How Cte Progresses Is Still Unknown

1041 WordsMar 17, 20175 Pages
The exact pathophysiology of how CTE progresses is still unknown. Dr. Bennet Omalu was one of the first authors who published a report describing CTE when he performed an autopsy on retired football player Mike Webester. In his report, Dr. Omalu took tissue samples from each layer and each part of Webster’s brain. The samples were first stained using the traditional hematoxylin and eosin stain (H&E). The H&E is the most widely used stain in histology and is referred to as the gold standard for microbiology. Eosin is an acidic compound that when applied to tissue that is basic in nature, turns the structure pink while hematoxylin is basic and turns acidic structures purple. For example, deoxyribonucleic acid (DNA), ribonucleic acid (RNA)…show more content…
1D), NFTs, neuritic threads, or Lewy bodies. The subcortical nuclei and brainstem, including the substantia nigra, contained no diffuse amyloid plaques, NFTs, neuritic threads, or Lewy bodies. There was no histological evidence of cerebral amyloid angiopathy. In Dr. Omalu’s published article in the journal entitled Clinical Neurosurgery, he explains that his clinical findings are similar to those discovered in a retired boxer during the 1950s. Twenty years later (from 1950), analogous findings were seen in an additional 15 former boxers who were recently deceased. At this time, these players were diagnosed with “punch-drunk” syndrome (McKee, et al., 2009). The common findings in both the retired boxers and Mike Webster were the presence of the “τ - neurofibrillary tangles (NFTs), the neocortical τ immunopositive neuritis, and amyloid plaques” (McKee, et al., 2009). The fact that the hippocampus was not affected by the neurofibrillary tangles is a distinct feature that is not seen in Alzheimer’s disease or in a standard aging brain (Omalu et al, 2005). Different biological cascades brought on by repeated head trauma are presumed to be the cause for these anatomical changes in the brain. Ischemic changes, vascular damage, and axonal destruction that are experienced in a head injury generate a chain of events that disrupt the normal neuronal cytoskeletal metabolism, resulting in a buildup of these

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