. However, our NEURO-Trauma Assessment Test™ can be given at any time, from right after the injury occurred to any point forward, there is no time limit.

Our NEURO-Trauma Assessment Test™ can work in concert with other interpretive, functional or subjective tests including:

  • Visual Occulomotor testing

  • CT, MRI, Diffuse Tensor Imaging

  • Exercise intolerance (autonomic dysfunction)

  • Neuro exam

  • Neuropsychological exam

Brazos Neuroscience’s NEURO-Trauma Assessment Test™ employs a number of biomarkers to help diagnose and manage the TBI patient:

Blood Protein Biomarkers used for Diagnosis                                                         

  • GFAP (Glial Fibrillary Acidic Protein)                                              

  • UCH-L1 (Ubiquitin C-Terminal Hydrolase L1)

Genes used for Diagnosis                                            

  • APOE (Apolipoprotein E)

  • MTHFR (Methylenetetrahydrofolate Reductase)

If you are a medical provider and would like to order our NEURO-Trauma Assessment Test™, please click on the link below:

Protein Blood Biomarkers

1. Glial Fibrillary Acidic Protein (GFAP)

What It Does: GFAP is an intermediate filament protein expressed by astrocytes. It is crucial for maintaining the structural integrity of the brain and plays a role in repair processes following brain injury.

Pertinence to TBI Diagnosis: GFAP levels increase in response to astrocyte activation and damage, making it a specific marker for astrocytic or neuronal injury. Elevated GFAP levels in the bloodstream are indicative of TBI and predicting outcomes.

 

2. Ubiquitin C-Terminal Hydrolase-L1 (UCH-L1)

What It Does: UCH-L1 is a protein highly abundant in neurons, where it plays a role in protein degradation and synaptic function. It is involved in the ubiquitin-proteasome system, critical for protein turnover and cellular homeostasis.

Pertinence to TBI Diagnosis: Like GFAP, elevated levels of UCH-L1 in the blood are a marker of neuronal damage. Its presence outside of the central nervous system indicates that brain cells have been damaged or disintegrating and are leaking their contents into the bloodstream. UCH-L1 levels can provide information on the timing and severity of injury, making it valuable for both diagnosis and monitoring the progression of TBI.

Genes

1. APOE (Apolipoprotein E)

What It Does: APOE is a gene that codes for the apolipoprotein E protein, which is involved in lipid metabolism and is crucial for the normal catabolism of triglyceride-rich lipoprotein constituents. There are three major isoforms of the APOE protein: ε2, ε3, and ε4, encoded by three alleles (ε2, ε3, ε4) of the APOE gene. APOE ε4, in particular, has been linked to an increased risk of Alzheimer's disease and cardiovascular disease.

Involvement in TBI Outcomes: Individuals with the APOE ε4 allele have been found to have worse outcomes after TBI, including a higher risk of developing chronic traumatic encephalopathy (CTE), poorer cognitive recovery, and an increased likelihood of neurodegenerative complications. The ε4 allele may affect the brain's response to injury, including impaired lipid metabolism and increased susceptibility to neuronal damage.

2. MTHFR (Methylenetetrahydrofolate Reductase)

What It Does: MTHFR is a gene that encodes the enzyme methylenetetrahydrofolate reductase. This enzyme plays a critical role in the body's folate and methionine metabolism pathways. Specifically, it catalyzes the conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, a reaction that is necessary for the re-methylation of homocysteine to methionine. Methionine is essential for the synthesis of S-adenosylmethionine (SAMe), a major methyl donor in numerous methylation reactions, including DNA methylation. This process is crucial for gene expression regulation, protein function, and cell cycle control. MTHFR mutations also correlate with the degree of brain white matter disease and injury and predict cerebrovascular disease and dementia.

Involvement in TBI Outcomes: Variants in the MTHFR gene, particularly the C677T and A1298C polymorphisms, have been studied for their potential impact on health outcomes, including those related to TBI. These polymorphisms can lead to reduced activity of the MTHFR enzyme, affecting folate metabolism and leading to elevated levels of homocysteine, a condition known as hyperhomocysteinemia. Elevated homocysteine levels are associated with increased oxidative stress and vascular risk factors, which can contribute to neurovascular damage and cognitive decline in TBI.

Reduced Enzyme Efficiency: The reduced efficiency of the MTHFR enzyme, due to these genetic variations, can impair the methylation cycle. This may influence brain repair mechanisms and neuronal plasticity following TBI. The proper function of the methylation cycle is crucial for DNA repair, neurotransmitter synthesis, and myelin sheath maintenance, all of which are important for recovery after brain injury.

Neuroinflammation and Oxidative Stress: The altered homocysteine levels and compromised folate metabolism can exacerbate neuroinflammation and oxidative stress, potentially worsening the outcomes after TBI. These conditions can lead to further neuronal damage and impede the recovery process.

Impact on Recovery and Rehabilitation: Individuals with MTHFR mutations may have a different response to TBI, affecting their recovery trajectory. Nutritional interventions, such as folate supplementation, could potentially mitigate some of these effects, suggesting a personalized approach to rehabilitation based on MTHFR genotype.