Boxing is undoubtedly an increasingly popular sport with as of 2016 there are over 205,000 people (• Boxing participation England 2006-2016 | UK Statistics,online, 12th December) participating in the sport. But however it is not all sunshine and rainbows for boxing as it is one of the most violent sports in the world where the main aim is to knock your opponent unconscious with brute force and well placed shots to the cranium (Head). This is the crux of the issue as this infamous, brutal and repeated head trauma is what cause the progressive degenerative brain disease Chronic traumatic encephalopathy, which in brief is when the repeated head trauma which causes the slow degeneration of the brain tissue and the introduction of the toxic protein known as Tau. So the question I am looking to answer is how can we protect those children under their age of 18 from this disease as the symptoms can appear years after the last head trauma and will have an exacerbated effect on the developing brain(Frequently Asked Questions about CTE | CTE Center, Online, 12th December),if has not become clear already this disease has an intrinsic link to boxing in that the disease is caused by repeated head trauma and this is the trademark of the sport. Hundreds of scientists and boxing professionals have attempted to solve this problem and I will be looking to their work fro inspiration, for example things such as “codswalloping” and going back to bare knuckle boxing, or the prospect of a full ban on boxing. In this extended project I will also be detailing the acute biological detail of the disease, who it affects and how, and lastly which rules and regulations require changing if any to make boxing a safer sport for the children under 18 years old.Though my stance on the issue will remain that we must endeavour to change as little as possible because the sport is becoming shorter and safer and to ruin the character of boxing would be criminal, changing all the rules and regulations and age limitations would be like changing the shape of a football so it doesn’t roll properly.Chronic traumatic encephalopathy was first discovered in 1928 by Dr. Harrison Martland who called it “punch drunk syndrome” because of the way it made sufferers behave in the short and long term. After this over the next 75 years many researchers reported finding similar symptoms in boxers and American football players. The actual pathology is very complex. There have been many studies of athletes ( e.g. Corsellis in 1973 in a study with 15 retired boxers, he first identified the pathology of Chronic traumatic encephalopathy) with repeated mild head trauma and these have produced consistent findings that have become the trademark signs of chronic traumatic encephalopathy. We see anterior Cavum septum pellucidum and posterior fenestrations as well, this happens when the impact shifts the brain within the head causing strain upon the tissues in the brain. There is also an enlargement of the lateral and third ventricle which has found to be common in chronic traumatic encephalopathy, as well as this enlargement we see a lot of atrophy in the brain, in the cerebrum the control centre for voluntary movement and complex sensory and neural function, this can thus lead to loss muscle and body control, like struggling to walk. Moreover as well as in the cerebrum there is an overall shrinkage in the brain and a reduction In brain mass which means there is a loss of brain cells and brain tissue and the components of the brain different lobes of the brain cannot properly perform their function, so we see symptoms such as memory loss and loss of cognitive function from the general atrophy of the brain. As I mentioned before, similar to Alzheimer’s disease we find a build up or clumping of the tau protein because of the fenestration of the microtubules and brain tissue the tau becomes phosphorylated and aggregates and polymerizes to form little colonies in a regionally irregular fashion in the brain. This accumulation of the tau protein becomes toxic to the brain which leads to neurodegeneration and the mood problems we see with short tempers and heavy mood swings as the limbic system becomes damaged thus the function is corrupted. The last consistent certain diagnosis we have for Chronic traumatic encephalopathy is the proteinopathy of the TDP-43 protein which is found in over 80% of chronic traumatic encephalopathy cases. It is found in the anterior horns of the spinal cord as well as the tau protein. The proteinopathy of the TDP-43 extends to the spine and manifest as motor neurone disease with an appearance that looks like amyotrophic lateral sclerosis which adds to the cognitive and body functionality problems experienced in the developed stages of the disease.