One of the numerous consequences of a traumatic brain injury (TBI) is an increased risk for Alzheimer’s disease at a later stage of life. A recent study in Nature, the International Weekly Journal of Science, suggests that researchers have found the driving cause behind the greater risk, along with an antibody that blocks the process.
What Causes Alzheimer’s Disease
As explained in the article, healthy tau proteins (trans P-tau) form scaffolding within nerve cells, which enables them to perform their correct duties. If the process works incorrectly, the resulting proteins are distorted (cis P-tau). They do not function properly, resulting in damage to the energy generators. This ultimately causes the cells to deteriorate and die.
To examine research mice, researchers utilized immunofluorescence, which is a brain imaging technique.
*They observed that one minor brain injury caused elevated levels of cis P-tau. This lasted about two weeks before levels returned to normal.
*One major brain injury or numerous minor injuries caused elevated levels that lasted about six months before returning to normal
*Chronic, continuous brain injury caused the spread of cis P-tau to various parts of the brain, resulting in the destruction of cells. This especially occurred in areas of the brain where memories form and behaviors are controlled.
The Proposed Cure
According to the article, researchers attempted to tackle the problem by creating an antibody that could contain the cis P-tau and prevent its expansion to healthy cells. The developed antibody was then tested on the research mice. The results were reported as follows:
*Mice receiving the antibodies demonstrated normal cis P-tau levels after two weeks of treatment
*Existing nerve damage that affected the axons and energy generators reversed, ceasing the destruction of cells
*The mice that were administered placebo treatments demonstrated extremely risky behaviors, similar to what is observed in people with traumatic brain injuries
*The mice that were administered the antibodies demonstrated caution and were less likely to engage in risky behaviors.
Kun Ping Lu is a professor of medicine at Harvard Medical School and senior co-author of the study. He is quoted in the article as stating, “Our subsequent and ongoing experiments show that pre-treatment and [brain] injection are not necessary… We can delay antibody treatment [hours] after TBI and give three to four antibody injections, which is effective. These results suggest that a short-term antibody treatment after TBI might be sufficient for treating TBI and preventing its long-term consequences if there is not further brain injury.”
Research regarding the effectiveness of the treatment on preventing Alzheimer’s continues, as the studied mice mature in age. According to the article, researchers are reportedly hopeful that this breakthrough may develop into a method of diagnosis, treatment and prevention of the disease.