Cobbers on the Brain

Chronic Traumatic Encephalopathy, commonly known as CTE, is a neurodegenerative disease caused by repeated impacts to the head that lead to devastating mental and physical consequences. People with CTE struggle with emotional problems like aggression, depression and anxiety, cognitive decline and physical decline resembling Parkinson’s (1). But the worst part of CTE is that the victims do not know that they have it, as it can only be diagnosed after death through an autopsy. This leads to misdiagnosis of diseases like Alzheimer’s or Parkinson’s, and a lack of understanding of the behavior of the person with CTE while they are living, often leading to interpersonal troubles. There are currently no treatments for CTE as it is a relatively new concept and there are many questions still unanswered. Therefore, CTE is scary not only because of what it can do to you, but also because there is nothing you can do about it. CTE is devastating disease for patients and their loved ones, that is why you should do everything you can to prevent developing it, and the first step to doing that is to understand how CTE works.

How does CTE work?

To understand how CTE works we must talk about a protein called tau. This protein is essential to stabilizing the structure of neurons. When someone has repeated head impacts, structures that have tau n them gets stretched out, and our body’s response phosphorylates the tau in the wrong way. When broken down into simpler terms, when you experience a head impact, it causes tau proteins to become loose from the microtubules. Once tau is loose, it is considered pathological, essentially meaning it is not good and can cause disease. Due to the repeated head impacts, this issue with tau phosphorylation never resolves and leads to the spread of disease even between injuries. Eventually, these loose tau proteins start to aggregate together and create something known neurofibrillary tangles, or NFTs for short. These NFTs act as barriers for cellular transport, almost like a spider web that things that are essential for cellular survival get caught in. When this happens, the cell cannot function properly and leads to the starvation of the cell and eventually degeneration and cell death. (2)

What can you do to prevent CTE?

While CTE can develop in anyone, most people who develop it are military personnel who worked with heavy explosives, such as artillerymen, and athletes of contact sports like football, soccer or hockey. Football players are especially at risk, experiencing multiple head impacts every time they play. A study by Boston University examined the brains of football players and found that 99% of former NFL players, 91% of college players and 21% of high school players had CTE. While the study experienced sample bias, with those who donated their brains having shown some signs of CTE rather than a wider population of players, these findings are still extremely alarming.

The only thing you can do to avoid CTE is to avoid head impacts altogether, although this isn’t very realistic for those who play contact sports (3). Finding ways to reduce the frequency of head hits and preventing more impactful hits that result in concussions is essential to avoiding CTE. One study (keep in mind it was not peer-reviewed) conducted by the NFL found that wearing a guardian cap reduced concussions by 50%. Also, making sure your gear is fitted properly is essential to maximizing the force the equipment absorbs. Another way to prevent CTE is to properly recover from concussions. One of the hardest things for an athlete to do it sit out and watch, especially when they feel more or less fine. While you may feel better after a couple days, it takes 2-4 weeks for a concussion to fully recover and returning to action while you are still recovering is not only detrimental for your recovery, but also a risk factor for CTE (4).

Be scared, but not too scared

CTE is a very scary disease for athletes and their parents. While you should definitely do everything you can to avoid repeated head impacts, it is important to remember that everybody experiences a countless number of head impacts throughout their lives. Constantly worrying about every hit your head takes will do you no good. Also, if you are a football player, it can be haunting to hear what CTE is and what it does to you but the majority of people who play football live long and fulfilling lives. It is important to wear protective equipment, wear the equipment properly, and to take the time to recover after getting a concussion. In all, be aware of CTE and its effects, but don’t let it stop you from living your life to the fullest!

