Chronic traumatic encephalopathy (CTE) is a type of neurodegenerative disease that includes ongoing and worsening problems with memory. CTE has been depicted in movies and television episodes–but not accurately.
Although CTE is a relatively new term, clinicians have known for almost a hundred years that repeated head trauma could cause memory problems. In 1928, Harrison Martland, a physician, published an article in the JAMA where he described “punch drunk syndrome” in boxers, especially those “of the slugging type who are usually poor boxers…and in second rate fighters used for training purposes.” [MARTLAND HS. PUNCH DRUNK. JAMA. 1928;91(15):1103–1107].Later termed “pugilistic dementia,” this syndrome included worsening memory problems, psychiatric problems (such as depression), personality changes, fluctuating emotions (such as inappropriate aggression), movement disorders (such as tremors), and unsteady gaits. In 1957, the term chronic traumatic encephalopathy arrived in the medical literature but there was very little scientific interest in the phenomenon because everyone thought this was a problem unique to boxers. In fact, from 1928 until 2005, scientific understanding of CTE came from post-mortem analysis of boxers’ brains. Scientists found neurofibrillary tangles and beta-amyloid plaque in the brains of these boxers. It wasn’t until 2005 when CTE pathology was found in the brain of a former National Football League player. In 2016, 11 years later, initial criteria for the neuropathological diagnosis of CTE were published.
CTE pathology have been discovered in the brains of football, soccer, rugby, and hockey players. The same pathology has also been noted in military personnel who experienced traumatic head injuries. But even research studies seem to contradict each other. For example, one group of researchers examined the brains of 226 deceased American football players and found CTE in 223 of the 226 brains. These same researchers concluded that the longer one played football, the greater the likelihood of CTE pathology. On the other hand, another group of researchers wanted to see if there was a relationship between length of one’s career, the position one played, and CTE if a group of professional hockey and football players. They analyzed the brains of 35 former football and former hockey players and discovered that less than half (48.6%) showed evidence of CTE. These same researchers did not find any relationship
between position played and duration of career with CTE pathology. However, this study is limited by its small sample size compared to the one with 266 participants.
Here is another bias that may affect these results. Families are more likely to approve brain donation if the person showed evidence of memory problems. This bias affects many studies because the brains that are donated are usually from people who showed signs of dementia. Individuals who played sports but who did not show signs of memory problems at the time of their death are less likely to have their brains donated to these research activities.
Is CTE the Same as Alzheimer’s Dementia?
Yes and no. Both Alzheimer’s dementia and CTE involve tau proteins. The tau proteins undergo the same changes that make them stick together and tangle up. It is the tangles in the neurons that kill off the neurons. The difference is where those tangles are found. In CTE, the tau tangles cluster close to blood vessels and in the “valleys” in the brain tissue, called sulci. We don’t see this in Alzheimer’s dementia. The tangles in AD seem to spread more evenly.
How are Alzheimer’s dementia, CTE, and Traumatic Brain Injuries Related?
Good question. According to the Alzheimer’s Association, people who have experienced traumatic brain injuries in early to midlife have a higher risk of developing dementia. There seems to be a “dose-dependent” relationship, meaning that more TBIs mean higher risks for AD. However, there has not been enough research to prove this relationship. There is some thought that TBIs cause CTE, which in turn cause Alzheimer’s. However, as I mentioned earlier, the CTE pathology is different from AD pathology.
Here is where the 3 may be connected. While we have biomarkers for AD—certain MRI findings, images from PET scans, and cerebral spinal fluid analyses—we don’t (yet) have ways of diagnosing CTE until after death. It may be that people who develop CTE are diagnosed with dementia, and maybe wrongly diagnosed with AD or another type of dementia. Another possibility is that damage from TBIs that result in CTE make the brain more vulnerable to AD. That is, the person may have had a risk for AD and the disease started nerve damage in the person’s 60s. However, they had enough neurons (cognitive reserve) to “make up” for the damage. But put two things together—AD AND CTE—and you see memory problems and other signs of dementia much earlier than if the traumatic brain injury and the resulting CTE never happened.
Does Having a TBI Automatically Mean Getting Dementia?
This is also where the research is all over the place. Two people experience a moderate TBI. One person never fully recovers—she has memory problems for years after the event. The second person does fully recover. Why? Nobody really knows.
What we do know is the what is good for the heart is good for the brain. If you have experienced a TBI and you are concerned about your risk for developing dementia down the road, you can help your odds of staying brain healthy by following some lifestyle changes. First, make sure you are doing everything you can do to improve your cardiovascular health. Exercise, get to your ideal body weight, keep your cholesterol numbers in the healthy range, and try the Mediterranean diet—it has been shown to be the best for brain health.
Second, rethink drinking patterns. Are you drinking more than the 1 standard daily drink for women, 2 standard daily drinks for men? Even if you are adhering to the guidelines, maybe cut down even more? I know in the past there were studies that suggested that one to two drinks a day were good for brain health. However, a recent study published from the UK analyzed MRIs from 36,678 health middle aged and older adults. They found that even 1-2 drinks a day were linked to shrinking brains—and the higher the alcohol amount, the more extensive the shrinkage! Yes, correlation does not equal causation, but these results were (no pun intended) sobering! Another study published in 2015 examined MRIs in recovering alcoholics. The MRIs were done after 1 week, 1 month, and 7.5 months of abstinence. White and grey brain matter volume increased during abstinence—in fact, positive changes were noted just after 7 days of abstinence.
Finally, exercise your brain: learn to do something new, perhaps an instrument or language or hobby. Recovery is an important part of exercise, which is why meditation is an important part of this balance. Meditation also helps to rein in anxiety and negative thoughts, further improving brain health. Spiritual practices also align with meditation.
In conclusion, there is not a lot that we do know about CTE. More research and studies are needed to better understand the relationship between TBIs and CTE.
 Mez J, Daneshvar DH, Abdolmohammadi B, Chua AS, Alosco ML, Kiernan PT, Evers L, Marshall L, Martin BM, Palmisano JN, Nowinski CJ, Mahar I, Cherry JD, Alvarez VE, Dwyer B, Huber BR, Stein TD, Goldstein LE, Katz DI, Cantu RC, Au R, Kowall NW, Stern RA, McClean MD, Weuve J, Tripodis Y, McKee AC. Duration of American Football Play and Chronic Traumatic Encephalopathy. Ann Neurol. 2020 Jan;87(1):116-131. doi: 10.1002/ana.25611. Epub 2019 Nov 23. PMID: 31589352; PMCID: PMC6973077.
 Schwab N, Wennberg R, Grenier K, Tartaglia C, Tator C, Hazrati LN. Association of Position Played and Career Duration and Chronic Traumatic Encephalopathy at Autopsy in Elite Football and Hockey Players. Neurology. 2021 Apr 6;96(14):e1835-e1843. doi: 10.1212/WNL.0000000000011668. Epub 2021 Feb 24. PMID: 33627496; PMCID: PMC8105967.
Dr. Rita Jablonski
Rita Jablonski, PhD, CRNP, FAAN, FGSA is a nurse practitioner, researcher, tenured professor, and former family caregiver. Her research and practice involve all aspects of dementia management; she is best known for non-drug strategies to address dementia-related behaviors.