Overview of Chronic Traumatic Encephalopathy

Chronic traumatic encephalopathy (CTE) is a progressive degenerative disease caused by repetitive blows to the head. This brain trauma typically comes in the form of concussions, a type of brain injury caused by a sudden blow to the head that jolts the brain and causes bruising, blood vessel damage and nerve injury. The nerve axons become damaged and adversely affect cell-to-cell communication, which gradually causes the brain to atrophy, or waste away. In addition, deposits of the proteins tau and TDP-43, and changes in white matter, occur in response to the disease.

Athletes that participate in sports like football, ice hockey and professional wresting are susceptible to CTE. It was first noticed in boxers, but it’s now apparent that the disease affects athletes of various sports and today its known that its prevalence is alarmingly high. In the December 2015 issue of Acta Neuropathologica, researchers at Mayo Clinic reported that about 33% of contact sport athletes would develop CTE. The team of scientists analyzed brains of former male contact-sport athletes. “About one-third of these men whose brains had been donated to the Mayo Clinic Brain Bank had evidence of CTE pathology,” the researchers at the Mayo Clinic explained in a press release.

The repetitive trauma to the brain causes symptoms that don’t become noticeable until about eight to 10 years after the repetitive trauma injury and the outset of the disease. Eventually, those with CTE will experience memory loss, confusion, impaired judgment, impulse control problems, depression, aggression, and in some cases, dementia.

While some of the changes that occur in the brain due to CTE are visible with brain imaging, currently, a diagnosis can only be made after death and during an autopsy. Once the pathological changes have begun, however, they will continue to have an effect and will progress throughout an individual’s life.

Currently, there is no cure for CTE. Preventing head injury is the best way to reduce the risk of CTE. In addition, following a concussion, an individual should be sure to follow the proper recovery protocol to help prevent additional brain injury.

Findings: Effects of Cannabis on Chronic Traumatic Encephalopathy

THC and other naturally occurring cannabinoids act on brain injury as a general neuroprotective agents with antioxidant properties, which can have crucial roles in treatment of Concussions, CTE and Traumatic Brain Injury.  Post-concussion syndrome is symptoms that can linger following a concussion. Studies have shown cannabis reduces damage caused from brain injuries and can help athletes manage the symptoms of the syndrome.

By definition, neuroprotection is an effect that may result in salvage, recovery or regeneration of the nervous system, its cells, structure and function. It is thought that there are many neurochemical modulators of nervous system damage. An antioxidant is a molecule that inhibits the oxidation of other molecules. Oxidation is a chemical reaction that can produce free radicals, leading to chain reactions that may damage cells. Antioxidants such as thiols or ascorbic acid (vitamin C) terminate these chain reactions. That’s right, just like vitamin C – THC and CBD all do the body good.

These cannabinoids as antioxidants and neuroprotectants are also why the U.S. Patent Office issued patent #6630507 to the U.S. Health and Human Services Department. The patent lists the use of certain cannabinoids found within the cannabis plant as useful in additional neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and HIV dementia.

Since cannabis contains compounds recognized and endorsed by an agency of the U.S. government- Why is it that cannabis remains on the Federal Schedule One list of drugs? As this patent is a direct contradiction of the government’s own definition for the classification of a Schedule I drug and it should provide the professional sports world reason enough to allow for the use of cannabis.

The non-psychoactive part of cannabis known, as CBD, also has the potential to treat and even prevent concussions. The NFL should set an example by investing in cannabis research to see how it can help improve the health of its players. The new studies have found that certain properties in cannabis can help shield the brain from injury. Like all cannabinoids, CBD helps the body by imitating the endocannabinoids produced in the body as part of the endocannabinoid system, and has also been found to have the potential to reduce inflammation in the brain when brain trauma occurs.

References

Castillo, A., Tolon, M.R., Fernandez-Ruiz, J., Romero, J., Martinez-Orgado, J. (2010, February). The neuroprotective effect of cannabidiol in an in vitro model of newborn hypoxic-ischemic brain damage in mice is mediated by CB(2) and adenosine receptors. Neurobiology of Disease, 37(2), 434-40.

Chronic traumatic encephalopathy. (2014, November 11). Mayo Clinic. Retrieved from http://www.mayoclinic.org/diseases-conditions/chronic-traumatic-encephalopathy/basics/definition/con-20113581.

Evidence suggests contact sports played by amateurs increase risk of degenerative disorder. (2015, December 1). Mayo Clinic. Retrieved from http://newsletter.carehubs.com/t/ViewEmail/j/2B6E3073A3AD413C/59F3204D88C0AFA89A8E73400EDACAB4.

Karantzoulis, S., and Randolph, C. (2013). Modern chronic traumatic encephalopathy in retired athletes: What is the evidence? Neuropsychology Review, 23, 350-360.

Ling, H., Kara, E., Revesz, T., Lees, A.J., Plant, G.T., Martino, D., Houlden, H., Hardy, J., and Holton, J. (2014). Concomitant progressive supranuclear palsy and chronic traumatic encephalopathy in a boxer. Acta Neuropathologica Communications, 2, 24.

Lopez-Rodriguez, A.B., Siopi, E., Finn, D.P., Marchand-Leroux, C., Garcia-Segura, L.M., Jafarian-Tehrani, M.H., and Viveros, M.P. (2013). CB1 and CB2 cannabinoid receptor antagonists prevent minocycline-induced neuroprotection following traumatic brain injury in mice. Cerebral Cortex. Retrieved from http://cercor.oxfordjournals.org/content/early/2013/08/19/cercor.bht202.abstract.

McKee, A. C., Cantu, R. C., Nowinski, C. J., Hedley-Whyte, E. T., Gavett, B. E., Budson, A. E., Santini, V.E., Lee, H.S., Kubilus, C.A., and Stern, R. A. (2009). Chronic Traumatic Encephalopathy in Athletes: Progressive Tauopathy following Repetitive Head Injury. Journal of Neuropathology and Experimental Neurology, 68(7), 709–735.

Pazos, M.R., Mohammed, N., Lafuente, H., Santos, M., Martinez-Pinilla, E., Moreno, E., Valdizan, E., Romero, J., Pazos, A., Franco, R., Hillard, C.J., Alvarez, F.J., Martinez-Orgado, J. (2013, August). Mechanisms of cannabidiol neuroprotection in hyopoxic-ischemic newborn pigs: role of 5HT(1A) and CB2 receptors. Neuropharmacology, 71, 282-91.

Shohami, E., Cohen-Yeshurun, A., Magid, L., Algali, M., & Mechoulam, R. (2011). Endocannabinoids and traumatic brain injury. British Journal of Pharmacology, 163(7), 1402–1410.

Tartaglia, M. C., Hazrati, L.-N., Davis, K. D., Green, R. E. A., Wennberg, R., Mikulis, D., Ezerins, L.J., Keightley, M., and, Tator, C. (2014). Chronic traumatic encephalopathy and other neurodegenerative proteinopathies. Frontiers in Human Neuroscience, 8, 30.

What is CTE? (n.d.). BU CTE Center. Retrieved from http://www.bu.edu/cte/about/what-is-cte/.

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