1. Lakhan, S. E., & Kirchgessner, A. (2012). Chronic traumatic encephalopathy: the dangers of getting “dinged”. SpringerPlus, 1, 2. https://doi.org/10.1186/2193-1801-1-2
2. Iqbal, K., Liu, F., Gong, C. X., Alonso, A.delC., & Grundke-Iqbal, I. (2009). Mechanisms of tau-induced neurodegeneration. Acta neuropathologica, 118(1), 53–69. https://doi.org/10.1007/s00401-009-0486-3
3. Cleveland Clinic. (2025). Chronic Traumatic Encephalopathy (CTE). Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/17686-chronic-traumatic-encephalopathy-cte
4. Giza, C. (2021). Recovering from a concussion: 5 tips for your child’s successful healing. UCLA Health. https://www.uclahealth.org/news/article/recovering-from-a-concussion-5-tips-for-your-childs-successful-healing

Concussions and Neuroinflammation: What Happens After Impact

When someone experiences a concussion, also known as a mild traumatic brain injury (mTBI), the damage is not always apparent through symptoms. Instead, much of the injury occurs on a chemical level inside the brain. After the initial impact, researchers have observed multiple pathologies to TBIs, including ionic flux, glutamate release, energy crisis, cytoskeletal damage, axonal dysfunction, and altered neurotransmission.[1] To read more about these processes, click here. One of the most important pathologies involved is neuroinflammation.

Many people assume inflammation in the brain only happens when the blood-brain barrier is damaged, allowing harmful substances to leak in. However, neuroinflammation can occur independently of changes in blood-brain barrier permeability. Brain cells, such as microglia and astrocytes, can trigger an inflammatory response and secrete cytokines on their own. These cells become activated after a concussion and invoke an immune response in the brain, including neuroinflammation.[2]

The Brain’s Inflammatory Response After a Concussion:

Inflammation following a mild traumatic brain injury can be either beneficial or detrimental, depending on how long it lasts and how intense it becomes. In the early stages, inflammation can help protect neurons and support recovery. Problems arise when this response becomes excessive or prolonged.

Several cytokines play major roles in this process:[3]

Interleukin-1 (IL-1) is part of a family of cytokines, although the most important forms are IL-1α and IL-1β. IL-1α spikes immediately after a concussion, while IL-1β increases gradually over several days. The levels of these cytokines depend on the severity of the trauma. IL-1β also stimulates the release of other pro-inflammatory molecules, including tumor necrosis factor-alpha. When IL-1 is hypersecreted, it can create a toxic inflammatory environment that can result in cell death in severe cases.

Tumor Necrosis Factor-Alpha (TNF-α) rises rapidly and usually returns to normal within 24 hours of the initial injury. TNF-α can also be protective or harmful. Its response depends on which receptor it binds to. Binding to the p55 receptor is associated with pathological effects, while binding to the p75 receptor supports neuroprotection.

Interleukin-6 (IL-6) has both pro- and anti-inflammatory roles and is stimulated by TNF-α. High levels of IL-6 have been detected for weeks after severe injury. One benefit of IL-6 is that it increases the production of nerve growth factor in astrocytes, which helps suppress TNF-α and IL-1β. This suppression keeps levels from rising too high and causing neurotoxicity.

Transforming Growth Factor-β (TGF-β) is an anti-inflammatory cytokine that peaks within 24 hours of injury and promotes tissue repair by suppressing inflammation. However, excessive levels can interfere with the brain’s own repair mechanisms and increase vulnerability to infection.

If you are interested in reading more about the involvement and effects of these cytokines in neuroinflammation, click here.

Why This Matters:

Although neuroinflammation can be harmful, it is also essential for neuronal growth and recovery after concussion and can even be used as a promising treatment option.  Understanding the timing and interaction of these cytokines suggests that future treatments may focus on carefully timed combinations of pro- and anti-inflammatory molecules to reduce long-term neurological deficits after mTBI.[4]

[1] Giza and Hovda, “The New Neurometabolic Cascade of Concussion.”

[2] Patterson and Holahan, “Understanding the Neuroinflammatory Response Following Concussion to Develop Treatment Strategies.”

[3] Patterson and Holahan, “Understanding the Neuroinflammatory Response Following Concussion to Develop Treatment Strategies.”

[4] Patterson and Holahan, “Understanding the Neuroinflammatory Response Following Concussion to Develop Treatment Strategies.”