Abnormally high levels of a brain protein called tau have been linked to acute traumatic brain injury (TBI) complications. New research from the National Institutes of Health (NIH) has found that accumulations of tau may also be responsible for long-term complications from traumatic brain injury (TBI).1
Possible tau-related neurological symptoms, include:
- Post-concussive disorder (PCD);
- Chronic traumatic encephalopathy (CTE);
- Post-traumatic stress disorder (PTSD); and
- Depression.
Tau proteins are most numerous in the neurons of the central nervous system. Evidence suggests tau levels are elevated after severe head trauma, and a decrease in tau levels is connected to clinical improvement.2
Other recent research has found that this protein may play a role in blood-brain barrier (BBB) damage. The new data suggests abnormally high levels of tau can initiate the breakdown of the BBB, and that reducing tau levels can precipitate BBB recovery.3
What all of this research indicates is that medical intervention reducing the levels of tau could prevent acute and chronic TBI symptoms and complications.
“With further study, our findings may provide a framework for identifying patients who are most at risk for experiencing chronic symptoms related to TBI. Identifying those at risk early in the progression of the disease provides the best opportyinity for therapies that can lesson the cognitive declines that may result from these long-term effects,” said Dr. Jessica Gill, the lead author of the NIH study.
The team used ultrasensitive immunoassay technology to measure tau levels in the blood. This is a promising technology4 that may someday be used as standard practice to assess damage after a traumatic brain injury and dictate treatment.
The work has begun on treatments for TBI centered on tau reduction. One study found sodium selenate may reduce levels of this protein, and thereby improve the patient’s immediate post-injury condition and long-term prognosis.5
Works Cited
1. Olivera, A., et al. “Peripheral total tau in military personnel who sustain traumatic brain injuries during deployment.” JAMA Neurology. Published online August 3, 2015.
2. Franz, G., et al. “Amyloid beta 1-42 and tau in cerebrospinal fluid after severe traumatic brain injury.” Neurology 60.9 (2003): 1457-1461.
3. Blair, Laura J., et al. “Tau depletion prevents progressive blood-brain barrier damage in a mouse model of tauopathy.” Acta neuropathologica communications 3.1 (2015): 1-22.
4. Rubenstein, Richard, et al. “A Novel, Ultrasensitive Assay for Tau: Potential for Assessing Traumatic Brain Injury in Tissues and Biofluids.” Journal of neurotrauma 32.5 (2015): 342-352.
5. Shultz, Sandy R., et al. “Sodium selenate reduces hyperphosphorylated tau and improves outcomes after traumatic brain injury.” Brain (2015): awv053.
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