Last month the US National Institutes of Health (NIH) published a paper in the Acta Neuropathologica medical journal titled “Seeding selectivity and ultrasensitive detection of tau aggregate conformers of Alzheimer disease.” That paper detailed a new test that could lead to dramatically better diagnostic tools and treatment for both Alzheimer disease (AD) and chronic traumatic encephalopathy (CTE).
CTE is a degenerative brain disease that is caused by clumps of Tau protein that spread throughout the brain, killing cells. As the Tau destroys cells the sufferer can experience symptoms that include dementia, impulse control problems, paranoia, depression, and suicidiality.
Repeated blows to the head have been shown to cause the kinds of clusters of Tau protein that cause CTE. It was previously believed that blows to the head that triggered a concussion were responsible for the release and clumping of Tau protein, but a recent study has shown that repeated blows to the head which do not cause a concussion can also result in Tau spreading through the brain.
Due to the nature of both sports and combat, many professional athletes and military personnel have been affected by CTE. In 2017, CNN reported that CTE was discovered in 99% (110 out of 111) of the deceased NFL players’ brains that had been donated to scientific research.
CTE has also been discovered in the brains of former NHL players and at least one professional soccer player. Bellator veteran Jordan Parsons, who was killed by a drunk driver in 2016, is the first — and currently only — MMA fighter to have been officially diagnosed with CTE.
Diagnosing CTE can only be done, with certainty, by examining brain tissue post-mortem. For this reason, the medical science community is eager to find methods to test CTE in living patients so that treatment can begin early and damaging behaviour can be stopped.
The latest NIH study, which was conducted by that organization’s National Institute of Allergy and Infectious Diseases, was focused primarily on Alzheimer Disease with brain samples from 16 AD patients. The study also included samples from two boxers with CTE and numerous control cases involving other brain diseases.
Like CTE, AD is caused by tangles of Tau protein in the brain. Although, the Tau tangles appear in different parts of the brain in AD sufferers compared to CTE sufferers. Unlike CTE, the causes of AD are largely unknown. Both conditions are currently considered incurable.
A press release from the NIH explained just how refined the new test for corrupted Tau proteins was:
The test is extremely sensitive. For example, if a pinhead-sized sample of brain tissue from an Alzheimer’s patient were pulverized and diluted into a thousand gallons of liquid, the test still could detect tau seeds in a pinhead-sized volume of that dilution. The test is called AD RT-QuIC: Alzheimer’s disease real-time quaking induced conversion.
This kind of testing was first developed by the NIH a decade ago, geared towards detecting Creutzfeldt-Jakob Disease. Since then it has been tweaked to identify various other brain diseases, including Parkinson’s Disease (which is also caused by Tau protein clusters) and other forms of dementia.
Since this test was adapted to detect (and analyze the seeding activity of) Tau clumps associated with both AD and CTE, there are hopes that biological markers for those conditions might be discovered.
If the biological marker was discovered to be something that could be tested for in a living specimen, then treatment for AD and CTE could begin far earlier than what is currently possible. In their study the NIH scientists stated that cerebrospinal fluid (CSF) — the fluid that exists between the brain and the skull — might be the key to this.
Scientists believe that the AD RT-QuIC test could be developed to detect Tau seeds in CSF, which is something that can be collected from a living patient. The NIH study also stated that this new testing for Tau could also help research CTE and, “aid interpretation of experimental attempts to manipulate or halt the spread of pathological Tau aggregation throughout the brain.”