Studies have shown that TBI induces the rapid accumulation of proteins in brain tissue (in the cortex) similar to those found in neurodegenerative diseases, namely AD. The primary clue that indicated a potential link between AD and TBI was the Aβ (amyloid-Beta) plaque, a hallmark of AD, which was found within days in up to 30% of patients who died from a single incident of brain trauma in a study conducted by Roberts et al. 1994. A study on a pig model conducted by Smith et al., 1999 revealed that the plaques were found mainly in the white matter with axonal pathology as well as in layer III of the cortex; although, some models did reveal some accumulation in the grey matter. Aβ is derived via the sequential cleavage of the amyloid precursor protein (APP) by the β- and γ- secretase (Uryu et al., 2007). To be more precise, its aggregation is mediated by β-site APP-cleaving enzyme 1 (BACE1) of the β-secretase and presenilin, which is the active site of the γ- secretase (Blennow, …show more content…
The changes to the brain may occur in months or even years after the last trauma to the head. The concept of CTE was first introduced as the term “punch drunk” in 1928 by Martland and has been recognised as dementia pugilistica ever since. It is a disease characterised by the accumulation of the microtubule associated protein tau as neurofibrillary tangles (NFTS) and astrocytic tangles in several regions of the brain including the frontal and temporal cortices, diencephalon, basal ganglia, brainstem and cortical sulci . The tau pathology is perivascular in arrangement where it accumulates in damaged axons with impaired transport. In addition, Baugh and colleagues demonstrated that neuronal loss is evident in the hippocampus, entorhinal cortex, amygdala, and cerebral cortex, all which play a major role in the symptoms resulting from