By NORBERT HERZOG and DAVID NIESEL

All it takes is the instantaneous crash of an oncoming car.

The heavy blow of a linebacker’s tackle. The explosion of a roadside bomb in Afghanistan. All these instances and more can cause traumatic brain injury (TBI). It used to be considered a one-time event, but its long-lasting impairments make it more of a chronic disease.

Sadly, there are no cures for TBI and each person experiences them in their own way. Just as each person is different, no two brain injuries are exactly alike. This makes it a very challenging condition to study and to treat.
A silent injury, the damage of TBI is not outwardly visible, unlike a broken arm or an amputated leg. Some people have been accused of faking a brain injury, and some denied medical assistance because their injury is undetectable.

Others think they are fine, but their reaction times are slower and they may have trouble with memory, focus, attention, and motor skills. Even a mild concussion can produce these effects.

What’s more, someone with TBI is at a greater risk of developing dementia. Autopsies of the brains of athletes who had multiple concussions prove this connection.

Their brains revealed that they had chronic traumatic encephalopathy (CTE), which has symptoms similar to Alzheimer’s disease.

There isn’t a way to detect CTE and dementia other than through an autopsy, so it is difficult to know who has it for sure.

In the lab, CTE is recognizable through the detection of a protein called tau in certain areas of the brain. The presence of tau can impair normal cellular processes and result in trouble thinking or remembering.

It seems like an easy fix — remove the tau and repair the dysfunctional brain cells. Unfortunately, it’s not that simple. Tau plays an important role in stabilizing the structure of brain cells, so removing all the tau from the brain would cause damage and dysfunction.

Too much tau is not good either. Then, individual units of tau protein accumulate and form structures of their own such as neurofibrillary tangles.

These interfere with cells’ ability to communicate with each other. Aggregate tau can be toxic as well and is suspected to perpetuate the cell death processes that occur in the hours and weeks after an initial injury.

Researchers with the Sealy Center for Vaccine Development at UTMB have developed an antibody that detects this toxic form of tau protein without interrupting the processes of normal tau proteins. Using this antibody, they were able to find toxic tau tangles in animal brains after TBI.

Next, they plan to use a similar antibody to inactivate the tau tangles with the hope of preventing further damage.
This antibody appears to improve learning and memory in rodents with Alzheimer’s disease. In the future, it might be used as a therapeutic vaccine for many neurodegenerative disorders.

Right now though, researchers are working to ensure this therapy is safe and effective in animals before moving on to clinical trials with people.

Professors Norbert Herzog and David Niesel are biomedical scientists at the University of Texas Medical Branch. Learn more at medicaldiscoverynews.com.