Forensic pathologist Dr. Bennet Omalu (who was played by Will Smith in the recent “Concussion” movie) first discovered that football players were susceptible to CTE. Initially, CTE was referred to as dementia pugilistica, or punch-drunk syndrome, and had only been diagnosed in boxers. After discovering CTE in former Pittsburgh Steelers’ Hall of Famer Mike Webster’s brain, Omalu named the syndrome chronic traumatic encephalopathy. “Chronic meant long-term, traumatic referred to trauma, and encephalopathy was a damaged brain,” so its earlier use could be referenced in medical literature.
Omalu explored Mike Webster’s brain on a hunch. Webster died at the age of fifty of a heart attack, but Omalu found everything surrounding his death fairly unusual in light of Webster’s erratic behavior towards the end of his life. Although Webster’s cause of death was a heart attack, Omalu decided to investigate further than the routine autopsy and study Webster’s brain.
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At first Omalu, who is certified in neuropathology (as well as a number of other medical fields), did not notice any abnormalities from looking at Webster’s brain, nor from the CT and MRI scans. It was not until Omalu actually sliced the brain and analyzed it on specialized stained slides under a microscope that he found what caused Webster’s demise: large accumulations of tau proteins that killed his brain cells, including cells in regions that control emotions and executive functions. A brain affected by CTE will gradually deteriorate over time, and eventually the brain itself can even lose mass.
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Thus far, the only definitive detection method of CTE must be done posthumously; therefore, the focus of the National Institutes of Health’s (NIH) research is to develop a diagnosis for living patients. Once researchers can establish who actually has CTE, they can begin to understand why certain players are susceptible. Eventually, the goal is to find ways to prevent players from having CTE, but first more research must be conducted in order to develop a better understanding of the disease.
Since Omalu’s discovery and rise in public awareness of CTE, many questions have been raised regarding the disease mechanism and diagnosis. In 2013, a potential detection method for CTE in living patients was studied at the Semel Institute for Neuroscience and Human Behavior at UCLA. The study looked at five former NFL players, all of whom were at least 45 years old, who suffered at least one concussion during their careers. The retired players all were given positron emission tomography (PET) scans after receiving intravenous injections of FDDNP.
FDDNP is a chemical marker that can bind tau protein tangles, as well as amyloid beta plaques, that are deposited in the brain. It is often utilized to identify Alzheimer’s disease in the brain. FDDNP can be detected by PET scans, proving as a potential neuro-imaging marker by revealing which of the players had accumulations of tau proteins consistent with those who have been diagnosed with CTE posthumously.
The Brain Injury Research Institute, co-founded by Dr. Julian Bailes, Dr. Bennet Omalu, and Robert P. Fitzsimmons, funded UCLA’s study. Bailes spoke of the results from this study, “For the first time, it opens the possibility we can intervene and stop the inexorable decline [of those suffering from CTE]… We are connecting more dots. This was the holy grail of C.T.E.”
New findings from the original 2013 study were published in 2015, advancing this potential detection method. Fourteen former NFL players were given PET scans with FDDNP in an attempt to identify tau distributions consistent with those confirmed to have CTE posthumously. The tau deposits that were identified in PET scans also appeared to be distinctively different from Alzheimer’s disease patients. Bailes noted that “Our preliminary data seems very strong that the areas of the brain and density of the tau signals correlates exactly with what we have found at autopsy.” The players who were identified as showing signs of CTE, based on the results of the PET scan, were informed of their status.
The Food and Drug Administration (FDA) criticized the researchers of the UCLA study for overstating the capabilities of FDDNP after the players that were informed that they exhibited signs of CTE publicly announced that they actually had CTE. The FDA wrote that “these claims and presentations suggest in a promotional context that FDDNP, an investigational new drug, is safe or effective for such uses, when F.D.A. has not approved FDDNP for any use,” in a letter to the UCLA researchers.
Although the results were not completely conclusive in diagnosing CTE, this research demonstrates that researchers have taken another step in the direction of finding a diagnosis tactic.
In April 2015, a neuropathological criteria for diagnosing CTE was established—perivascular patterned accumulations of tau in neurons and neurites. This pattern, that was reported by Ann McKee, MD, of Boston University, was identified as being specific to CTE. A component specific to CTE was noted: the accumulations of tau were often distributed around blood vessels, which made CTE unique from other tauopathies. “This defines, crystallizes, and objectifies some of the uncertainties of CTE, and establishes by expert consensus the standards for the neuropathological tissue diagnosis of CTE,” explained Bailes. Further validating previous findings regarding CTE, these indications were only found on patients that had suffered brain trauma, and were more prevalent in those who had suffered multiple brain traumas.
