The Tau of Dementia

Dec. 27, 2013

By Medical Discovery News

The Tau of Dementia

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.

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An Early Start to Alzheimer’s

April 12, 2013

By Medical Discovery News

More and more data suggest that treatment for Alzheimer’s disease may be more effective if started early, even before symptoms appear. In addition, recent clinical trials of treatments for mild to moderate Alzheimer’s have failed, suggesting that waiting to treat the disease until these stages may be too late, and once the degenerative process has started it cannot be stopped. But since Alzheimer’s has no identifiable markers in its early stages, how would doctors know when and whom to treat?


Alzheimer’s is a form of dementia that causes an irreversible loss in brain function and gradually gets worse over time, affecting memory, thinking, and behavior. Buildup of insoluble proteins in the brain causes amyloid plaques or neurofibrillary tangles, two hallmarks of the disease along with a loss in connections between electrically active nerve cells called neurons. There is no definite diagnosis, other than autopsy.

A recent study of an extended family of 5,000 people from Colombia who inherited a form of Alzheimer’s revealed that the disease begins much earlier, and the deterioration of the brain occurs in more ways than previously thought. Affected family members had mild problems thinking and remembering at an average age of 45 and dementia at 53. However, researchers also noticed changes in affected family members at younger ages, before the first signs of plaques in the brain.

The study compared twenty 18- to 26-year-old family members who carried a mutation called presenilin1 E280A and were very likely to develop early onset Alzheimer’s with 24 non-carriers. Both groups underwent a variety of tests including MRIs, memory tests, cognitive tests, blood tests, and cerebral spinal fluid sampling. The groups did not differ significantly in their dementia ratings or psychological scores. However, carriers had fewer neurons in several regions of the brain that are affected by Alzheimer’s. Carriers also had higher levels of the amyloid protein that causes plaques in their cerebral spinal fluid. 

Previous studies of Alzheimer’s patients showed they have lower levels of amyloid than normal, which had been attributed to amyloid accumulating in the brain. Based on this information, scientists thought Alzheimer’s was explained by the progressive buildup of amyloid in plaques that causes brain cells to die, leading to symptoms of Alzheimer’s. This new study suggests that there are early changes in the brain even before amyloid plaques. 

This challenges what we know about when and how Alzheimer’s develops. Inherited, early onset Alzheimer’s may be caused by the body producing too much amyloid, while late onset Alzheimer’s may be the result of the body’s inability to clear amyloid from the brain. Researchers are now focusing on family members ages seven to 17 to determine if they can detect any brain differences even earlier.

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