Chronic Traumatic Encephalopathy

What is CTE?

Chronic traumatic encephalopathy (CTE) is a condition, first noted in boxers, and now recognized as a serious problem for athletes in collision-contact sports, such as football and related sports and occupations. Encephalopathy refers to any disease, wide-spread throughout the brain, that changes the structure or functionality of the brain. It is evidenced by dementia, erratic thinking and behavior, and personality changes. It caused by repeated blows to the head, but symptoms may not appear until many years after the injuries.1 It appears that such trauma is necessary to the development of CTE, but is not alone the cause.2

CTE can be caused by some of the same events that give rise to PTSD. CTE is caused by repeated brain impact such as that experienced by military personnel exposed to explosive blast force, as well as numerous hits to the head from sports involvement. Researchers used MRSI to compare the hippocampal areas of veterans with blast-related mild traumatic brain injury and PTSD, finding that those exposed to blasts had more severe cognitive and neuromotor impairment.3


Beta-amyloid Plaque

CTE is similar to Alzheimer’s and Parkinson’s in that tau protein becomes too plentiful (hyperphosphorylated) leading to fibrous tangles around small blood vessels. Sometimes beta-amyloid plaque is present. Unlike Alzheimer’s, the aggregates are observed more quickly than in AD. And, unlike AD, they form around blood vessels in the furrows (sulci) of the wrinkled surface of the cerebral cortex, and then spread unevenly in the cortex. Researchers have discovered that the fibrous tangles first noted around blood vessels in the sulci also develop within the nucleus basalis neurons (an important cluster of neurons in the forebrain that are part of the cholinergic system), and contribute to disconnection of messaging. These neurons are rich in the transmitter acetylcholine with widespread connections to other parts of the brain.


The midbrain, which regulates movement (such as eye movement), is especially vulnerable to repeated mild impact. Researchers found that the amount of neurodegeneration in the midbrain is related to the amount of rotational acceleration experienced, and it was noted that some damage occurs even after a single season of college football.4 In addition, researchers have found that CTE also causes increased expression of phosphorylated tau and amyloid proteins in hippocampal (important for memory) and septal neurons (that play a role in reward/reinforcement mechanisms), resulting in diminishing these capabilities.

Metabolic Changes

N-acetyl-aspartate Levels Decrease.

There is evidence (in college ice hockey players) that after repetitive head impacts N-acetyl aspartate (NAA) levels decrease significantly in post-season compared to pre-season.5 The decrease in NAA was also noted in former NFL players. NAA, contained in neurons, is essential for neuronal mitochondrial function. Its presence indicates both density of nerve cells and nerve mitochondria integrity and reduced concentrations of NAA are common to different psychiatric disorders.

Choline Levels Decrease

In post-season ice hockey players researchers noted a decrease in choline.6 Choline is essential for keeping homocysteine levels low and preventing over-activation of the microglial system which removes waste products.

Glutamate, Glutathione, and Myo-inositol Levels Decrease

In the anterior of the brains of former NFL football players there was direct positive correlation between changed mood/ behavior and levels of: glutamate, 32% change; glutathione, 29%; myo-inositol, 26% change.7 Glutamate is an excitatory neurotransmitter with an important role in learning and memory. Myo-inositol is a carbohydrate that affects levels of neurotransmitters and how we experience anxiety. The antioxidant glutathione, when deficient, contributes to seizures, intellectual disability, and loss of coordination.8

Creatine Levels Decrease.

Early studies of NFL players that have suffered from concussions indicate that white matter signal abnormalities can occur, which as a result is associated with cognitive decline. This type of brain tissue helps you think fast, walk straight, and keeps you from falling.9


At early stages symptoms are:

Memory difficulties,
explosivity, and
executive dysfunction.

As the condition develops, patients experience problems with:

mood swings,
visuospatial difficulties,
progressive dementia, and

Risk Factors

The primary risk factor appears to be the number of times the head is struck, not the severity of individual blows as they can be mild.10 In the case of boxing, researchers found that the number of rounds fought was more indicative of CTE development rather than the number of knockouts. Researchers, however, are also beginning to think that CTE is caused by multiple factors. Any one of the following can account for many of the symptoms11

Repeated neurotrauma is necessary but not sufficient alone to cause CTE
Substance abuse
Chronic pain
Emotional stress such as athletic career transition stress

Other researchers suggest that the following are also factors.12

Neurodevelopmental disorders
Normal aging
Surgeries and anesthesia
Sleep difficulties .

Next: CTE Support


Note: additional sources of the above information are available in our guide to brain care, Natural Brain Care, or upon request.

1. Alzheimer's Association. Chronic Traumatic Encephalopathy. Retrieved Oct 1 2019 from
2. Gaetz M. (2017). The multi-factorial origins of Chronic Traumatic Encephalopathy (CTE) symptomology in post-career athletes: The athlete post-career adjustment (AP-CA) model. Med Hypotheses. May;102:130-143.
3. Kontos AP, Van Cott AC, Roberts J, Pan JW, Kelly MB, et al. (2017). Clinical and Magnetic Resonance Spectroscopic Imaging Findings in Veterans with Blast Mild Traumatic Brain Injury and Post-Traumatic Stress Disorder. Mil Med. Mar;182(S1):99-104.
4. Hirad AA, Bazarian JJ, Merchant-Borna K, Garcea FE, Heilbronner S, et al. (2019). A common neural signature of brain injury in concussion and subconcussion. Sci Adv. Aug 7;5(8):eaau3460.
5. Panchal H, Sollman N, Pasternak O, Alosco ML, Kinzel P, et al. (2018). Neuro-Metabolite Changes in a Single Season of Unniversity Ice Hockey Using Magnetic Resonance Spectroscopy. Front Neurol. Aug 20;9:616.
6. Ibid. Panchal. (2018).
7. Alosco ML, Tripodis Y, Rowland B, Chua AS, Liao H, et al. (2019). A magnetic resonance spectroscopy investigation in symptomatic former NFL players. Brain Imaging Behav. Mar 8.
8. NIH. Glutathione synthetase deficiency. Retrieved Oct 2 2019 from
9. Alosco ML, Koerte IK, Tripodis Y, Mariani M, Chua AS, et al. (2018). White matter signal abnormalities in former National Football League players. Alzheimers Dement (Amst). 2018:10:56-65.
10. Katsumoto A, Takeuchi H, Tanaka F. (2019). Tau Pathology in Chronic Traumatic Encephalopathy and Alzheimer's Disease: Similarities and Differences. Front Neurol. Sep 10;10:980.
11. Gaetz M. (2017). The multi-factorial origins of Chronic Traumatic Encephalopathy (CTE) symptomology in post-career athletes: The athlete post-career adjustment (AP-CA) model. Med Hypotheses. May;102:130-143.
12. Asken BM, Sullan MJ, Snyder AR, Houck ZM, Bryant VE, et al. (2016). Factors Influencing Clinical Correlates of Chronic Encephalopathy (CTE): a Review. Neuropsychol Rev. Dec;26(4):340-363.