The NIH launched a research effort to define and differentiate the pathological characteristics of CTE from a cognitive impairment like Alzheimer’s disease in 2013, since there were critiques from researchers that CTE is not distinctive enough to be its own disease. The NIH has the ultimate goal of diagnosing CTE in living patients with imaging tools and by establishing a neuropathological criteria. This research has officially shown tangible results, which according to McKee is the the first advancement in characterizing CTE, although there still are no established correlations between clinical symptoms and the trademark pathological components of CTE—thus, further research is still necessary.
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NFL players are highly susceptible to brain trauma, which heightens the correlation of players developing a brain disease like CTE after playing a career in the NFL. The NIH’s study on this pressing issue is considered to be a very ambitious project that could yield groundbreaking results. The NFL was supposed to fund the seven-year, $16 million initiative from the $30 million research grant the League gave the NIH. Instead, Boston University announced that this project will be funded by the NIH. The NIH awarded this research initiative to Dr. Robert Stern, a researcher from Boston University.
ESPN reported that the NFL was not contributing to this research initiative, though the NFL challenged that report for its inaccuracies. In their report, ESPN indicated that the NFL prohibited the NIH from using funds from the League’s grant for this study. ESPN also noted that the NFL vetoed the grant money being used because of the selection of Dr. Stern for the study, likely since he has criticized the NFL in the past.
In response, the League stressed that it was the NIH’s decision to fund this project and that their $30 million grant is still available for use at the NIH’s discretion. The Foundation for the NIH released a statement that confirmed the NFL’s claims: “The NFL funding commitment to SHRP remains intact. NFL was willing to contribute to the Boston University CTE study headed by Dr. Stern. NIH made the decision to fund this study in its entirety and to issue a Request for Applications (RFA) early next year to support an additional study on CTE using funds from SHRP, which will double the support for research in this area.”
The conflicting reports between the NFL and ESPN concerned House Democrats over whether the NFL has “veto power” over how the NIH distributes the funds from the League’s grant. Representatives Frank Pallone Jr. (D-NJ), Gene Green (D-TX), Jan Schakowsky (D-IL), and Diana DeGette (D-CO) wrote in a letter to NIH Director Francis Collins that “We are concerned about the potential implications of outside entities attempting to exercise ‘veto power’ or other influence over the selection of NIH research applicants, and we therefore seek to better understand the role the NFL has played in the allocation and administration of its $30 million ‘unrestricted’ donation.”
Rather than directing the NFL’s funds to the NIH’s project that is looking to diagnose CTE in living patients, the League’s money has been dispersed to smaller research initiatives on spinal cord injuries and a project looking at the prevalence of CTE and how to diagnose it posthumously.
Diagnosis through an autopsy has already been established, so it seems odd to focus on that aspect of the disease when its diagnosis in living patients would likely be more effective since it is still unknown. Then again, the NFL has attempted to minimize all of the previous work done on CTE (and how to diagnose it posthumously).
In fact, after Omalu published his first paper on CTE, Dr. Elliot Pellman (a rheumatologist without experience in neuroscience) led the NFL’s Mild Traumatic Brain Injury (MTBI) committee to request a retraction of the paper stating, “Omalu et al’s description of chronic traumatic encephalopathy is completely wrong. The diagnosis of a chronic condition requires a medical history indicating a long-standing nature of the illness… Such a history is completely lacking in [Omalu et al.s’] report.” Pellman’s eventual replacement, Dr. Ira Casson, actually denied the existence of a connection between brain injuries in NFL players and long-term problems like depression, dementia, or any other brain damage.
The NFL further damaged their credibility on traumatic brain injuries after Casson said, “In my opinion, the only scientifically valid evidence of a chronic encephalopathy in athletes is in boxers and in some Steeplechase jockeys. It’s never been scientifically validly documented in any other athletes… Anecdotes do not make scientifically valid evidence. I am a man of science. I believe in empirically determined scientifically valid data. And that is not scientifically valid data.”
The NFL has certainly taken strides in concussion management with initiatives like the NFL Head Health Challenge, but actually attempting to understand CTE is noteworthy after significantly polarizing itself from most of the neuroscience community. Maybe the NFL is finally looking to understand CTE from the very beginning of its discovery in NFL players, which began with diagnosis through an autopsy.
On the other hand, that research has been done numerous times already and could be understood by reviewing the already published studies, so the NFL’s resources could be better utilized in an area that actually needs further research.
If the NFL does not have any power in controlling the distribution of the grant, then this could simply be a decision of the NIH. By using funds from the NFL, the NIH could feel unintentionally restrained in researching something that will most likely further damage the NFL’s reputation, or that the integrity of the study could be questioned because of the link to the League. While the NIH does not have a duty to protect the NFL, they may feel an obligation when using their funds. Whether this was a decision of the NFL or NIH, the credibility of the NFL in regards to concussions and CTE has already been tarnished, which is why many are so skeptical of the League’s intentions and are so quick to believe ESPN’s scathing report.
Regardless, the potentially groundbreaking research is being funded and conducted, and the NIH has the freedom to find an answer without being concerned with any potential restraints due to any underlying obligations from using NFL funds.