User:Dscarpenter/sandbox

Screening Procedures
To date, all screening procedures that examine football players for brain damage have been post mortem. In 2013, Dr. Gary Small and colleagues developed an in vivo chemical tracer that can detect tau protein build up in living players. Dr. Small and his team invented this new chemical tracer, 2-(1-{6-[(2-[F-18]fluoroethyl)(methyl)amino]-2-naphthyl}ethylidene)malononitrile, or FDDNP, that could be used in positron emission tomography (PET). This new tracer measures for tau protein and amyloid plaque accumulation in human brains; symptoms of repetitive brain trauma among other things. Although tracers have been developed to screen for the build-up of tau proteins in the human brain, FDDNP is the first PET tracer that can be used in vivo in human trails. FDDNP was originally developed in an effort to detect Alzheimer’s in elderly individuals, thus the article was published in the journal of the American Association for Geriatric Psychiatry. However, because there are similarities between Alzheimer’s and the effects of chronic traumatic encephelopathy (CTE), FDDNP was used to study the extent of brain trauma in consenting, retired NFL players.

Dr. Small and colleagues performed a controlled experiment on retired NFL players and an equal number of control participants. Unfortunately the sample size was very small as only 5 players of the 19 contacted were eligible for the study. Though the sample size was small, a good range of positions were represented (linebacker, quarterback, offensive lineman, defensive lineman, and a center) and all players had played in the league at least 10 years. The players had to be at least 45 years of age and currently exhibit symptoms of cognitive and mood disruption. Control participants had to meet certain criteria as well to ensure that they were as similar as possible to the NFL players in order to eliminate any biases or confounding variables. Age, Body Mass Index (BMI), years of education, and family history of dementia were all selected as the selection criteria for control participants. All participants received intravenous injections of the FDDNP tracer and were tested over 4 weeks using PET imaging technology. The injection of the FDDNP tracer was successful, and the results of the study showed significant differences between the NFL players and control participants. The NFL players had significantly higher FDDNP signals than control participants, indicating a greater amount of tau protein accumulation. The cortical regions of all the participants studied showed no significant difference, but the NFL players had FDDNP levels that were significantly higher in the caudate, putamen, thalamus, sub thalamus, midbrain, and cerebellar white matter regions of the brain as compared to the control participants. In addition, a positive correlation was found between the number of head injuries the players sustained and the levels of FDDNP binding. This suggests that players with a more severe history of head trauma will likely have significantly more accumulation of tau protein. This, in turn, gives rise to the suggestion that a more sever history of head trauma will result in greater deterioration of the brain, cognitive functioning, and mood regulation.

The findings of the study were consistent with previous autopsy studies of individuals with CTE. The important distinction to make, however, is that the patients in Dr. Small’s study were not on the slab and walked out after testing was completed. This is monumental in the field of brain trauma and concussion research.